Journal articles on the topic 'PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)'
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Veetil, Aneesh T., Junyi Zou, Katharine W. Henderson, Maulik S. Jani, Shabana M. Shaik, Sangram S. Sisodia, Melina E. Hale, and Yamuna Krishnan. "DNA-based fluorescent probes of NOS2 activity in live brains." Proceedings of the National Academy of Sciences 117, no. 26 (June 17, 2020): 14694–702. http://dx.doi.org/10.1073/pnas.2003034117.
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Innate immune cells destroy pathogens within a transient organelle called the phagosome. When pathogen-associated molecular patterns (PAMPs) displayed on the pathogen are recognized by Toll-like receptors (TLRs) on the host cell, it activates inducible nitric oxide synthase (NOS2) which instantly fills the phagosome with nitric oxide (NO) to clear the pathogen. Selected pathogens avoid activating NOS2 by concealing key PAMPs from their cognate TLRs. Thus, the ability to map NOS2 activity triggered by PAMPs can reveal critical mechanisms underlying pathogen susceptibility. Here, we describe DNA-based probes that ratiometrically report phagosomal and endosomal NO, and can be molecularly programmed to display precise stoichiometries of any desired PAMP. By mapping phagosomal NO produced in microglia of live zebrafish brains, we found that single-stranded RNA of bacterial origin acts as a PAMP and activates NOS2 by engaging TLR-7. This technology can be applied to study PAMP−TLR interactions in diverse organisms.
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Chen, Jiann Chu. "The complex of damage-associated molecular pattern and its inducer, pathogen-associated molecular pattern enhance triggering innate immunity in shrimp (VET1P.1128)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 146.16. http://dx.doi.org/10.4049/jimmunol.194.supp.146.16.
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Abstract Peptidoglycan (PG) derived commonly from Gram-positive bacteria, is one of pathogen-associated molecular pattern (PAMP). Incubating hemocytes of shrimp in PG caused degranulation, changes in cell size, reduction in the percentage of cell viability, necrosis of hemocytes, and released intracellular molecules containing damage-associated molecular pattern (DAMP) that is well known in mammals and teleosts. Incubating shrimp hemocytes in PAMP, DAMP or the mixture of PAMPs plus DAMPs all induced significant increases in phenoloxidase (PO) activity and respiratory burst (RB, release of superoxide anion) in vitro. The PO activity and RB induced by the mixture of DAMP-PAMP were much greater than that induced by DAMP alone or PAMP alone. In conclusion, the mixture of DAMP-PAMP cause enhancement in eliciting innate immunity of shrimp. This is the first study to confirm that cell necrosis caused by PAMPs releases intracellular molecules, DAMPs, and the mixture of DAMP-PAMP elicit the innate immunity in an invertebrate.
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Göhre, Vera, Alexandra M. E. Jones, Jan Sklenář, Silke Robatzek, and Andreas P. M. Weber. "Molecular Crosstalk Between PAMP-Triggered Immunity and Photosynthesis." Molecular Plant-Microbe Interactions® 25, no. 8 (August 2012): 1083–92. http://dx.doi.org/10.1094/mpmi-11-11-0301.
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The innate immune system allows plants to respond to potential pathogens in an appropriate manner while minimizing damage and energy costs. Photosynthesis provides a sustained energy supply and, therefore, has to be integrated into the defense against pathogens. Although changes in photosynthetic activity during infection have been described, a detailed and conclusive characterization is lacking. Here, we addressed whether activation of early defense responses by pathogen-associated molecular patterns (PAMPs) triggers changes in photosynthesis. Using proteomics and chlorophyll fluorescence measurements, we show that activation of defense by PAMPs leads to a rapid decrease in nonphotochemical quenching (NPQ). Conversely, NPQ also influences several responses of PAMP-triggered immunity. In a mutant impaired in NPQ, apoplastic reactive oxygen species production is enhanced and defense gene expression is differentially affected. Although induction of the early defense markers WRKY22 and WRKY29 is enhanced, induction of the late markers PR1 and PR5 is completely abolished. We propose that regulation of NPQ is an intrinsic component of the plant's defense program.
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Peng, Yujun, Rowan van Wersch, and Yuelin Zhang. "Convergent and Divergent Signaling in PAMP-Triggered Immunity and Effector-Triggered Immunity." Molecular Plant-Microbe Interactions® 31, no. 4 (April 2018): 403–9. http://dx.doi.org/10.1094/mpmi-06-17-0145-cr.
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Plants use diverse immune receptors to sense pathogen attacks. Recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors localized on the plasma membrane leads to PAMP-triggered immunity (PTI). Detection of pathogen effectors by intracellular or plasma membrane–localized immune receptors results in effector-triggered immunity (ETI). Despite the large variations in the magnitude and duration of immune responses triggered by different PAMPs or pathogen effectors during PTI and ETI, plasma membrane–localized immune receptors activate similar downstream molecular events such as mitogen-activated protein kinase activation, oxidative burst, ion influx, and increased biosynthesis of plant defense hormones, indicating that defense signals initiated at the plasma membrane converge at later points. On the other hand, activation of ETI by immune receptors localized to the nucleus appears to be more directly associated with transcriptional regulation of defense gene expression. Here, we review recent progress in signal transductions downstream of different groups of plant immune receptors, highlighting the converging and diverging molecular events.
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Yan, Qing, Conner J. Rogan, and Jeffrey C. Anderson. "Development of a Pseudomonas syringae–Arabidopsis Suspension Cell Infection System for Investigating Host Metabolite-Dependent Regulation of Type III Secretion and Pattern-Triggered Immunity." Molecular Plant-Microbe Interactions® 32, no. 5 (May 2019): 527–39. http://dx.doi.org/10.1094/mpmi-10-18-0295-fi.
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The importance of pattern-triggered immunity (PTI) in plant defense has been clearly established through genetic studies of mutants lacking functional pattern recognition receptors (PRRs) and signaling components downstream of PRR activation. Despite extensive knowledge of PRR-mediated signaling responses to pathogen-associated molecular patterns (PAMPs), little is known about which of these responses, if any, are directly responsible for limiting bacterial growth. In this work, we established a protocol for coculturing the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and Arabidopsis suspension cells. The system closely mirrors infection processes that occur in leaves, with bacteria relying on the type III secretion system (T3SS) for maximal growth and PAMP-induced plant defenses effectively limiting bacterial growth. To demonstrate the utility of this system, we investigated the molecular basis of PAMP-induced growth inhibition and discovered that T3SS-associated genes are inhibited when DC3000 is cocultured with PAMP-treated plant suspension cells. To determine the underlying mechanism of decreased T3SS gene expression, we performed metabolomics and biochemical analyses of suspension cell exudates and identified 14 metabolites that significantly increased or decreased following PAMP treatment. Citric acid, a known inducer of T3SS gene expression in DC3000, was among several organic acids decreased in exudates from PAMP-treated plant cells. Exogenous addition of citric acid increased T3SS gene expression and partially recovered growth of DC3000 in the presence of PAMP-treated cells, indicating that a portion of PAMP-induced defense in this system is decreased extracellular release of this metabolite. We envision that the well-defined infection conditions of this coculture system will be valuable for quantitative studies of type III effector delivery by P. syringae. Furthermore, this system provides a unique ‘top-down’ approach to unravel the molecular basis of PTI against P. syringae.
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Shen, Qiujing, Gildas Bourdais, Huairong Pan, Silke Robatzek, and Dingzhong Tang. "Arabidopsis glycosylphosphatidylinositol-anchored protein LLG1 associates with and modulates FLS2 to regulate innate immunity." Proceedings of the National Academy of Sciences 114, no. 22 (May 15, 2017): 5749–54. http://dx.doi.org/10.1073/pnas.1614468114.
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Plants detect and respond to pathogen invasion with membrane-localized pattern recognition receptors (PRRs), which recognize pathogen-associated molecular patterns (PAMPs) and activate downstream immune responses. Here we report that Arabidopsis thaliana LORELEI-LIKE GPI-ANCHORED PROTEIN 1 (LLG1), a coreceptor of the receptor-like kinase FERONIA, regulates PRR signaling. In a forward genetic screen for suppressors of enhanced disease resistance 1 (edr1), we identified the point mutation llg1-3, which suppresses edr1 disease resistance but does not affect plant growth and development. The llg1 mutants show enhanced susceptibility to various virulent pathogens, indicating that LLG1 has an important role in plant immunity. LLG1 constitutively associates with the PAMP receptor FLAGELLIN SENSING 2 (FLS2) and the elongation factor-Tu receptor, and forms a complex with BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 in a ligand-dependent manner, indicating that LLG1 functions as a key component of PAMP-recognition immune complexes. Moreover, LLG1 contributes to accumulation and ligand-induced degradation of FLS2, and is required for downstream innate immunity responses, including ligand-induced phosphorylation of BOTRYTIS-INDUCED KINASE 1 and production of reactive oxygen species. Taken together, our findings reveal that LLG1 associates with PAMP receptors and modulates their function to regulate disease responses. As LLG1 functions as a coreceptor of FERONIA and plays central roles in plant growth and development, our findings indicate that LLG1 participates in separate pathways, and may suggest a potential connection between development and innate immunity in plants.
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Pandya, Unnati, Chinaza Egbuta, Trefa Abdullah Norman, Chih-Yuan Chiang, Valerie Wiersma, Rekha Panchal, Edwin Bremer, Paul Eggleton, and Leslie Gold. "The Biophysical Interaction of the Danger-Associated Molecular Pattern (DAMP) Calreticulin with the Pattern-Associated Molecular Pattern (PAMP) Lipopolysaccharide." International Journal of Molecular Sciences 20, no. 2 (January 18, 2019): 408. http://dx.doi.org/10.3390/ijms20020408.
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The endoplasmic reticulum (ER) chaperone protein, calreticulin (CRT), is essential for proper glycoprotein folding and maintaining cellular calcium homeostasis. During ER stress, CRT is overexpressed as part of the unfolded protein response (UPR). In addition, CRT can be released as a damage-associated molecular pattern (DAMP) molecule that may interact with pathogen-associated molecular patterns (PAMPs) during the innate immune response. One such PAMP is lipopolysaccharide (LPS), a component of the gram-negative bacterial cell wall. In this report, we show that recombinant and native human placental CRT strongly interacts with LPS in solution, solid phase, and the surface of gram-negative and gram-positive bacteria. Furthermore, LPS induces oilgomerization of CRT with a disappearance of the monomeric form. The application of recombinant CRT (rCRT) to size exclusion and anion exchange chromatography shows an atypical heterogeneous elution profile, indicating that LPS affects the conformation and ionic charge of CRT. Interestingly, LPS bound to CRT is detected in sera of bronchiectasis patients with chronic bacterial infections. By ELISA, rCRT dose-dependently bound to solid phase LPS via the N- and C-domain globular head region of CRT and the C-domain alone. The specific interaction of CRT with LPS may be important in PAMP innate immunity.
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Goto, Yukihisa, Noriko Maki, Yasunori Ichihashi, Daisuke Kitazawa, Daisuke Igarashi, Yasuhiro Kadota, and Ken Shirasu. "Exogenous Treatment with Glutamate Induces Immune Responses in Arabidopsis." Molecular Plant-Microbe Interactions® 33, no. 3 (March 2020): 474–87. http://dx.doi.org/10.1094/mpmi-09-19-0262-r.
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Plant resistance inducers (PRIs) are compounds that protect plants from diseases by activating immunity responses. Exogenous treatment with glutamate (Glu), an important amino acid for all living organisms, induces resistance against fungal pathogens in rice and tomato. To understand the molecular mechanisms of Glu-induced immunity, we used the Arabidopsis model system. We found that exogenous treatment with Glu induces resistance against pathogens in Arabidopsis. Consistent with this, transcriptome analyses of Arabidopsis seedlings showed that Glu significantly induces the expression of wound-, defense-, and stress-related genes. Interestingly, Glu activates the expression of genes induced by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns at much later time points than the flg22 peptide, which is a bacterial-derived PAMP. The Glu receptor-like (GLR) proteins GLR3.3 and GLR3.6 are involved in the early expression of Glu-inducible genes; however, the sustained expression of these genes does not require the GLR proteins. Glu-inducible gene expression is also not affected by mutations in genes that encode PAMP receptors (EFR, FLS2, and CERK1), regulators of pattern-triggered immunity (BAK1, BKK1, BIK1, and PBL1), or a salicylic acid biosynthesis enzyme (SID2). The treatment of roots with Glu activates the expression of PAMP-, salicylic acid-, and jasmonic acid-inducible genes in leaves. Moreover, the treatment of roots with Glu primes chitin-induced responses in leaves, possibly through transcriptional activation of LYSIN-MOTIF RECEPTOR-LIKE KINASE 5 (LYK5), which encodes a chitin receptor. Because Glu treatment does not cause discernible growth retardation, Glu can be used as an effective PRI.
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Stączek, Sylwia, Agnieszka Zdybicka-Barabas, Iwona Wojda, Adrian Wiater, Paweł Mak, Piotr Suder, Krzysztof Skrzypiec, and Małgorzata Cytryńska. "Fungal α-1,3-Glucan as a New Pathogen-Associated Molecular Pattern in the Insect Model Host Galleria mellonella." Molecules 26, no. 16 (August 23, 2021): 5097. http://dx.doi.org/10.3390/molecules26165097.
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Recognition of pathogen-associated molecular patterns (PAMPs) by appropriate pattern recognition receptors (PRRs) is a key step in activating the host immune response. The role of a fungal PAMP is attributed to β-1,3-glucan. The role of α-1,3-glucan, another fungal cell wall polysaccharide, in modulating the host immune response is not clear. This work investigates the potential of α-1,3-glucan as a fungal PAMP by analyzing the humoral immune response of the greater wax moth Galleria mellonella to Aspergillus niger α-1,3-glucan. We demonstrated that 57-kDa and 61-kDa hemolymph proteins, identified as β-1,3-glucan recognition proteins, bound to A. niger α-1,3-glucan. Other hemolymph proteins, i.e., apolipophorin I, apolipophorin II, prophenoloxidase, phenoloxidase activating factor, arylphorin, and serine protease, were also identified among α-1,3-glucan-interacting proteins. In response to α-1,3-glucan, a 4.5-fold and 3-fold increase in the gene expression of antifungal peptides galiomicin and gallerimycin was demonstrated, respectively. The significant increase in the level of five defense peptides, including galiomicin, corresponded well with the highest antifungal activity in hemolymph. Our results indicate that A. niger α-1,3-glucan is recognized by the insect immune system, and immune response is triggered by this cell wall component. Thus, the role of a fungal PAMP for α-1,3-glucan can be postulated.
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Imamura, Yasuhiro, Yoshimasa Makita, Kazuya Masuno, and Hourei Oh. "Inhibitory Mechanism of IL-6 Production by Orento in Oral Squamous Cell Carcinoma Cell Line CAL27 Stimulated by Pathogen-Associated Molecular Patterns from Periodontopathogenic Porphyromonas gingivalis." International Journal of Molecular Sciences 24, no. 1 (December 31, 2022): 697. http://dx.doi.org/10.3390/ijms24010697.
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Orento is a traditional Japanese medicinal kampo preparation that is also prescribed in oral care. In oral squamous cell carcinoma cell line CAL27, orento significantly inhibited periodontopathogenic bacterium Porphyromonas gingivalis lipopolysaccharide (LPS) and lipoproteins (PAMP)-stimulated production of interleukin (IL)-6. This suggests that orento negatively regulates PAMP-mediated toll-like receptor (TLR) signaling. Orento significantly suppressed PAMP-stimulated activation of the IL-6 promoter, indicating that orento may suppress the production of IL-6 by PAMP at the transcriptional level. Orento also suppressed TLR-mediated activation of transcription factor nuclear factor-kappa B (NF-kB) that was stimulated by PAMP. This finding indicates that orento may suppress the function and activation of factors involved in TLR signaling, thereby suppressing NF-kB-dependent expression of various genes. Orento suppressed IL-1 receptor-associated kinase (IRAK4), IRAK1, and c-Jun N-terminal kinase (JNK) phosphorylation in PAMP-stimulated CAL27 cells. This result indicates that orento is involved in the initiation of TLR signaling by PAMP and suppresses the downstream signaling pathways of myeloid differentiation primary response gene 88 (MyD88) such as mitogen-activated protein kinase (MAPK) and NF-kB cascades. These findings suggest that orento has an inhibitory effect on the production of inflammatory cytokines.
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Ziske Maritska and Rachmat Hidayat. "The Role of Pattern Recognition Receptor (PRR) in the Body's Defense System: A Narrative Literature Review." Open Access Indonesian Journal of Medical Reviews 3, no. 2 (May 8, 2023): 394–97. http://dx.doi.org/10.37275/oaijmr.v3i2.300.
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Each cell has receptors on the cell surface that specifically bind to solutes (ligands) produced during tissue damage or infection. This review aimed to describe the role of PRR in the human body's defense system. The binding of the ligand to its receptor results in the activation of intracellular signaling pathways and cell activation. The B and T lymphocytes of the adaptive immune system have developed surface receptors (that is, the T-cell receptor, or TCR, and the B-cell receptor, or BCR) that bind a broad spectrum of antigens. The cells involved in innate resistance have developed a distinct set of receptors that recognize a much more limited array of specific molecules. These are called pattern recognition receptor (PRR), and they recognize the molecular patterns in infectious agents or their products (pathogen-associated molecular patterns, or PAMP) or products of cellular damage (necrosis or apoptosis; molecular pattern-associated damage, or DAMPs). In conclusion, the pattern recognition receptor (PRR) is a receptor complex that interacts with various molecules, such as PAMP and DAMPs. PRR bonds with these various molecules and play a role in various actions of innate immunity and adaptive immunity.
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Idris, Adi. "Cellular Responses to Cytosolic Double-stranded RNA–-The Role of the Inflammasome." Immunology and Immunogenetics Insights 6 (January 2014): III.S17839. http://dx.doi.org/10.4137/iii.s17839.
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Sensing the presence of a pathogen is an evolutionarily ancient trait, especially for cells of the innate immune system. The innate immune response against pathogens, such as viruses, begins with recognition of pathogen-associated molecular patterns (PAMPs) by specific pattern-recognition receptors (PRRs). Cytosolic double-stranded RNA (dsRNA) is emerging as a critical PAMP in the detection of viral infections. This recognition results in the production of antiviral and proinflammatory cytokines and, often, the death of the virus-infected cell. This review focuses on the current developments in the role of inflammasomes in response to the presence of cytosolic dsRNA in host cells. More importantly, it highlights important unanswered questions that if addressed will help us better understand the ways in which host cells respond to viral infection, in particular RNA viruses.
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Thiel, Steffen, Troels R. Kjær, Thomas Wittenborn, Eva L. Petersen, and Jens C. Jensenius. "M-ficolin, a monocyte pathogen-associated molecular pattern (PAMP) recognition molecule (PRM)." Molecular Immunology 46, no. 14 (September 2009): 2869–70. http://dx.doi.org/10.1016/j.molimm.2009.05.329.
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Oth, Tammy, Joris Vanderlocht, Catharina H. M. J. Van Elssen, Gerard M. J. Bos, and Wilfred T. V. Germeraad. "Pathogen-Associated Molecular Patterns Induced Crosstalk between Dendritic Cells, T Helper Cells, and Natural Killer Helper Cells Can Improve Dendritic Cell Vaccination." Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/5740373.
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A coordinated cellular interplay is of crucial importance in both host defense against pathogens and malignantly transformed cells. The various interactions of Dendritic Cells (DC), Natural Killer (NK) cells, and T helper (Th) cells can be influenced by a variety of pathogen-associated molecular patterns (PAMPs) and will lead to enhanced CD8+effector T cell responses. Specific Pattern Recognition Receptor (PRR) triggering during maturation enables DC to enhance Th1 as well as NK helper cell responses. This effect is correlated with the amount of IL-12p70 released by DC. Activated NK cells are able to amplify the proinflammatory cytokine profile of DC via the release of IFN-γ. The knowledge on how PAMP recognition can modulate the DC is of importance for the design and definition of appropriate therapeutic cancer vaccines. In this review we will discuss the potential role of specific PAMP-matured DC in optimizing therapeutic DC-based vaccines, as some of these DC are efficiently activating Th1, NK cells, and cytotoxic T cells. Moreover, to optimize these vaccines, also the inhibitory effects of tumor-derived suppressive factors, for example, on the NK-DC crosstalk, should be taken into account. Finally, the suppressive role of the tumor microenvironment in vaccination efficacy and some proposals to overcome this by using combination therapies will be described.
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Furukawa, Takehito, Hiroaki Inagaki, Ryota Takai, Hiroyuki Hirai, and Fang-Sik Che. "Two Distinct EF-Tu Epitopes Induce Immune Responses in Rice and Arabidopsis." Molecular Plant-Microbe Interactions® 27, no. 2 (February 2014): 113–24. http://dx.doi.org/10.1094/mpmi-10-13-0304-r.
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Plants sense potential pathogens by recognizing conserved pathogen-associated molecular patterns (PAMPs) that cause PAMP-triggered immunity (PTI). We previously reported that rice recognizes flagellin from the rice-incompatible N1141 strain of Acidovorax avenae and subsequently induces immune responses. Cell extracts isolated from flagellin-deficient N1141 (Δfla1141) still induced PTI responses, suggesting that Δfla1141 possesses an additional PAMP distinct from flagellin. Here, we show that elongation factor Tu (EF-Tu), one of the most abundant bacterial proteins, acts as a PAMP in rice and causes several PTI responses. In Brassicaceae species, EF-Tu and an N-acetylated peptide comprising the first 18 amino acids of the N-terminus, termed elf18, are fully active as inducers of PTI responses. By contrast, elf18 did not cause any immune responses in rice, whereas an EF-Tu middle region comprising Lys176 to Gly225, termed EFa50, is fully active as a PAMP in rice. In the leaves of rice plants, EF-Tu induced H2O2 generation and callose deposition, and also triggered resistance to coinfection with pathogenic bacteria. Taken together, these data demonstrate that rice recognizes EFa50, which is distinct from elf18, and that this epitope induces PTI responses.
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Wallecha, Anu, Laurence Wood, Zhen-Kun Pan, Paulo C. Maciag, Vafa Shahabi, and Yvonne Paterson. "Listeria monocytogenes-Derived Listeriolysin O Has Pathogen-Associated Molecular Pattern-Like Properties Independent of Its Hemolytic Ability." Clinical and Vaccine Immunology 20, no. 1 (November 7, 2012): 77–84. http://dx.doi.org/10.1128/cvi.00488-12.
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ABSTRACTThere is a constant need for improved adjuvants to augment the induction of immune responses against tumor-associated antigens (TAA) during immunotherapy. Previous studies have established that listeriolysin O (LLO), a cholesterol-dependent cytolysin derived fromListeria monocytogenes, exhibits multifaceted effects to boost the stimulation of immune responses to a variety of antigens. However, the direct ability of LLO as an adjuvant and whether it acts as a pathogen-associated molecular pattern (PAMP) have not been demonstrated. In this paper, we show that a detoxified, nonhemolytic form of LLO (dtLLO) is an effective adjuvant in tumor immunotherapy and may activate innate and cellular immune responses by acting as a PAMP. Our investigation of the adjuvant activity demonstrates that dtLLO, either fused to or administered as a mixture with a human papillomavirus type 16 (HPV-16) E7 recombinant protein, can augment antitumor immune responses and facilitate tumor eradication. Further mechanistic studies using bone marrow-derived dendritic cells suggest that dtLLO acts as a PAMP by stimulating production of proinflammatory cytokines and inducing maturation of antigen-presenting cells (APC). We propose that dtLLO is an effective adjuvant for tumor immunotherapy, and likely for other therapeutic settings.
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Kell, Alison, Mark Stoddard, Hui Li, Joe Marcotrigiano, George M. Shaw, and Michael Gale. "Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length." Journal of Virology 89, no. 21 (August 26, 2015): 11056–68. http://dx.doi.org/10.1128/jvi.01964-15.
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ABSTRACTDespite the introduction of direct-acting antiviral (DAA) drugs against hepatitis C virus (HCV), infection remains a major public health concern because DAA therapeutics do not prevent reinfection and patients can still progress to chronic liver disease. Chronic HCV infection is supported by a variety of viral immune evasion strategies, but, remarkably, 20% to 30% of acute infections spontaneously clear prior to development of adaptive immune responses, thus implicating innate immunity in resolving acute HCV infection. However, the virus-host interactions regulating acute infection are unknown. Transmission of HCV involves one or a few transmitted/founder (T/F) variants. In infected hepatocytes, the retinoic acid-inducible gene I (RIG-I) protein recognizes 5′ triphosphate (5′ppp) of the HCV RNA and a pathogen-associated molecular pattern (PAMP) motif located within the 3′ untranslated region consisting of poly-U/UC. PAMP binding activates RIG-I to induce innate immune signaling and type 1 interferon antiviral defenses. HCV poly-U/UC sequences can differ in length and complexity, suggesting that PAMP diversity in T/F genomes could regulate innate immune control of acute HCV infection. Using 14 unique poly-U/UC sequences from HCV T/F genomes recovered from acute-infection patients, we tested whether RIG-I recognition and innate immune activation correlate with PAMP sequence characteristics. We show that T/F variants are recognized by RIG-I in a manner dependent on length of the U-core motif of the poly-U/UC PAMP and are recognized by RIG-I to induce innate immune responses that restrict acute infection. PAMP recognition of T/F HCV variants by RIG-I may therefore impart innate immune signaling and HCV restriction to impact acute-phase-to-chronic-phase transition.IMPORTANCERecognition of nonself molecular patterns such as those seen with viral nucleic acids is an essential step in triggering the immune response to virus infection. Innate immunity is induced by hepatitis C virus infection through the recognition of viral RNA by the cellular RIG-I protein, where RIG-I recognizes a poly-uridine/cytosine motif in the viral genome. Variation within this motif may provide an immune evasion strategy for transmitted/founder viruses during acute infection. Using 14 unique poly-U/UC sequences from HCV T/F genomes recovered from acutely infected HCV patients, we demonstrate that RIG-I binding and activation of innate immunity depend primarily on the length of the uridine core within this motif. T/F variants found in acute infection contained longer U cores within the motif and could activate RIG-I and induce innate immune signaling sufficient to restrict viral infection. Thus, recognition of T/F variants by RIG-I could significantly impact the transition from acute to chronic infection.
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Nguyen, Hanh P., Suma Chakravarthy, André C. Velásquez, Heather L. McLane, Lirong Zeng, Hitoshi Nakayashiki, Duck-Hwan Park, Alan Collmer, and Gregory B. Martin. "Methods to Study PAMP-Triggered Immunity Using Tomato and Nicotiana benthamiana." Molecular Plant-Microbe Interactions® 23, no. 8 (August 2010): 991–99. http://dx.doi.org/10.1094/mpmi-23-8-0991.
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Understanding the molecular basis of plant responses to pathogen-associated molecular patterns (PAMPs) is an active area of research in the field of plant–microbe interactions. A growing number of plant genes involved in various steps of PAMP-triggered immunity (PTI) pathways and microbial factors involved in the elicitation or suppression of PTI have been identified. These studies have largely relied on Arabidopsis thaliana and, therefore, most of the PTI assays have been developed and optimized for that model plant system. Although PTI is a conserved feature among plants, the response spectra vary across different species. Thus, there is a need for robust PTI assays in other pathosystems, such as those involving Solanaceae plant–pathogen interactions, which include many economically important plants and their diseases. We have optimized molecular, cellular, and whole-plant methods to measure PTI responses in two widely studied solanaceous species, tomato (Solanum lycopersicum) and Nicotiana benthamiana. Here, we provide detailed protocols for measuring various PTI-associated phenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition, activation of mitogen-activated protein kinases, and a luciferase-based reporter system. These methods will facilitate limited genetic screens and detailed characterization of potential PTI-related genes in model and economically important Solanaceae spp.–pathogen interactions.
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Heiniö, Camilla, Riikka Havunen, Joao Santos, Klaas de Lint, Victor Cervera-Carrascon, Anna Kanerva, and Akseli Hemminki. "TNFa and IL2 Encoding Oncolytic Adenovirus Activates Pathogen and Danger-Associated Immunological Signaling." Cells 9, no. 4 (March 26, 2020): 798. http://dx.doi.org/10.3390/cells9040798.
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In order to break tumor resistance towards traditional treatments, we investigate the response of tumor and immune cells to a novel, cytokine-armed oncolytic adenovirus: Ad5/3-d24-E2F-hTNFa-IRES-hIL2 (also known as TILT-123 and OAd.TNFa-IL2). There are several pattern recognition receptors (PRR) that might mediate adenovirus-infection recognition. However, the role and specific effects of each PRR on the tumor microenvironment and treatment outcome remain unclear. Hence, the aim of this study was to investigate the effects of OAd.TNFa-IL2 infection on PRR-mediated danger- and pathogen-associated molecular pattern (DAMP and PAMP, respectively) signaling. In addition, we wanted to see which PRRs mediate an antitumor response and are therefore relevant for optimizing this virotherapy. We determined that OAd.TNFa-IL2 induced DAMP and PAMP release and consequent tumor microenvironment modulation. We show that the AIM2 inflammasome is activated during OAd.TNFa-IL2 virotherapy, thus creating an immunostimulatory antitumor microenvironment.
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Lloyd, Simon R., Henk-jan Schoonbeek, Martin Trick, Cyril Zipfel, and Christopher J. Ridout. "Methods to Study PAMP-Triggered Immunity in Brassica Species." Molecular Plant-Microbe Interactions® 27, no. 3 (March 2014): 286–95. http://dx.doi.org/10.1094/mpmi-05-13-0154-fi.
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The first layer of active defense in plants is based on the perception of pathogen-associated molecular patterns (PAMPs) leading to PAMP-triggered immunity (PTI). PTI is increasingly being investigated in crop plants, where it may have potential to provide durable disease resistance in the field. Limiting this work, however, is an absence of reliable bioassays to investigate PAMP responses in some species. Here, we present a series of methods to investigate PTI in Brassica napus. The assays allow measuring early responses such as the oxidative burst, mitogen-activated protein kinase phosphorylation, and PAMP-induced marker gene expression. Illumina-based RNA sequencing analysis produced a genome-wide survey of transcriptional changes upon PAMP treatment seen in both the A and C genomes of the allotetraploid B. napus. Later responses characterized include callose deposition and lignification at the cell wall, seedling growth inhibition, and PAMP-induced resistance to Pseudomonas syringae and Botrytis cinerea. Furthermore, using these assays, we demonstrated substantial variation in PAMP responses within a collection of diverse B. napus cultivars. The assays reported here could have widespread application in B. napus breeding and mapping programs to improve selection for broad-spectrum disease resistance.
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Mitchell, Jane A., Mark J. Paul-Clark, Graham W. Clarke, Shaun K. McMaster, and Neil Cartwright. "Critical role of toll-like receptors and nucleotide oligomerisation domain in the regulation of health and disease." Journal of Endocrinology 193, no. 3 (June 2007): 323–30. http://dx.doi.org/10.1677/joe-07-0067.
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Pathogens are sensed by pattern recognition receptors (PRRs), which are germ line-encoded receptors, including transmembrane Toll-like receptors (TLRs) and cytosolic nucleotide oligomerisation domain (NOD) proteins, containing leucine-rich repeats (NLRs). Activation of PRRs by specific pathogen-associated molecular patterns (PAMPs) results in genomic responses in host cells involving activation transcription factors and the induction of genes. There are now at least 10 TLRs in humans and 13 in mice, and 2 NLRs (NOD1 and NOD2). TLR signalling is via interactions with adaptor proteins including MyD88 and toll-receptor associated activator of interferon (TRIF). NOD signalling is via the inflammasome and involves activation of Rip-like interactive clarp kinase (RICK). Bacterial lipopolysaccharide (LPS) from Gram-negative bacteria is the best-studied PAMP and is activated by or ‘sensed’ by TLR4. Lipoteichoic acid (LTA) from Gram-positive bacteria is sensed by TLR2. TLR4 and TLR2 have different signalling cascades, although activation of either results in symptoms of sepsis and shock. This review describes the rapidly expanding field of pathogen-sensing receptors and uses LPS and LTA as examples of how these pathways parallel and diverge from each other. The role of pathogen-sensing pathways in disease is also discussed.
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Dewey, Elyse C., Min Jie Alvin Tan, Martin Hibberd, and Michael J. Gale. "Programming of RIG-I signaling through co-factor interactions." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 203.7. http://dx.doi.org/10.4049/jimmunol.196.supp.203.7.
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Abstract Retinoic acid-inducible gene I (RIG-I) functions as a cytosolic pathogen recognition receptor by binding the pathogen associated molecular patterns (PAMPs) in viral RNA. The molecular signature for RIG-I recognition has been identified as 5′-triphosphate-containing short double stranded or poly-uridine RNA (5′pppRNA) structures found in RNA species that amass in the cytoplasm during virus infection. PAMP-mediated activation of RIG-I triggers many signaling cascades that mediates its effector functions in innate immunity and apoptosis. In the innate immune response to virus infection, RIG-I sets off both IRF3/7 and NF-κB signaling to induce type I interferon (IFN) and pro-inflammatory cytokine production respectively. PAMP-induced RIG-I activation can also induce apoptosis in cancer cells. Since PAMP RNA can act as the activator of RIG-I’s pro-apoptotic and innate immune functions, we hypothesized that the induction of these separate pathways is programmed through differential RIG-I-cofactor interactions. We have identified and characterized novel co-factors of RIG-I by using a systems proteomic approach. These co-factors serve to program apoptotic versus innate immune signaling actions through their interaction with RIG-I. These co-factors and their biologic functions will be presented.
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Mogensen, Trine H. "Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses." Clinical Microbiology Reviews 22, no. 2 (April 2009): 240–73. http://dx.doi.org/10.1128/cmr.00046-08.
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SUMMARY The innate immune system constitutes the first line of defense against invading microbial pathogens and relies on a large family of pattern recognition receptors (PRRs), which detect distinct evolutionarily conserved structures on pathogens, termed pathogen-associated molecular patterns (PAMPs). Among the PRRs, the Toll-like receptors have been studied most extensively. Upon PAMP engagement, PRRs trigger intracellular signaling cascades ultimately culminating in the expression of a variety of proinflammatory molecules, which together orchestrate the early host response to infection, and also is a prerequisite for the subsequent activation and shaping of adaptive immunity. In order to avoid immunopathology, this system is tightly regulated by a number of endogenous molecules that limit the magnitude and duration of the inflammatory response. Moreover, pathogenic microbes have developed sophisticated molecular strategies to subvert host defenses by interfering with molecules involved in inflammatory signaling. This review presents current knowledge on pathogen recognition through different families of PRRs and the increasingly complex signaling pathways responsible for activation of an inflammatory and antimicrobial response. Moreover, medical implications are discussed, including the role of PRRs in primary immunodeficiencies and in the pathogenesis of infectious and autoimmune diseases, as well as the possibilities for translation into clinical and therapeutic applications.
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Yamamoto, Ayumi, Noriko N. Miura, Toshiaki Oharaseki, Kei Takahashi, Shiro Naoe, Kazuo Suzuki, and Naohito Ohno. "Suppression of PAMPs, Pathogen-Associated Microbial Patterns, Induced Cytokine Synthesis of PBMC, Human Blood Mononuclear Cells, by Immunoglobulin Preparation." Open Allergy Journal 5, no. 1 (August 24, 2012): 53–61. http://dx.doi.org/10.2174/1874838401205010053.
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The applications of immunoglobulin preparation for intravenous injection (IVIg) for various intractable diseases are increasing. The two major clinical indications for IVIg are the replacement therapy and the anti-inflammation therapy for a variety of acute and chronic autoimmune diseases. One of the proposed mechanisms of IVIg activity is the modulation of cytokine expression and function; therefore, we analyzed the effect of IVIg on pathogen-associated molecular pattern (PAMP)-induced cytokine production by peripheral blood mononuclear cells (PBMCs). The production of tumor necrosis factor-α (TNF-α) as a result of stimulation with lipopolysaccharide (LPS), polyinosinic-polycytidylic acid sodium salt (Poly I:C), or Pam3CysSerLys4 (Pam3) was significantly inhibited by sulfonated-IVIg (S-IVIg), or by F(ab')2. Assessed by one-color microarray analysis, the expressions of 229 genes were inhibited to 1/200 or less by F(ab')2. On the other hand, the expressions of 159 genes were increased by more than 100-fold by F(ab')2. According to these results, it was suggested that IVIg inhibits inflammatory PAMPs-induced cytokine production by PBMCs, due to the modulation of varieties of gene expression.
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Cedzyński, Maciej, and Anna S. Świerzko. "Components of the Lectin Pathway of Complement in Haematologic Malignancies." Cancers 12, no. 7 (July 4, 2020): 1792. http://dx.doi.org/10.3390/cancers12071792.
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The complement system is activated cascadically via three distinct major routes: classical pathway (CP), alternative pathway (AP) or lectin pathway (LP). The unique factors associated with the latter are collectins (mannose-binding lectin, collectin-10, collectin-11), ficolins (ficolin-1, ficolin-2, ficolin-3) and proteins of the mannose-binding lectin-associated serine protease (MASP) family (MASP-1, MASP-2, MASP-3, MAp19, MAp44). Collectins and ficolins are both pattern-recognising molecules (PRM), reactive against pathogen-associated molecular patterns (PAMP) or danger-associated molecular patterns (DAMP). The MASP family proteins were first discovered as complexes with mannose-binding lectin (MBL) and therefore named MBL-associated serine proteases, but later, they were found to interact with ficolins, and later still, collectin-10 and collectin-11. As well as proteolytic enzymes (MASP-1, MASP-2, MASP-3), the group includes non-enzymatic factors (MAp19, MAp44). In this review, the association-specific factors of the lectin pathway with haematologic malignancies and related infections are discussed.
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Nicaise, Valerie, and Thierry Candresse. "Plum pox virus capsid protein suppresses plant pathogen-associated molecular pattern (PAMP)-triggered immunity." Molecular Plant Pathology 18, no. 6 (August 8, 2016): 878–86. http://dx.doi.org/10.1111/mpp.12447.
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Yan, Yu, Dan Yao, and Xiaoyu Li. "Immunological Mechanism and Clinical Application of PAMP Adjuvants." Recent Patents on Anti-Cancer Drug Discovery 16, no. 1 (May 25, 2021): 30–43. http://dx.doi.org/10.2174/1574892816666210201114712.
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Background: The host innate immune system can recognize Pathogen-Associated Molecular Patterns (PAMPs) through Pattern Recognition Receptors (PRRs), thereby initiating innate immune responses and subsequent adaptive immune responses. PAMPs can be developed as a vaccine adjuvant for modulating and optimizing antigen-specific immune responses, especially in combating viral infections and tumor therapy. Although several PAMP adjuvants have been successfully developed they are still lacking in general, and many of them are in the preclinical exploration stage. Objective: This review summarizes the research progress and development direction of PAMP adjuvants, focusing on their immune mechanisms and clinical applications. Methods: PubMed, Scopus, and Google Scholar were screened for this information. We highlight the immune mechanisms and clinical applications of PAMP adjuvants. Results: Because of the differences in receptor positions, specific immune cells targets, and signaling pathways, the detailed molecular mechanism and pharmacokinetic properties of one agonist cannot be fully generalized to another agonist, and each PAMP should be studied separately. In addition, combination therapy and effective integration of different adjuvants can increase the additional efficacy of innate and adaptive immune responses. Conclusion: The mechanisms by which PAMPs exert adjuvant functions are diverse. With continuous discovery in the future, constant adjustments should be made to build new understandings. At present, the goal of therapeutic vaccination is to induce T cells that can specifically recognize and eliminate tumor cells and establish long-term immune memory. Following immune checkpoint modulation therapy, cancer treatment vaccines may be an option worthy of clinical testing.
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Saur, Isabel M. L., Yasuhiro Kadota, Jan Sklenar, Nicholas J. Holton, Elwira Smakowska, Youssef Belkhadir, Cyril Zipfel, and John P. Rathjen. "NbCSPR underlies age-dependent immune responses to bacterial cold shock protein inNicotiana benthamiana." Proceedings of the National Academy of Sciences 113, no. 12 (March 4, 2016): 3389–94. http://dx.doi.org/10.1073/pnas.1511847113.
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Plants use receptor kinases (RKs) and receptor-like proteins (RLPs) as pattern recognition receptors (PRRs) to sense pathogen-associated molecular patterns (PAMPs) that are typical of whole classes of microbes. After ligand perception, many leucine-rich repeat (LRR)-containing PRRs interact with the LRR-RK BRI1-ASSOCIATED KINASE 1 (BAK1). BAK1 is thus expected to interact with unknown PRRs. Here, we used BAK1 as molecular bait to identify a previously unknown LRR-RLP required for the recognition of the csp22 peptide derived from bacterial cold shock protein. We established a method to identify proteins that interact with BAK1 only after csp22 treatment. BAK1 was expressed transiently inNicotiana benthamianaand immunopurified after treatment with csp22. BAK1-associated proteins were identified by mass spectrometry. We identified several proteins including known BAK1 interactors and a previously uncharacterized LRR-RLP that we termed RECEPTOR-LIKE PROTEIN REQUIRED FOR CSP22 RESPONSIVENESS (NbCSPR). This RLP associates with BAK1 upon csp22 treatment, andNbCSPR-silenced plants are impaired in csp22-induced defense responses.NbCSPRconfers resistance to bacteria in an age-dependent and flagellin-induced manner. As such, it limits bacterial growth andAgrobacterium-mediated transformation of floweringN. benthamianaplants. Transgenic expression ofNbCSPRintoArabidopsis thalianaconferred responsiveness to csp22 and antibacterial resistance. Our method may be used to identify LRR-type RKs and RLPs required for PAMP perception/responsiveness, even when the active purified PAMP has not been defined.
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Yang, Huan, Haichao Wang, Sangeeta Chavan, Timothy Billiar, Al-Abed Yousef, and Kevin Tracey. "The HMGB1-MD-2 axis as a novel therapeutic target in inflammatory diseases (CCR5P.210)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 186.12. http://dx.doi.org/10.4049/jimmunol.194.supp.186.12.
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Abstract Innate immune cells express receptors for pathogen-associated molecular patterns (PAMP e.g. LPS) as well as damage-associated molecular patterns (DAMP e.g. HMGB1), and orchestrate inflammatory responses to both infection and sterile injury. Secreted by activated immune cells or passively released by damaged cells, HMGB1 is subjected to redox modulation that distinctly influences its extracellular functions. Previously, it was unknown how the TLR4 signalosome distinguishes between HMGB1 isoforms. Here we demonstrate that the TLR4 adaptor molecule, myeloid differentiation factor 2 (MD-2), binds specifically to the cytokine-inducing disulfide HMGB1 isoform, to the exclusion of other isoforms. Screening of HMGB1 peptide libraries identified a tetramer (FSSE, designated as P5779) as a specific MD-2-antagonist preventing MD-2/HMGB1 interaction and subsequent TLR4 signaling mediating cytokine and chemokine release. Moreover, P5779 does not interfere with LPS-induced cytokine production, thereby preserving PAMP-mediated TLR4-MD2 responses. P5779 conferred protection in animal models of hepatic ischemia/reperfusion injury, chemical toxicity and sepsis. Taken together, these findings reveal a novel mechanism by which innate systems selectively recognize specific HMGB1 isoforms and suggest strategies to attenuate DAMP-mediated inflammatory responses while preserving anti-microbial immune responsiveness.
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Watkins, Rebekah, Pamela Tiet, Robert Junkins, Matthew Gallovic, Ning Chen, Brandon Johnson, Eric Bachelder, Kristy Ainslie, and Jenny P. Y. Ting. "Particulate Delivery of Innate Immune Agonist for Cancer Immunotherapy." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 58.11. http://dx.doi.org/10.4049/jimmunol.200.supp.58.11.
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Abstract Immunotherapies have dramatically improved cancer patient survival; however, certain forms of cancer still rely on conventional chemotherapies and radiation. We have designed a novel cancer treatment that utilizes an immunotherapeutic to augment the adaptive immune system. Many FDA-approved immunotherapies have several drawbacks including high cost, short half-life, and flu-like side effects leading to patient noncompliance. To overcome these difficulties, we have utilized pathogen-associated molecular patterns (PAMP) to stimulate an innate immune response and induce a potent cytokine response. However, the receptor for the PAMP is located in the cytosol, and the PAMP cannot transverse the cell membrane. To overcome this, we have designed a polymeric microparticle (MP) to deliver the PAMP (PAMP MPs) into the cytosol. The polymeric MP is composed of a dextran-based, biodegradable polymer. It has several critical advantages over other FDA-approved delivery vehicles, such as liposomes, including greater stability, higher encapsulation efficiency (EE) of hydrophilic cargo, ease and reproducibility of production, and ease of end point sterilization. Treatment with PAMP MPs resulted in reduced tumor burden compared to mice treated with the soluble PAMP in a model of melanoma, suggesting that the MPs increase the biological activity. Intratumoral treatment with PAMP MPs resulted in increased natural killer cells and professional antigen presenting cells in the tumor environment. In conclusion, our PAMP MPs resulted in significant anti-tumor efficacy in an aggressive murine model of melanoma, and the data suggest that this anti-tumor function is due to an increased immune response within the tumor.
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Fabro, Georgina, Yanina Soledad Rizzi, and María Elena Alvarez. "Arabidopsis Proline Dehydrogenase Contributes to Flagellin-Mediated PAMP-Triggered Immunity by Affecting RBOHD." Molecular Plant-Microbe Interactions® 29, no. 8 (August 2016): 620–28. http://dx.doi.org/10.1094/mpmi-01-16-0003-r.
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Plants activate different defense systems to counteract the attack of microbial pathogens. Among them, the recognition of conserved microbial- or pathogen-associated molecular patterns (MAMPs or PAMPs) by pattern-recognition receptors stimulates MAMP- or PAMP-triggered immunity (PTI). In recent years, the elicitors, receptors, and signaling pathways leading to PTI have been extensively studied. However, the contribution of organelles to this program deserves further characterization. Here, we studied how processes altering the mitochondrial electron transport chain (mETC) influence PTI establishment. With particular emphasis, we evaluated the effect of proline dehydrogenase (ProDH), an enzyme that can load electrons into the mETC and regulate the cellular redox state. We found that mETC uncouplers (antimycin or rotenone) and manganese superoxide dismutase deficiency impair flg22-induced responses such as accumulation of reactive oxygen species (ROS) and bacterial growth limitation. ProDH mutants also reduce these defenses, decreasing callose deposition as well. Using ProDH inhibitors and ProDH inducers (exogenous Pro treatment), we showed that this enzyme modulates the generation of ROS by the plasma membrane respiratory burst NADPH oxidase homolog D. In this way, we contribute to the understanding of mitochondrial activities influencing early and late PTI responses and the coordination of the redox-associated mitochondrial enzyme ProDH with defense events initiated at the plasma membrane.
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Navarrete, Fernando, Nenad Grujic, Alexandra Stirnberg, Indira Saado, David Aleksza, Michelle Gallei, Hazem Adi, et al. "The Pleiades are a cluster of fungal effectors that inhibit host defenses." PLOS Pathogens 17, no. 6 (June 24, 2021): e1009641. http://dx.doi.org/10.1371/journal.ppat.1009641.
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Biotrophic plant pathogens secrete effector proteins to manipulate the host physiology. Effectors suppress defenses and induce an environment favorable to disease development. Sequence-based prediction of effector function is impeded by their rapid evolution rate. In the maize pathogen Ustilago maydis, effector-coding genes frequently organize in clusters. Here we describe the functional characterization of the pleiades, a cluster of ten effector genes, by analyzing the micro- and macroscopic phenotype of the cluster deletion and expressing these proteins in planta. Deletion of the pleiades leads to strongly impaired virulence and accumulation of reactive oxygen species (ROS) in infected tissue. Eight of the Pleiades suppress the production of ROS upon perception of pathogen associated molecular patterns (PAMPs). Although functionally redundant, the Pleiades target different host components. The paralogs Taygeta1 and Merope1 suppress ROS production in either the cytoplasm or nucleus, respectively. Merope1 targets and promotes the auto-ubiquitination activity of RFI2, a conserved family of E3 ligases that regulates the production of PAMP-triggered ROS burst in plants.
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Zhang, Rongzhi, Fengya Zheng, Shugen Wei, Shujuan Zhang, Genying Li, Peijian Cao, and Shancen Zhao. "Evolution of Disease Defense Genes and Their Regulators in Plants." International Journal of Molecular Sciences 20, no. 2 (January 15, 2019): 335. http://dx.doi.org/10.3390/ijms20020335.
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Biotic stresses do damage to the growth and development of plants, and yield losses for some crops. Confronted with microbial infections, plants have evolved multiple defense mechanisms, which play important roles in the never-ending molecular arms race of plant–pathogen interactions. The complicated defense systems include pathogen-associated molecular patterns (PAMP) triggered immunity (PTI), effector triggered immunity (ETI), and the exosome-mediated cross-kingdom RNA interference (CKRI) system. Furthermore, plants have evolved a classical regulation system mediated by miRNAs to regulate these defense genes. Most of the genes/small RNAs or their regulators that involve in the defense pathways can have very rapid evolutionary rates in the longitudinal and horizontal co-evolution with pathogens. According to these internal defense mechanisms, some strategies such as molecular switch for the disease resistance genes, host-induced gene silencing (HIGS), and the new generation of RNA-based fungicides, have been developed to control multiple plant diseases. These broadly applicable new strategies by transgene or spraying ds/sRNA may lead to reduced application of pesticides and improved crop yield.
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Филатов, О. Ю., and В. А. Назаров. "Image-recognizing receptors of the innate immunity and their role in immunotherapy (review)." Nauchno-prakticheskii zhurnal «Patogenez», no. 4 (December 25, 2020): 4–15. http://dx.doi.org/10.25557/2310-0435.2020.04.4-15.
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Данная статья обобщает накопившуюся на сегодняшний день информацию о многообразии образраспознающих рецепторов, их роли в регуляции иммунной системы. Распознавание патогена врожденным иммунитетом происходит с помощью рецепторов к широкому спектру антигенов за счет выделения нескольких высоко консервативных структур микроорганизмов. Эти структуры были названы патоген-ассоциированные образы (Patogen-Associated Molecular Patterns - PAMP). Наиболее изученными являются липополисахарид грамм отрицательных бактерий (LPS), липотейхоевые кислоты, пептидогликан (PGN), CpG мотивы ДНК и РНК. Рецепторы, распознающие PAMP, называются PRR. Данная группа рецепторов также распознает молекулы, образующиеся при повреждении собственных тканей. Такие молекулярные структуры называются Damage-Associated Molecular Patterns (DAMP), или образы, ассоциированные с повреждением. В качестве DAMP могут выступать белки теплового шока, хроматин, фрагменты ДНК. В зависимости от локализации, образраспознающие рецепторы принято разделять на: расположенные на мембране Toll-подобные рецепторы (Toll-like receptors, TLR) и рецепторы лектина С-типа (C-type lectin receptors, CLR), а также расположенные в цитоплазме NOD-подобные рецепторы (NOD-like receptors, NLR) и цитоплазматические РНК- и ДНК-сенсоры. Сегодня у человека известно 10 типов TLR, часть из которых расположена на поверхности (TLR1-TLR6, TLR10) большинства клеток, в том числе макрофагов, В-лимфоцитов и дендритных клеток, а часть - в эндосомах (TLR3, TLR7-TLR9). CLR представляет из себя семейство рецепторов, расположенных на мембране и имеющих домены распознавания углеводов (CRD), или структурно сходные лектиноподобные домены типа C (CTLD). В данном семействе рецепторов принято по происхождению и структуре выделять 17 групп. CLR активно участвуют в противогрибковой иммунной защите, а также они играют роль в защите и от других типов микроорганизмов. NOD (нуклеотидсвязывающий и олигомеризационный домен)-подобные рецепторы расположены в цитоплазме. Благодаря этим рецепторам, патоген, который избежал распознавания на поверхности мембраны, сталкивается со вторым уровнем распознавания уже внутри клетки. В данной статье рассматриваются пути активации образраспознающих рецепторов, их эффекты и применение данных эффектов в медицине. This article summarizes currently available information about the variety of image-recognizing receptors and their role in regulation of the immune system. Pathogen recognition by the innate immunity is mediated by receptors to a wide range of antigens via recognition of several highly conservative structures of microorganisms. These structures were named pathogen-associated images or PAMP (pathogen-associated molecular pattern). The best studied types of such structures include lipopolysaccharide (LPS) of gram-negative bacteria, lipoteichoic acids, peptidoglycan (PGN), and CpG DNA and RNA motifs. PAMP-recognizing receptors (PRRS) are a group of receptors, which also recognize molecules released during damage of host tissues. Such molecular structures are called DAMPS (damage-associated molecular patterns) or damage-associated images. Heat shock proteins, chromatin, and DNA fragments may act as DAMPS. Depending on the localization, image-recognizing receptors are generally classified as membrane-located Toll-like receptors (TLR) and C-type lectin receptors (CLR), as well as cytoplasmic NOD-like receptors (NLR) and cytoplasmic RNA and DNA sensors. Today, 10 types of human TLR are known. Some of them are located on the surface (TLR1-TLR6, TLR10) of most cells, including macrophages, B-cells, and dendritic cells, and some are present in endosomes (TLR3, TLR7-TLR9). CLR is a family of membrane receptors that have carbohydrate recognition domains (CRD) or structurally similar lectin-like type C domains (CTLD). Seventeen groups are distinguished within this receptor family based on their origin and structure. CLRs are actively involved in antifungal immune defense and also play a role in protection against other types of microorganisms. NOD (nucleotide-binding and oligomerization domain)-like receptors are present in the cytoplasm. These receptors provide the second level of recognition inside the cell for the pathogens that have escaped recognition on the membrane surface. This article discusses activation pathways of image-recognizing receptors, their effects, and the use of such effects in medicine.
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Zhang, Wei, Feng Zhao, Lihui Jiang, Cun Chen, Lintao Wu, and Zhibin Liu. "Different Pathogen Defense Strategies in Arabidopsis: More than Pathogen Recognition." Cells 7, no. 12 (December 7, 2018): 252. http://dx.doi.org/10.3390/cells7120252.
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Plants constantly suffer from simultaneous infection by multiple pathogens, which can be divided into biotrophic, hemibiotrophic, and necrotrophic pathogens, according to their lifestyles. Many studies have contributed to improving our knowledge of how plants can defend against pathogens, involving different layers of defense mechanisms. In this sense, the review discusses: (1) the functions of PAMP (pathogen-associated molecular pattern)-triggered immunity (PTI) and effector-triggered immunity (ETI), (2) evidence highlighting the functions of salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET)-mediated signaling pathways downstream of PTI and ETI, and (3) other defense aspects, including many novel small molecules that are involved in defense and phenomena, including systemic acquired resistance (SAR) and priming. In particular, we mainly focus on SA and (JA)/ET-mediated signaling pathways. Interactions among them, including synergistic effects and antagonistic effects, are intensively explored. This might be critical to understanding dynamic disease regulation.
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Deng, Wen-Ling, Yuan-Chun Lin, Rong-Hwa Lin, Chia-Fong Wei, Yi-Chiao Huang, Hwei-Ling Peng, and Hsiou-Chen Huang. "Effects of galU Mutation on Pseudomonas syringae–Plant Interactions." Molecular Plant-Microbe Interactions® 23, no. 9 (September 2010): 1184–96. http://dx.doi.org/10.1094/mpmi-23-9-1184.
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Bacterial galU coding for a uridine diphosphate-glucose pyrophosphorylase plays an important role in carbohydrates biosynthesis, including synthesis of lipopolysaccharides (LPS), membrane-derived oligosaccharides, and capsular polysaccharides. In this study, we characterized the galU mutant of Pseudomonas syringae pv. syringae 61 (Psy61), a necrotizing plant pathogen whose pathogenicity depends on a functional type III secretion system (T3SS), and showed that the Psy61 galU mutant had reduced biofilm formation ability, was nonmotile, and had an assembled T3SS structure but failed to elicit hypersensitive response in resistant plants and necrotic lesions in susceptible plants. Moreover, the defective LPS and other pathogen-associated molecular patterns (PAMPs) on the surface of the Psy61 galU mutant were capable of inducing PAMP-triggered immunity, which severely compromised the ability of the Psy61 galU mutant to survive in planta. Our results demonstrated that the complete LPS protected plant-pathogenic bacteria from host innate immunity, similar to what was found in animal pathogens, prior to the translocation of T3S effectors and bacterial multiplication.
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Chen, Yu-Yuan, Jiann-Chu Chen, Yong-Chin Lin, Suwaree Kitikiew, Hui-Fang Li, Jia-Chin Bai, Kuei-Chi Tseng, et al. "Endogenous Molecules Induced by a Pathogen-Associated Molecular Pattern (PAMP) Elicit Innate Immunity in Shrimp." PLoS ONE 9, no. 12 (December 17, 2014): e115232. http://dx.doi.org/10.1371/journal.pone.0115232.
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Castaño, Andrea, and Margarita María Velásquez. "Psoriasis pustulosa generalizada: de la inmunopatogénesis a la clínica." Revista de la Asociación Colombiana de Dermatología y Cirugía Dermatológica 25, no. 2 (April 1, 2017): 130–42. http://dx.doi.org/10.29176/2590843x.9.
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El síndrome DITRA (Interleukin-36-Receptor Antagonist Deficiency) es una enfermedad autoinflamatoria debida a mutaciones del gen IL36RN que producen deficiencia del antagonista del receptor de la IL-36, lo que induce una cascada inflamatoria que lleva a un cuadro clínico grave de psoriasis pustulosa generalizada. Ante desencadenantes externos, como los componentes de agentes infecciosos que son activadores de los receptores de inmunidad innata, denominados PAMP (Pathogen-Associated Molecular Patterns), o los asociados a estrés celular, llamados DAMP (Damage-Associated Molecular Patterns), se activa el receptor con gran homología a los TLR (Toll-Like Receptors) y se amplifica a través del receptor de la IL-36, que en ausencia de su antagonista, conlleva a mayor activación celular en el principal órgano blanco, que es la piel.El síndrome DITRA debe sospecharse en todo paciente con psoriasis pustulosa generalizada grave, para enfocar apropiadamente su tratamiento.
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Kato, Hiroaki, Kiyoshi Onai, Akira Abe, Motoki Shimizu, Hiroki Takagi, Chika Tateda, Hiroe Utsushi, et al. "Lumi-Map, a Real-Time Luciferase Bioluminescence Screen of Mutants Combined with MutMap, Reveals Arabidopsis Genes Involved in PAMP-Triggered Immunity." Molecular Plant-Microbe Interactions® 33, no. 12 (December 2020): 1366–80. http://dx.doi.org/10.1094/mpmi-05-20-0118-ta.
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Plants recognize pathogen-associated molecular patterns (PAMPs) to activate PAMP-triggered immunity (PTI). However, our knowledge of PTI signaling remains limited. In this report, we introduce Lumi-Map, a high-throughput platform for identifying causative single-nucleotide polymorphisms (SNPs) for studying PTI signaling components. In Lumi-Map, a transgenic reporter plant line is produced that contains a firefly luciferase (LUC) gene driven by a defense gene promoter, which generates luminescence upon PAMP treatment. The line is mutagenized and the mutants with altered luminescence patterns are screened by a high-throughput real-time bioluminescence monitoring system. Selected mutants are subjected to MutMap analysis, a whole-genome sequencing-based method of rapid mutation identification, to identify the causative SNP responsible for the luminescence pattern change. We generated nine transgenic Arabidopsis reporter lines expressing the LUC gene fused to multiple promoter sequences of defense-related genes. These lines generate luminescence upon activation of FLAGELLIN-SENSING 2 (FLS2) by flg22, a PAMP derived from bacterial flagellin. We selected the WRKY29-promoter reporter line to identify mutants in the signaling pathway downstream of FLS2. After screening 24,000 ethylmethanesulfonate-induced mutants of the reporter line, we isolated 22 mutants with altered WRKY29 expression upon flg22 treatment (abbreviated as awf mutants). Although five flg22-insensitive awf mutants harbored mutations in FLS2 itself, Lumi-Map revealed three genes not previously associated with PTI. Lumi-Map has the potential to identify novel PAMPs and their receptors as well as signaling components downstream of the receptors. [Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
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Ulloa, Brittany, and Michael Gale. "Abstract A16: RIG-I-mediated cell death pathways activated by PAMP RNA in hepatic tumor cells." Cancer Immunology Research 10, no. 12_Supplement (December 1, 2022): A16. http://dx.doi.org/10.1158/2326-6074.tumimm22-a16.
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Abstract Most malignant cells are poorly immunogenic and fail to elicit an effective antitumor response. However, some viral infections of cancer cells can trigger intracellular innate immune defenses that initiate cancer cell death, known as “oncolytic signaling.” Our lab has identified a viral pathogen associated molecular pattern (PAMP) RNA motif from the hepatitis C virus (HCV) genome that is recognized by the pathogen recognition receptor, retinoic acid-inducible gene I (RIG-I), to induce innate immune signaling when delivered to cells in a liposomal formulation. We found that PAMP RNA can direct RIG-I-dependent signaling to drive cell death in tumor cells, indicating that PAMP activation of the RIG-I pathway has applications for oncolytic destruction of tumors. However, the exact cell death pathways that are activated by PAMP are not clearly defined. We hypothesize that PAMP activates a RIG-I-mediated form of apoptosis and that cancer cells are more susceptible than non-cancer cells to death by this apoptotic pathway. In vitro studies using CRISPR knockout cell lines confirmed that PAMP-induced cell death signaling requires RIG-I, mitochondrial antiviral-signaling protein (MAVS), and interferon regulatory factor 3 (IRF3). Further, our analyses show that PAMP-induced cell death is regulated by type 1 interferon, and that cell death outcomes can be blocked by treatment of cells with caspase inhibitor. Thus, PAMP-induced RIG-I signaling triggers cell death through linkage with caspase signaling. This research will define cell death pathways activated by PAMP and RIG-I signaling by interrogating multiple cell death programs and will reveal the potential of designing antitumor therapeutics leveraging PAMP. Citation Format: Brittany Ulloa, Michael Gale. RIG-I-mediated cell death pathways activated by PAMP RNA in hepatic tumor cells [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr A16.
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Chalifour, Anick, Pascale Jeannin, Jean-François Gauchat, Aline Blaecke, Martine Malissard, Thien N'Guyen, Nathalie Thieblemont, and Yves Delneste. "Direct bacterial protein PAMP recognition by human NK cells involves TLRs and triggers α-defensin production." Blood 104, no. 6 (September 15, 2004): 1778–83. http://dx.doi.org/10.1182/blood-2003-08-2820.
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Abstract Although human CD56+CD3- natural killer (NK) cells participate in immune responses against microorganisms, their capacity to directly recognize and be activated by pathogens remains unclear. These cells encode members of the Toll-like receptor (TLR) family, involved in innate cell activation on recognition of pathogen-associated molecular patterns (PAMPs). We therefore evaluated whether the 2 bacterial protein PAMPs, the outer membrane protein A from Klebsiella pneumoniae (KpOmpA) and flagellin, which signal through TLR2 and TLR5, respectively, may directly stimulate human NK cells. These proteins induce interferon-γ (IFN-γ) production by NK cells and synergize with interleukin-2 (IL-2) and proinflammatory cytokines in PAMP-induced activation. Similar results were obtained using CD56+CD3+ (NKR-expressing) T cells. NK cells from TLR2-/- mice fail to respond to KpOmpA, demonstrating TLR involvement in this effect. Defensins are antimicrobial peptides expressed mainly by epithelial cells and neutrophils that disrupt the bacterial membrane, leading to pathogen death. We show that NK cells and NKR-expressing T cells constitutively express α-defensins and that KpOmpA and flagellin rapidly induce their release. These data demonstrate for the first time that highly purified NK cells directly recognize and respond to pathogen components through TLRs and evidence defensins as a novel and direct cytotoxic pathway involved in NK cell-mediated protection against microorganisms. (Blood. 2004;104:1778-1783)
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Chen, Shiu-Jau, Tzer-Bin Lin, Hsien-Yu Peng, Cheng-Hsien Lin, An-Sheng Lee, Hsiang-Jui Liu, Chun-Chieh Li, and Kuang-Wen Tseng. "Protective Effects of Fucoxanthin Dampen Pathogen-Associated Molecular Pattern (PAMP) Lipopolysaccharide-Induced Inflammatory Action and Elevated Intraocular Pressure by Activating Nrf2 Signaling and Generating Reactive Oxygen Species." Antioxidants 10, no. 7 (July 7, 2021): 1092. http://dx.doi.org/10.3390/antiox10071092.
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Inflammation and oxidative stress are closely related processes in the pathogenesis of various ocular diseases. Uveitis is a disorder of the uvea and ocular tissues that causes extreme pain, decreases visual acuity, and can eventually lead to blindness. The pharmacological functions of fucoxanthin, isolated from brown algae, induce a variety of therapeutic effects such as oxidative stress reduction and repression of inflammation reactions. However, the specific anti-inflammatory effects of fucoxanthin on pathogen-associated molecular pattern (PAMP) lipopolysaccharide-induced uveitis have yet to be extensively described. Therefore, the aim of present study was to investigate the anti-inflammatory effects of fucoxanthin on uveitis in rats. The results showed that fucoxanthin effectively enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in ocular tissues. Furthermore, fucoxanthin significantly increased the ocular activities of superoxide dismutase and decreased the levels of malondialdehyde stimulated by PAMP-induced uveitis. Ocular hypertension and the levels of inflammatory cells and proinflammatory cytokine tumor necrosis factor-alpha in the aqueous humor were alleviated with fucoxanthin treatment. Consequently, compared to the observed effects in lipopolysaccharide groups, fucoxanthin treatment significantly preserved iris sphincter innervation and pupillary function. Additionally, PAMP-induced corneal endothelial disruption was significantly inhibited by fucoxanthin treatment. Overall, these findings suggest that fucoxanthin may protect against inflammation from PAMP-induced uveitis by promoting the Nrf2 pathway and inhibiting oxidative stress.
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Zhang, Jie, Haibin Lu, Xinyan Li, Yan Li, Haitao Cui, Chi-Kuang Wen, Xiaoyan Tang, Zhen Su, and Jian-Min Zhou. "Effector-Triggered and Pathogen-Associated Molecular Pattern–Triggered Immunity Differentially Contribute to Basal Resistance to Pseudomonas syringae." Molecular Plant-Microbe Interactions® 23, no. 7 (July 2010): 940–48. http://dx.doi.org/10.1094/mpmi-23-7-0940.
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Pathogens induce pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants. PAMPs are microbial molecules recognized by host plants as nonself signals, whereas pathogen effectors are evolved to aid in parasitism but are sometimes recognized by specific intracellular resistance proteins. In the absence of detectable ETI determining classical incompatible interactions, basal resistance exists during compatible and nonhost interactions. What triggers the basal resistance has remained elusive. Here, we provide evidence that ETI contributes to basal resistance during both compatible and nonhost Arabidopsis–Pseudomonas syringae interactions. Mutations in RAR1 and NDR1, two genes required for ETI, compromise basal resistance in both compatible and nonhost interactions. Complete nonhost resistance to P. syringae pv. tabaci required a functional type III secretion system. PTI appears to play a greater role in nonhost resistance than basal resistance during compatible interactions, because abrogation of PTI compromises basal resistance during nonhost but not compatible interactions. Strikingly, simultaneous abrogation of ETI and flagellin-induced PTI rendered plants completely susceptible to the nonadapted bacterium P. syringae pv. tabaci, indicating that ETI and PTI act synergistically during nonhost resistance. Thus, both nonhost resistance and basal resistance to virulent bacteria can be unified under PTI and ETI.
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Sidor, Karolina, and Tomasz Skirecki. "A Bittersweet Kiss of Gram-Negative Bacteria: The Role of ADP-Heptose in the Pathogenesis of Infection." Microorganisms 11, no. 5 (May 17, 2023): 1316. http://dx.doi.org/10.3390/microorganisms11051316.
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Due to the global crisis caused by the dramatic rise of drug resistance among Gram-negative bacteria, there is an urgent need for a thorough understanding of the pathogenesis of infections of such an etiology. In light of the limited availability of new antibiotics, therapies aimed at host–pathogen interactions emerge as potential treatment modalities. Thus, understanding the mechanism of pathogen recognition by the host and immune evasion appear to be the key scientific issues. Until recently, lipopolysaccharide (LPS) was recognized as a major pathogen-associated molecular pattern (PAMP) of Gram-negative bacteria. However, recently, ADP-L-glycero-β-D-manno-heptose (ADP-heptose), an intermediate carbohydrate metabolite of the LPS biosynthesis pathway, was discovered to activate the hosts’ innate immunity. Therefore, ADP-heptose is regarded as a novel PAMP of Gram-negative bacteria that is recognized by the cytosolic alpha kinase-1 (ALPK1) protein. The conservative nature of this molecule makes it an intriguing player in host–pathogen interactions, especially in the context of changes in LPS structure or even in its loss by certain resistant pathogens. Here, we present the ADP-heptose metabolism, outline the mechanisms of its recognition and the activation of its immunity, and summarize the role of ADP-heptose in the pathogenesis of infection. Finally, we hypothesize about the routes of the entry of this sugar into cytosol and point to emerging questions that require further research.
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Asiamah, Emmanuel K., Sarah Adjei-Fremah, Bertha Osei, Kingsley Ekwemalor, and Mulumebet Worku. "An Extract of Sericea Lespedeza Modulates Production of Inflammatory Markers in Pathogen Associated Molecular Pattern (PAMP) Activated Ruminant Blood." Journal of Agricultural Science 8, no. 9 (August 5, 2016): 1. http://dx.doi.org/10.5539/jas.v8n9p1.
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<p>Programs based on antibiotics are failing to control diseases due to increase in resistance of pathogens to antibiotics. Food safety, animal welfare and public health concerns have fueled interest in the use of plant-based alternatives. This study was conducted to evaluate the effect of a plant (Sericea Lespedeza, SL), and pathogen associated molecular patterns (PAMPs) (Lipopolysaccharide (LPS) and peptidoglycan (PGN)) on gene activation in ruminant blood. A water extract of SL, was used as a source of plant-derived tannins. Blood was collected from Holstein-Friesian cows (N = 4), Spanish × Boer goats (N = 4), St Croix sheep (N = 4) and incubated with 100 ng/mL of SL in the presence or absence of LPS or PGN. Samples maintained in Phosphate-buffered saline (PBS) served as negative control. The total protein concentration, WNT5a, and prostaglandin E2 in plasma were determined. Total RNA was isolated, reverse transcribed and Real time-PCR was performed using gene specific primers for TLR2, TLR4, WNT5a, and FZD. TLR2 and FZD were up-regulated in response to PAMPs. WNT5a and TLR4 genes were undetected in PAMP treated blood. SL regulated protein and prostaglandin concentration in all species. SL reduced PGE2 in sheep and cow blood. WNT5a was only secreted in LPS treated cow blood. Transcription and translation of genes involved in innate and adaptive immunity and the WNT signaling pathway in ruminant blood were responsive to diverse PAMPS, and can be modulated by SL. This suggests that dietary tannins may promote the health of ruminants. Further studies are needed to determine the significance of these changes in immune gene expression on ruminant health.</p>
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Nakamura, Kiwamu, Akiko Miyazato, Shinobu Saijo, Yoichiro Iwakura, Mitsuo Kaku, and Kazuyoshi Kawakami. "Role of TLR2 and dectin-1 in the host response to Penicillium marneffei (51.10)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S98. http://dx.doi.org/10.4049/jimmunol.178.supp.51.10.
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Abstract Pathogen-associated molecular patterns (PAMP) are recognized by Toll-like receptors (TLR) and C-type lectin receptors including Dectin-1. In the current study, we examined the role of TLR2 and 4 and dectin-1, a β-glucan receptor, in the host response to Penicillium marneffei, an opportunistic fungal pathogen in AIDS patients. IL-12p40 production by bone marrow-derived dendritic cells (BMDCs) stimulated with yeast cells of this fungal pathogens was significantly reduced in TLR2KO and MyD88KO mice, but not in TLR4KO and C3H/HeJ mice, compared to that in control mice. Such production was significantly lower in dectin-1KO mice than wild-type mice. In further experiments, HEK293 cells transfected with TLR2 and/or dectin-1 genes were stimulated with P. marneffei for a NFκB promoter assay. Compared to the cells transfected with control vector, significantly higher activity of NFκB was detected in TLR2-transfectant, but this response was not further enhanced by co-transfection with dectin-1. Taken together, these results demonstrated that TLR2 and dectin-1 played an important role in the recognition of P. marneffei by BMDCs.
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Liu, Po-Pu, Yue Yang, Eran Pichersky, and Daniel F. Klessig. "Altering Expression of Benzoic Acid/Salicylic Acid Carboxyl Methyltransferase 1 Compromises Systemic Acquired Resistance and PAMP-Triggered Immunity in Arabidopsis." Molecular Plant-Microbe Interactions® 23, no. 1 (January 2010): 82–90. http://dx.doi.org/10.1094/mpmi-23-1-0082.
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Methyl salicylate (MeSA), which is synthesized in plants from salicylic acid (SA) by methyltransferases, has roles in defense against microbial and insect pests. Most of the MeSA that accumulates after pathogen attack is synthesized by benzoic acid/SA carboxyl methyltransferase 1 (AtBSMT1). To investigate the role of AtBSMT1 in plant defense, transgenic Arabidopsis with altered AtBSMT1 function or expression were assessed for their ability to resist pathogen infection. A knockout mutant (Atbsmt1) failed to accumulate MeSA following pathogen infection; these plants also failed to accumulate SA or its glucoside in the uninoculated leaves and did not develop systemic acquired resistance (SAR). However, the Atbsmt1 mutant exhibited normal levels of effector-triggered immunity and pathogen-associated molecular pattern (PAMP)-triggered immunity to Pseudomonas syringae and Hyaloperonospora arabidopsidis. Analyses of transgenic Arabidopsis plants overexpressing AtBSMT1 revealed that they accumulate elevated levels of MeSA in pathogen-infected leaves but fail to develop SAR. Since the levels of SA and its glucoside were reduced in uninoculated systemic leaves of these plants whereas MeSA levels were elevated, AtBSMT1-mediated conversion of SA to MeSA probably compromised SAR development by suppressing SA accumulation in uninoculated leaves. PAMP-triggered immunity also was compromised in the AtBSMT1 overexpressing plants, although effector-triggered immunity was not.
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Li, Guangjin, Tong Chen, Zhanquan Zhang, Boqiang Li, and Shiping Tian. "Roles of Aquaporins in Plant-Pathogen Interaction." Plants 9, no. 9 (September 1, 2020): 1134. http://dx.doi.org/10.3390/plants9091134.
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Aquaporins (AQPs) are a class of small, membrane channel proteins present in a wide range of organisms. In addition to water, AQPs can facilitate the efficient and selective flux of various small solutes involved in numerous essential processes across membranes. A growing body of evidence now shows that AQPs are important regulators of plant-pathogen interaction, which ultimately lead to either plant immunity or pathogen pathogenicity. In plants, AQPs can mediate H2O2 transport across plasma membranes (PMs) and contribute to the activation of plant defenses by inducing pathogen-associated molecular pattern (PAMP)-triggered immunity and systemic acquired resistance (SAR), followed by downstream defense reactions. This involves the activation of conserved mitogen-activated protein kinase (MAPK) signaling cascades, the production of callose, the activation of NPR1 and PR genes, as well as the opening and closing of stomata. On the other hand, pathogens utilize aquaporins to mediate reactive oxygen species (ROS) signaling and regulate their normal growth, development, secondary or specialized metabolite production and pathogenicity. This review focuses on the roles of AQPs in plant immunity, pathogenicity, and communications during plant-pathogen interaction.
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Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 1—Innate and Humoral Immunity and the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 198–208. http://dx.doi.org/10.1177/154405910608500301.
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Based on the results of recent research in the field, the present paper will discuss the protective and destructive aspects of the innate vs. adaptive (humoral and cell-mediated) immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) the Toll-like receptors (TLR), the innate immune repertoire for recognizing the unique molecular patterns of microbial components that trigger innate and adaptive immunity for effective host defenses, in some general non-oral vs. periodontal microbial infections; (ii) T-cell-mediated immunity, Th-cytokines, and osteoclastogenesis in periodontal disease progression; and (iii) some molecular techniques developed and used to identify critical microbial virulence factors or antigens associated with host immunity (using Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species). Therefore, further understanding of the molecular interactions and mechanisms associated with the host’s innate and adaptive immune responses will facilitate the development of new and innovative therapeutics for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; and TLR, Toll-like receptors.
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Tuleski, Thalita Regina, Jennifer Kimball, Fernanda P. do Amaral, Tomas P. Pereira, Michelle Zibetti Tadra-Sfeir, Fabio de Oliveira Pedrosa, Emanuel Maltempi de Souza, Peter Balint-Kurti, Rose Adele Monteiro, and Gary Stacey. "Herbaspirillum rubrisubalbicans as a Phytopathogenic Model to Study the Immune System of Sorghum bicolor." Molecular Plant-Microbe Interactions® 33, no. 2 (February 2020): 235–46. http://dx.doi.org/10.1094/mpmi-06-19-0154-r.
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Herbaspirillum rubrisubalbicans is the causal agent of red stripe disease (RSD) and mottle stripe disease of sorghum and sugarcane, respectively. In all, 63 genotypes of Sorghum bicolor were inoculated with H. rubrisubalbicans, with 59 showing RSD symptoms. Quantitative trait loci (QTL) analysis in a recombinant inbred line (RIL) population identified several QTL associated with variation in resistance to RSD. RNA sequencing analysis identified a number of genes whose transcript levels were differentially regulated during H. rubrisubalbicans infection. Among those genes that responded to H. rubrisubalbicans inoculation were many involved in plant–pathogen interactions such as leucine-rich repeat receptors, mitogen-activated protein kinase 1, calcium-binding proteins, transcriptional factors (ethylene-responsive element binding factor), and callose synthase. Pretreatment of sorghum leaves with the pathogen-associated molecular pattern (PAMP) molecules flg22 and chitooctaose provided protection against subsequent challenge with the pathogen, suggesting that PAMP-triggered immunity plays an important role in the sorghum immunity response. These data present baseline information for the use of the genetically tractable H. rubrisubalbicans–sorghum pathosystem for the study of innate immunity and disease resistance in this important grain and bioenergy crop. Information gained from the use of this system is likely to be informative for other monocots, including those more intractable for experimental study (e.g., sugarcane).