Academic literature on the topic 'PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)'
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Journal articles on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
1
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.
Dissertations / Theses on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
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Boltaña, Harms Sebastian. "Molecular characterisation of the underlying mechanisms of pathogen-associated molecular pattern (PAMP) recognition in fish." Doctoral thesis, Universitat Autònoma de Barcelona, 2011. http://hdl.handle.net/10803/42005.
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La respuesta inmune innata es basada en la activación de receptores
genotípicamente codificados, llamados receptores de reconocimiento de patógenos
(PRR). Los PRR pueden ser proteínas solubles tal como las proteínas plasmáticas
PGRPs o pueden estar anclados en las membranas celulares como los TLR. Estos
receptores son capaces de reconocer a los patógenos o a sus patrones moleculares
(PAMPs). La interacción PAMP-PRR provoca la activación de genes diana y
promueve la producción de mediadores pro- e inflamatorios. El principal objetivo
de esta tesis doctoral fue la caracterización de las respuestas de macrófagos de la
trucha arcoíris Oncorhynchus mykiss, y de la dorada tratados con diferentes
PAMPs y la subsecuente exploración de cambios en la expresión de genes
relacionados con la respuesta inmune así como cambios globales en la respuesta
transcriptómica de los macrófagos. Un objetivo especifico de este estudio fue
registrar los cambios en los macrófagos activados hacia un fenotipo inflamatorio
después de tratamientos con lipopolisacarido (LPS) crudo de bacterias Gram
negativas, enfatizando que el peptidoglicano (PGN) es un contaminante
encontrado en las preparaciones crudas de LPS. PGN es capaz de inducir la
expresión de mRNA de IL-1β y IL-6 e inducir la liberación de productos
inflamatorios como prostaglandinas. Los análisis de microarray fueron hechos
para describir la concentración y la dependencia en el tiempo de las modulaciones
transcriptómicas en los macrófagos de trucha y dorada tratados con PGN o LPS.
En el caso de dorada, se diseño y valido un microarray de oligonucleótidos. Los
resultados revelaron la sobre-regulación de transcritos específicos que están
cercanamente relacionados con la síntesis de prostaglandinas y las vías de
señalización activadas a partir de TLR. Así, el reconocimiento de PGN en peces
resulta del reconocimiento de mecanismos específicos que no incluyen TLR pero si
otros grupos de receptores como PGRPs o NODs. Estos mecanismos parecen ser
conservados en la respuesta de defensa innata a lo largo del grupo de los
vertebrados.The innate immune response is based upon the activation of a restricted number of genotypic encoded receptors, the pathogen recognition receptors (PRRs). PRRs can be soluble proteins such as plasmatic PGRPs or cell membraneanchored TLRs able to recognize pathogens or their pathogen-associated molecular patterns (PAMPs). PAMP-PRR interaction results in the activation of target genes and promotes the production of pro- and inflammatory mediators. The main goal of this dissertation was to characterise the responses of rainbow trout, Oncorhynchus mykiss, and gilthead seabream, Sparus aurata, macrophages treated with different PAMPs and to explore subsequent changes in the expression of immune related genes or global shifts in the macrophage transcriptome. A specific goal of this study was to register changes in macrophages activated toward an inflammatory phenotype after treatments with crude gram negative bacterial lipopolysaccharide (LPS) preparations, highlighting that peptidoglycan (PGN) is a contaminant within crude LPS. PGN is able to induce the mRNA expression of IL- 1β and IL-6 and release inflammatory products such as prostaglandins. Microarray analyses were made to describe concentration and time-dependent transcriptional modulations both in trout and seabream macrophages treated with PGN or LPS. In the case of sea bream, a specific oligonucleotide microarray was designed and validated for these studies. Results reveal up-regulation of specific mRNA transcripts that are closely related to prostaglandin synthesis and TLR signalling pathways. Thus PGN recognition in fish is a result of recognition mechanisms including non-TLR PRRs such as PGRPs and NODs. These mechanisms appear to be conserved throughout the vertebrate innate immune response.
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AMBIKA, KM. "ROLE OF LACTOSMART AS A NOVEL THERAPEUTIC AGENT IN ANTIMICROBIAL DEFENSE." Thesis, DELHI TECHNOLOGICAL UNIVERSITY, 2021. http://dspace.dtu.ac.in:8080/jspui/handle/repository/18433.
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The emergence of multi – drug resistance (MDR ) in microorganisms against
antibiotics has become a global problem [1,2,3]. Various conventional drugs with
promised efficacy and specificity are unable to withstand the threat of antibiotic drug
resistance [4,5,6].
The rising crisis of MDR bacteria has led to the channelization of relevant
research in the direction of antimicrobial molecules from natural sources as potential
novel antibiotics. The spectrum of innate immune proteins and their potent
fragments herald a promising approach to fight the problem of drug resistance. Among
the natural antimicrobial proteins, Lactoferrin (LF) has been identified as a potent
host defense system based on its wide spectrum bactericidal and bacteriostatic activities
[7,8,9,10,11,12,13] . In the past , several studies have demonstrated the antibacterial and
antifungal effects of LF and its derivative peptides, for instance, lactoferricin B
[14,15,16,17,18,19] and lactoferrampin [20,21].
Structurally, LF consists of two iron bound lobes, N -lobe (1-333) and C -lobe
(345-692) [22,23,24,25]. Amongst the two lobes , the highly cationic properties of N- lobe
are responsible for membrane disruption by interacting with anionic components
present on bacterial surface [26,27]. It has been established that the lipid A component
of the LPS is a known drug target for antimicrobial therapeutics [ 28,29]. One of the
mechanisms by which Lf acts as an antimicrobial agent is through binding to pathogen
associated molecular patterns (PAMP) such as Lipopolysaccharide (LPS), thereby
disrupting the bacterial membrane integrity and activating the chemical signaling pathway[30-
32]. This leads to the secretion of pro- inflammatory responses which down regulates the release of cytokine production [33,34]. In the past, it had been
reported that LF binds to LPS with its hexameric sequence present in the 18 - loop region
of the lactoferricin [35-37] .
In the present study , we have performed the partial digestion of LF with trypsin
which generates a potent antimicrobial molecule of the size of about 21kDa (85-281).
We have proposed its name as Lactosmart due to its higher potency against pathogens
when compared to native LF as a whole protein . The lactosmart has been tested for
antibacterial and antifungal properties along with its inhibitory potential of biofilm
formation by Pseudomonas aeruginosa through established assays [41]. Our primary
focus was on the comparison of LPS binding properties of lactosmart with native LF
using surface plasmon resonance technique . The docking and molecular dynamics
simulations (MD) studies with LPS have also been performed to further substantiate our
claims. Through our studies , we have demonstrated that LF sequesters LPS through
two binding sites which are situated on the N- lobe.
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Janakiraman, Vani. "Réponse immunitaire innée et adaptative pour des motifs moléculaire associés aux mycobactéries pathogènes (« PAMPs »)." Paris 6, 2010. http://www.theses.fr/2010PA066291.
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La tuberculose causée par Mycobacterium tuberculosis est la plus mortelle des maladies infectieuses. Les mycobactéries sont des pathogènes intra-cellulaires qui ont développé des mécanismes d’évasion spécifiques pour survivre au sein de leur hôte. Une réponse immune anti-mycobatérienne efficace met en jeu l’activation des cellules T CD4+ Th1 ainsi que la génération d’IFN- microbicide. Cependant, des patients ayant une tuberculose active présentent une réponse immune de type Th2 durant les stades les plus tardifs de l’infection. L’association de ce pathogène avec le VIH chez les patients atteints du SIDA et l’émergence de souches extrêmement résistantes aux traitements actuelles font de la tuberculose une « urgence mondiale ». Ainsi, découvrir les interactions moléculaires des motifs antigéniques associés aux mycobactéries pathogènes (« PAMPs ») avec le système immunitaire de l’hôte est important pour comprendre la pathogenèse de la tuberculose et pour permettre une immunointervention thérapeutique efficace. La mise en place d’une réponse immune contre M. Tuberulosis met en jeu l’interaction entre les systèmes immunitaires innés et adaptatifs. Les cellules de l’immunité innée comme les cellules dendritiques (CD) sont impliquées dans la reconnaissance du pathogène et des antigènes qui en dérives, dans la présentation de peptides antigéniques aux cellules T et dans la sécrétion d’un large panel de cytokines qui permettent la différenciation et l’expansion des cellules T CD4+ et T CD8+. Les cellules T CD4+ Th fournissent l’aide nécessaire aux lymphocytes B pour la production des anticorps. Outre la production d’anticorps, les cellules B peuvent aussi agir comme cellules présentatrices de l’antigène et produire différentes cytokines et chimiokines immunorégulatrices qui modulent la réponse immune et l’inflammation. Durant ma thèse, j’ai étudié l’interaction moléculaire des « PAMPs » de M. Tuberculosis avec des CD et des cellules B humaines et j’ai examiné in vivo les réponses immunes dirigées contre les « PAMPs » en association avec différentes molécules adjuvantes. Dans un premier temps, j’ai étudié la régulation des fonctions des CD humaines par un antigène mycobactérien de surface mannosylé : le mannose lipoarabinomannan (ManLAM). Le ManLAM est un composant principal de la membrane cellulaire des mycobactéries et est impliqué dans l’immunopathogenèse de la tuberculose. J’ai démontré que le ManLAM induisait la maturation des CD vers une réponse immune de type Th2 et la production de chimiokines impliquées dans la migration des cellules T Th2 et T régulatrice (Treg). De plus, les cellules B ont été retrouvées sur le site de réactions granulomateuses chez l’homme et la souris atteints de la tuberculose. Cependant le rôle des cellules B dans la réponse immune contre la tuberculose reste inconnu. A cet effet, j’ai étudié l’interaction du ManLAM avec des cellules B humaines issues de donneurs sains. J’ai démontré que le ManLAM stimulait la prolifération des cellules B avec une forte production d’IL-8 et d’IL-6. Mes résultats montrent de même que la prolifération des cellules B stimulées par le ManLAM avait pour origine l’interaction entre le ManLAM et le TLR-2. Ainsi, les cellules B éduquées par le ManLAM propagent la réponse immune de type Th2. L’ensemble de mes résultats démontrent que le ManLAM module la fonction des CD et des cellules B afin d’échapper à la réponse cellulaire T efficace contre M. Tuberculosis. PE, PPE sont de nouvelles familles de protéines qui ont été identifiées après que le génome de M. Tuberculosis ait été entièrement séquencé. Ces classes de protéines sont propres aux mycobactéries et la plupart d’entre elles sont des protéines de surface qui ont la capacité d’interagir avec les cellules du système immunitaire. J’ai étudié l’interaction de PE_PGRS 62 (Rv3812) avec les CD humaines et j’ai montré que PE_PGRS 62 agissait comme un ligant de TLR-2 et induisait la maturation des CD vers des réponses de type Th1. De plus, j’ai démontré que PE_PGRS 62 générait de fortes réponses immunitaires in vivo dans différents modèles expérimentaux. L’ensemble de ces résultats montre que PE_PGRS 62 met en place une réponse cellulaire de type Th1 en présence ou non d’antigènes immunorégulateurs tels que le ManLAM et la protéine gp120 du VIH. Ceci permet d’envisager l’utilisation de PE_PGRS 62 comme vaccin candidat pour combattre la tuberculose.
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Hadebe, Sabelo Goodman. "The role of pathogen associated molecular patterns in the pathogenesis of asthma." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=215573.
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Asthma is a complex obstructive airway disease characterised by airway hyper-reactivity to innocuous allergens. It may be categorised as either classical eosinophilic, T helper 2 type of disease or as one driven by neutrophils that may be associated with T helper 17 cells and that is corticosteroid resistant. While the pathogenesis of the disease is not fully understood, there is increasing evidence for the role of environmentally-derived pathogen-associated molecular patterns (PAMPs) including fungal β-(1,3)-glucans and bacterial lipopolysaccharide (LPS) in inducing and exacerbating airway inflammation. We investigated the effects of these components, either alone or in combination, in several models of pulmonary inflammation and discovered that they modified airway responses in vivo. Notably, a combination of PAMPs drove a profound neutrophilia that was associated with synergistic CCL5 production. Moreover, in allergic models using house dust mite, sensitisation with these agonists resulted in corticosteroid resistant airway hyper-responsiveness. Interestingly, we found severe asthmatics with corticosteroid resistant neutrophilia to have upregulated CCL5 mRNA levels when compared to moderate asthmatics or controls. Interactions of environmental PAMPs from multiple sources could present a key determinant in the development and pathogenesis of corticosteroid resistant asthma.
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Durand, Vanessa Magali Marie. "Shaping of adaptive immune responses to soluble protein antigens by pathogen-associated molecular patterns." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444644/.
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Invading organisms are detected by the innate immune system, through the recognition of conserved microbial structures. Innate responses are known to influence the development of adaptive immune responses, which are crucial for preventing infection and eliminating pathogens. Characterising the signals that initiate the induction of efficient cellular and humoral adaptive immune responses is particularly relevant for the rational design of new vaccines. The aims of this study were first to assess the ability of a broad range of conserved microbial stimuli to induce CD8+ T cells responses by cross-priming and enhance antibody responses against exogenous soluble protein antigens, and secondly to investigate the mechanisms by which microbial stimuli induced cross-priming. Stimulation of Toll like receptors (TLR) is believed to play a major role in the activation of innate and subsequent adaptive responses. All TLR agonists tested enhanced antigen-specific antibody responses, and in particular zymosan (TLR2/6), poly(I:C) (TLR3), LPS from E. coli (TLR4) and CpG DNA (TLR9) promoted IgG2a responses, which are thought to contribute effectively to protective mechanisms against pathogens in mice. However, only poly(I:C), LPS from E. coli and CpG DNA were able to stimulate the induction of cross-priming, whereas zymosan, peptidoglycan (TLR2/) and R-848 (TLR7) were ineffective. It is known that LPS from different bacteria species can elicit different immune responses. LPSs from Klebsiella pneumoniae and from Neisseria meningitidis, but not the unconventional LPS from Porphyromonas gingivalis, were able to induce cross-priming. Microbial mannose structures, as present in yeast mannan, Influenza hemagglutinin and polymannose LPS, were demonstrated for the first time to be able to induce functional cross-priming. In addition, mannan and polymannose LPS were found to enhance antigen-specific antibody responses and promote IgG2a responses. IFN-a/p and signalling through costimulatory molecules play a central role in the licensing of cross-priming. Experiments using knock-out mice showed that in all cases licensing of cross- priming was dependent on IFN-a/pR signalling, albeit to a varying degree. In contrast, signalling through CD40 was not required for induction of cross-priming by mannan and polymannose LPS. Induction of cross-priming by LPS from E. coli and by mannan was TLR4-dependent, whereas induction by polymannose LPS was TLR4-independent. This study thus identifies LPS from some bacteria species as cross-priming-inducing stimuli. It also confirms that activation of TLR can initiate induction of cross- priming, while indicating the existence of TLR-independent pathways. In addition, this work illustrates the importance of IFN-oc/pR signalling as a cross-priming licensing stimulus.
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Sawyer, Daniel Thomas. "The Involvement of Hsp70 in the Innate Immune Recognition of Pathogen Associated Molecular Patterns." Thesis, University of Sussex, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517138.
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Barghahn, Sina [Verfasser]. "Pathogen-induced cell wall remodeling and production of Danger Associated Molecular Patterns (DAMPs) / Sina Barghahn." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1230137998/34.
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Turner, Matthew L. "The effect of bacterial pathogen-associated molecular patterns and metabolism on innate immunity in the bovine endometrium." Thesis, Swansea University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678484.
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Myskiw, Chad. "Role of the Vaccinia Virus E3 protein and its poxvirus orthologues in suppressing innate immune responses activated by RNA-based pathogen-associated molecular patterns." American Society for Microbiology, 2009. http://hdl.handle.net/1993/4967.
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Poxviruses are a diverse family of double-stranded DNA viruses. A characteristic feature of poxviruses is that they express a vast array of immuno-modulatory proteins. Vaccinia virus is the prototypic member of the Orthopoxvirus genus, which also includes variola virus, the causative agent of smallpox. The vaccinia E3 protein is required for virus replication in vivo and in numerous cell culture systems. Although E3 function has received considerable study, many aspects of E3 biology remain to be addressed. While E3 can inhibit cytokine expression, the pathways targeted by E3 to block cytokine expression have not been identified. Furthermore, the factor(s) which stimulate innate immune responses during vaccinia infection are not known. In this study, E3 was found to target PKR and RIG-I-like receptor mediated signal transduction to differentially block expression of IFN-β, TNF-α and IL-6 in HeLa cells. RNA species generated in vaccinia infected cells were identified as pathogen-associated molecular patterns capable of inducing cytokine expression and activating apoptosis. Furthermore, PKR, RIG-I and MDA5 play non-overlapping and essential roles in mediating the innate immune response to these RNA species.
Orthologues of E3 are encoded by all poxviruses which infect vertebrate animals except the Avipoxviruses and molluscum contagiosum virus. However, orthologues of vaccinia E3 remain essentially uncharacterized. A comparative analysis of the ability of E3 orthologues encoded by sheeppox, yaba monkey tumour, swinepox and myxoma virus to complement deletion of E3 was performed. E3 orthologues of myxoma virus and swinepox virus suppress PKR activation and interferon induced antiviral activity and restore the host range function of E3 in culture. In contrast, the E3 orthologues of sheeppox virus and yaba monkey tumour virus are unable to inhibit PKR activation. While the sheeppox orthologue cannot restore the host range function of E3, the yaba monkey tumour virus orthologue partially restores E3 deficient vaccinia replication. However, none of these E3 orthologues restore pathogenicity to E3 deficient vaccinia in vivo. In summary, these results highlight the role of the vaccinia virus E3 protein and its poxvirus orthologues in suppressing innate immune responses activated by RNA-based pathogen-associated molecular patterns
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Voth, Stephanie. "MICROBIAL DNA RECEPTOR EXPRESSION IN CHRONIC PERIODONTITIS." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3129.
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AIM: The aim of this study was to determine the expression of microbial nucleic acid receptors including Toll like receptor 9 “TLR-9”, DNA-dependent activator of interferon-regulatory factors “DAI” and absent in melanoma “AIM-2” in chronic periodontitis (P) versus healthy (H) tissues. METHODS: 33 chronic periodontitis (P) and 27 periodontally-healthy (H) gingival biopsies were included. The gene and protein expression for each receptor was determined using real-time quantitative PCR and immunohistochemistry. RESULTS: Our results revealed statistically significant up-regulation of TLR-9 (p<0.006) and DAI (p<0.001) gene expression in P tissues compared to H sites. We were also able to demonstrate significant correlation among three DNA receptors (p<0.05). Immunohistochemistry further confirmed the expression of DNA sensors in gingival tissues. CONCLUSION: This study highlights a possible role for nucleic acid sensing in periodontal inflammation. Further investigations will determine whether cytoplasmic receptors and their ligands can be targeted to improve clinical outcomes in periodontitis.
Books on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.
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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Wiersinga, W. Joost, and Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.
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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.
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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
Book chapters on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
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Silva-Gomes, Sandro, Alexiane Decout, and Jérôme Nigou. "Pathogen-Associated Molecular Patterns (PAMPs)." In Compendium of Inflammatory Diseases, 1055–69. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_35.
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Silva-Gomes, Sandro, Alexiane Decout, and Jérôme Nigou. "Pathogen-Associated Molecular Patterns (PAMPs)." In Encyclopedia of Inflammatory Diseases, 1–16. Basel: Springer Basel, 2014. http://dx.doi.org/10.1007/978-3-0348-0620-6_35-1.
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Correa, Wilmar, Lena Heinbockel, Guillermo Martinez-de-Tejada, Susana Sánchez, Patrick Garidel, Tobias Schürholz, Walter Mier, et al. "Synthetic Anti-lipopolysaccharide Peptides (SALPs) as Effective Inhibitors of Pathogen-Associated Molecular Patterns (PAMPs)." In Advances in Experimental Medicine and Biology, 111–29. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3588-4_8.
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Cavaillon, Jean-Marc. "Pathogen-associated Molecular Patterns." In Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 17–56. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch2.
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Rathore, Jitendra Singh, and Chaitali Ghosh. "Pathogen-Associated Molecular Patterns and Their Perception in Plants." In Molecular Aspects of Plant-Pathogen Interaction, 79–113. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7371-7_4.
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Vidhyasekaran, P. "Switching on Plant Immune Signaling Systems Using Pathogen-Induced Molecular Patterns/Host-Associated Molecular Patterns." In Switching on Plant Innate Immunity Signaling Systems, 191–228. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26118-8_4.
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Krishnan, Jayalakshmi. "Pattern Recognition Receptors in Brain: Emphasis on Toll Like Receptors and their Types." In Toll-Like Receptors in Vector-borne Diseases, 6–11. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815124545123010004.
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The immune system is highly complex; it senses foreign invaders, thus protecting the body. The adaptive arm of the immune system confers long-term protection, whereas the innate immune system confers immediate protection. In the case of the immune system, the pattern recognition receptors offer various modes of sensing the pathogen-associated molecular patterns present in pathogens. The receptors that sense invading pathogens are called Pattern recognition receptors [1]. The adaptive immune system is very sophisticated, as it is trained to identify only the “specific antigen”, but PPRs are customised to sense a wide array of “common patterns” present in the pathogens. Cerebral pericytes are the cells that are seen as embedded in the basement membrane of capillaries. Matzinger [2] gave a new insight into the recognition of pathogens by PRRs as those that recognise PAMPs and DAMPs (Damage Associated Molecular Patterns). While PAMPs can be presented as exogenous ligands to the receptor, DAMPs are presented as endogenous ligands. Once these PRRs are activated either by PAMPs or DAMPs, they lead to the production of inflammation to clear the infection. However, over-activation during chronic conditions leads to pathological changes.
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Gilbert, Gregory S., and Ingrid M. Parker. "Physiology and genetics." In The Evolutionary Ecology of Plant Disease, 163–78. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/oso/9780198797876.003.0012.
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Abstract Plants lack antibody-based immune systems, but they do have a robust system of defenses against pathogens. Constitutive defenses are a broad array of constitutively-produced physical structures and chemical compounds that protect most plants from infection by most pathogens. The three major groups of plant chemical defenses are phenolics, terpenoids, and the nitrogen-containing alkaloids and glucosinolates. Pathogens have evolved enzymes and specialized growth structures to overcome the constitutive defenses of their host plants. Inducible (or induced) defenses are produced in response to pathogen attack, and they rely on the plant detecting the presence of the pathogen. Local induced defenses are initiated when pattern recognition receptors (PRR) recognize specific microbe-associated molecular patterns (MAMPs, otherwise known as pathogen-associated molecular patterns, PAMPs) or effectors and induce pattern-triggered immunity (PTI) or effector-triggered immunity (ETI). Defense responses can include production of toxic phytoalexins or reactive oxygen species (ROS). Host responses may include a hypersensitive response that leads to rapid cell death in the host, limiting colonization by biotrophic pathogens. In many cases, there is a correspondence between specific pathogen genes that code for effectors, which determine virulence (here meaning pathogenicity), and host R-genes that code for receptors, which determine resistance relative to that particular virulence genotype in the pathogen. This correspondence is the gene-for-gene system first discovered in flax rust. In addition to local defense responses, plants can mount systemic resistance defenses in response to pathogen attack, using signaling pathways based on salicyclic acid, jasmonic acid, or ethylene.
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Primrose, Sandy B. "Some Common Factors Involved in Host-Pathogen Interactions." In Microbiology of Infectious Disease, 15–22. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780192863843.003.0002.
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Many pathogens have evolved common mechanisms for effecting the early stages of infecting target organisms, be they plants or animals. These include secretion systems, iron-chelating systems (siderophores), and motility. Secretion systems are the protein complexes used by bacteria to transport substances, particularly proteins, across cell membranes. They are the cellular devices whereby pathogenic bacteria secrete virulence factors that they use either to invade host cells or attack cells biochemically. Pathogens require iron for virulence and have evolved chelation systems to ensure that they can absorb enough. Pathogenic microbes need to attach to epithelial cells and use motility and chemotaxis to penetrate the protective hydrogels that overlay the epithelium. The target organisms have evolved common mechanisms for recognizing when they are being attacked, such as the detection of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors. The pathogens fight back by mutating in various ways including using phagocytosis as an infection strategy.
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Rasheed Anjum, Faisal, Sidra Anam, Muhammad Luqman, Ameena A. AL-surhanee, Abdullah F. Shater, Muhammad Wasim Usmani, Sajjad ur Rahman, Muhammad Sohail Sajid, Farzana Rizvi, and Muhammad Zulqarnain Shakir. "Fungal Immunology: Mechanisms of Host Innate Immune Recognition and Evasion by Pathogenic Fungi." In Fungal Reproduction and Growth [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101415.
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For a fungal pathogen to successfully infect, colonize and spread inside a susceptible host, it must have overcome the host immune responses. The early recognition of the fungal pathogen-associated molecular patterns (PAMPS) by the host’s pattern recognition receptors (PRRs) results in the establishment of anti-fungal immunity. Although, our immune system has evolved several processes to combat these pathogens both at the innate and adaptive immune levels. These organisms have developed various escape strategies to evade the recognition by the host\'s innate immune components and thus interfering with host immune mechanisms. In this chapter, we will summarize the major PRRs involved in sensing fungal PAMPS and most importantly the fungal tactics to escape the host\'s innate immune surveillance and protective mechanisms.
Conference papers on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
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Tun, Aung M., Stephen Hefeneider, Sharon McCoy, Erin Danielson, and Jeffrey A. Gold. "Synthetic Peptides Derived From Vaccinia Virus Inhibit Pathogen Associated Molecular Patterns (PAMP) Induced Nf-kB Activation In Human Macrophages." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2501.
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Agler, Anne H., Brent S. Pedersen, Laura A. Warg, David A. Schwartz, and Ivana V. Yang. "Whole Genome Association Mapping To Identify Novel Innate Immunity Genes Using Macrophage Cytokine Response To Pathogen-Associated Molecular Patterns (PAMP)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1063.
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Yang, Ivana V., Laura A. Warg, Elizabeth J. Davidson, Samir N. P. Kelada, Kari Kubalanza, Francis S. Collins, Elissa J. Chesler, et al. "INNATE IMMUNE GENE DISCOVERY USING MACROPHAGE RESPONSE TO PATHOGEN-ASSOCIATED MOLECULAR PATTERNS (PAMPS)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1273.
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Leonardo, Steven M., Ross B. Fulton, Keith B. Gorden, Katy Fraser, Ben Harrison, Takashi Kangas, Adria Jonas, et al. "Abstract LB-080: Imprime PGG, a β-glucan PAMP (pathogen-associated molecular pattern) activates the direct killing functions of innate immune cells in concert with tumor targeting antibodies." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-080.
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Fulton, Ross B., Steven M. Leonardo, Adria B. Jonas, Kathryn A. Fraser, Anissa S. H. Chan, Nadine R. Ottoson, Michael E. Danielson, Nandita Bose, Jeremy R. Graff, and Keith Gorden. "Abstract LB-089: Imprime PGG, a β-glucan PAMP (pathogen-associated molecular pattern), effectively elicits in vivo maturation of antigen presenting cells in mice and humans, suggesting potential synergy with checkpoint inhibitor therapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-089.
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Nacher, Jose C., and Vladimir B. Ryabov. "Identifying genes induced by different pathogen-associated molecular patterns." In Annual International Conference on BioInformatics and Computational Biology & Annual International Conference on Advances in Biotechnology. Global Science and Technology Forum, 2011. http://dx.doi.org/10.5176/978-981-08-8119-1_bicb33.
Full textReports on the topic "PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMP)"
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Sessa, Guido, and Gregory B. Martin. molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597918.bard.
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The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease.
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Sessa, Guido, and Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604270.bard.
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Pattern-recognition receptors (PRRs) located on the plant cell surface initiate immune responses by perceiving conserved pathogen molecules known as pathogen-associated molecular patterns (PAMPs). PRRs typically function in multiprotein complexes that include transmembrane and cytoplasmickinases and contribute to the initiation and signaling of pattern-triggered immunity (PTI). An important challenge is to identify molecular components of PRR complexes and downstream signaling pathways, and to understand the molecular mechanisms that mediate their function. In research activities supported by BARD-4931, we studied the role of the FLAGELLIN SENSING 3 (FLS3) PRR in the response of tomato leaves to flagellin-derivedPAMPs and PTI. In addition, we investigated molecular properties of the tomato brassinosteroid signaling kinase 830 (BSK830) that physically interacts with FLS3 and is a candidate for acting in the FLS3 signaling pathway. Our investigation refers to the proposal original objectives that were to: 1) Investigate the role of FLS3 and its interacting proteins in PTI; 2) Investigate the role of BSK830 in PTI; 3) Examine molecular and phosphorylation dynamics of the FLS3-BSK830 interaction; 4) Examine the possible interaction of FLS3 and BSK830 with Pstand Xcveffectors. We used CRISPR/Cas9 techniques to develop plants carrying single or combined mutations in the FLS3 gene and in the paralogsFLS2.1 and FLS2.2 genes, which encode the receptor FLAGELLIN SENSING2 (FLS2), and analyzed their function in PTI. Domain swapping analysis of the FLS2 and FLS3 receptors revealed domains of the proteins responsible for PAMP detection and for the different ROS response initiated by flgII-28/FLS3 as compared to flg22/FLS2. In addition, in vitro kinase assays and point mutations analysis identified FLS2 and FLS3 domains required for kinase activity and ATP binding. In research activities on tomato BSK830, we found that it interacts with PRRs and with the co-receptor SERK3A and PAMP treatment affects part of these interactions. CRISPR/Cas9 bsk830 mutant plants displayed enhanced pathogen susceptibility and reduced ROS production upon PAMP treatment. In addition, BSK830 interacted with 8 Xanthomonastype III secreted effectors. Follow up analysis revealed that among these effectors XopAE is part of an operon, is translocated into plant cells, and displays E3 ubiquitinligase activity. Our investigation was also extended to other Arabidopsis and tomato BSK family members. Arabidopsis BSK5 localized to the plant cell periphery, interacted with receptor-like kinases, and it was phosphorylatedin vitro by the PEPR1 and EFRPRRs. bsk5 mutant plants displayed enhanced susceptibility to pathogens and were impaired in several, but not all, PAMP-induced responses. Conversely, BSK5 overexpression conferred enhanced disease resistance and caused stronger PTI responses. Genetic complementation suggested that proper localization, kinase activity, and phosphorylation by PRRs are critical for BSK5 function. BSK7 and BSK8 specifically interacted with the FLS2 PRR, their respective mutant plants were more susceptible to B. cinereaand displayed reduced flg22-induced responses. The tomato BSK Mai1 was found to interact with the M3KMAPKKK, which is involved in activation of cell death associated with effector-triggered immunity. Silencing of Mai1 in N. benthamianaplants compromised cell death induced by a specific class of immune receptors. In addition, co-expression of Mai1 and M3Kin leaves enhanced MAPKphosphorylation and cell death, suggesting that Mai1 acts as a molecular link between pathogen recognition and MAPK signaling. Finally, We identified the PP2C phosphatase Pic1 that acts as a negative regulator of PTI by interacting with and dephosphorylating the receptor-like cytoplasmickinase Pti1, which is a positive regulator of plant immunity. The results of this investigation shed new light on the molecular characteristics and interactions of components of the immune system of crop plants providing new knowledge and tools for development of novel strategies for disease control.
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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Sessa, Guido, and Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7699834.bard.
Full textAbstract:
The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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Sela, Hanan, Eduard Akhunov, and Brian J. Steffenson. Population genomics, linkage disequilibrium and association mapping of stripe rust resistance genes in wild emmer wheat, Triticum turgidum ssp. dicoccoides. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598170.bard.
Full textAbstract:
The primary goals of this project were: (1) development of a genetically characterized association panel of wild emmer for high resolution analysis of the genetic basis of complex traits; (2) characterization and mapping of genes and QTL for seedling and adult plant resistance to stripe rust in wild emmer populations; (3) characterization of LD patterns along wild emmer chromosomes; (4) elucidation of the multi-locus genetic structure of wild emmer populations and its correlation with geo-climatic variables at the collection sites. Introduction In recent years, Stripe (yellow) rust (Yr) caused by Pucciniastriiformis f. sp. tritici(PST) has become a major threat to wheat crops in many parts of the world. New races have overcome most of the known resistances. It is essential, therefore, that the search for new genes will continue, followed by their mapping by molecular markers and introgression into the elite varieties by marker-assisted selection (MAS). The reservoir of genes for disease and pest resistance in wild emmer wheat (Triticumdicoccoides) is an important resource that must be made available to wheat breeders. The majority of resistance genes that were introgressed so far in cultivated wheat are resistance (R) genes. These genes, though confering near-immunity from the seedling stage, are often overcome by the pathogen in a short period after being deployed over vast production areas. On the other hand, adult-plant resistance (APR) is usually more durable since it is, in many cases, polygenic and confers partial resistance that may put less selective pressure on the pathogen. In this project, we have screened a collection of 480 wild emmer accessions originating from Israel for APR and seedling resistance to PST. Seedling resistance was tested against one Israeli and 3 North American PST isolates. APR was tested on accessions that did not have seedling resistance. The APR screen was conducted in two fields in Israel and in one field in the USA over 3 years for a total of 11 replicates. We have found about 20 accessions that have moderate stripe rust APR with infection type (IT<5), and about 20 additional accessions that have novel seedling resistance (IT<3). We have genotyped the collection using genotyping by sequencing (GBS) and the 90K SNP chip array. GBS yielded a total 341K SNP that were filtered to 150K informative SNP. The 90K assay resulted in 11K informative SNP. We have conducted a genome-wide association scan (GWAS) and found one significant locus on 6BL ( -log p >5). Two novel loci were found for seedling resistance. Further investigation of the 6BL locus and the effect of Yr36 showed that the 6BL locus and the Yr36 have additive effect and that the presence of favorable alleles of both loci results in reduction of 2 grades in the IT score. To identify alleles conferring adaption to extreme climatic conditions, we have associated the patterns of genomic variation in wild emmer with historic climate data from the accessions’ collection sites. The analysis of population stratification revealed four genetically distinct groups of wild emmer accessions coinciding with their geographic distribution. Partitioning of genomic variance showed that geographic location and climate together explain 43% of SNPs among emmer accessions with 19% of SNPs affected by climatic factors. The top three bioclimatic factors driving SNP distribution were temperature seasonality, precipitation seasonality, and isothermality. Association mapping approaches revealed 57 SNPs associated with these bio-climatic variables. Out of 21 unique genomic regions controlling heading date variation, 10 (~50%) overlapped with SNPs showing significant association with at least one of the three bioclimatic variables. This result suggests that a substantial part of the genomic variation associated with local adaptation in wild emmer is driven by selection acting on loci regulating flowering. Conclusions: Wild emmer can serve as a good source for novel APR and seedling R genes for stripe rust resistance. APR for stripe rust is a complex trait conferred by several loci that may have an additive effect. GWAS is feasible in the wild emmer population, however, its detection power is limited. A panel of wild emmer tagged with more than 150K SNP is available for further GWAS of important traits. The insights gained by the bioclimatic-gentic associations should be taken into consideration when planning conservation strategies.