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1

Easton, Donna M., Shuhua Ma, Neeloffer Mookherjee, Pamela Hamill, David Lynn, Jennifer Gardy, Sarah Mullaly, et al. "Immunomodulatory activity of synthetic innate defence regulators (IDRs) (134.45)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 134.45. http://dx.doi.org/10.4049/jimmunol.182.supp.134.45.

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Abstract Cationic host defence (antimicrobial) peptides, e.g. cathelicidin LL-37, have a variety of immunomodulatory activities that favour the safe resolution of infections. We have studied novel synthetic cationic innate defence regulator peptides that are not directly antimicrobial but are anti-infective in vivo, due to modulation of innate immunity. A range of peptides derived from the small bovine peptide bactenecin were screened for immunomodulatory activities in vitro; e.g. promotion of chemokine production and suppression of pro-inflammatory cytokines. Since innate immunity is complex, involving >1,500 gene products, a systems biology approach was utilized to characterize peptide modulation of innate immunity, including analysis of receptors, signalling pathways, transcription factors and downstream genes. To permit visualization and bioinformatic analysis of complex events, an innate immunity database (www.innatedb.ca), a network visualization tool (Cerebral) and downstream analysis tools (e.g. pathway overrepresentation analysis) were developed and provided insight into how this selective modulation occurs. In vivo data indicate that these activities provide protection in animal model infections of Gram positive and Gram negative bacterial infections as well as severe malaria. Thus IDRs have great potential for use as novel anti-infective agents. Supported by Genome BC, FNIH and CIHR.
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2

Cederlund, Andreas, Gudmundur H. Gudmundsson, and Birgitta Agerberth. "Antimicrobial peptides important in innate immunity." FEBS Journal 278, no. 20 (September 19, 2011): 3942–51. http://dx.doi.org/10.1111/j.1742-4658.2011.08302.x.

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3

Ganz, Tomas. "Defensins: antimicrobial peptides of innate immunity." Nature Reviews Immunology 3, no. 9 (September 2003): 710–20. http://dx.doi.org/10.1038/nri1180.

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4

Moser, Christian, Daniel J. Weiner, Elena Lysenko, Robert Bals, Jeffrey N. Weiser, and James M. Wilson. "β-Defensin 1 Contributes to Pulmonary Innate Immunity in Mice." Infection and Immunity 70, no. 6 (June 2002): 3068–72. http://dx.doi.org/10.1128/iai.70.6.3068-3072.2002.

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ABSTRACT Innate immunity serves as a first line defense in vertebrate organisms by providing an initial barrier to microorganisms and triggering antigen-specific responses. Antimicrobial peptides are thought to be effectors of innate immunity through their antibiotic activity and direct killing of microorganisms. Evidence to support this hypothesis in vertebrates is indirect, based on expression profiles and in vitro assays using purified peptides. Here we investigated the function of antimicrobial peptides in vivo using mice deficient in an antimicrobial peptide, mouse β-defensin-1 (mBD-1). We find that loss of mBD-1 results in delayed clearance of Haemophilus influenzae from lung. These data demonstrate directly that antimicrobial peptides of vertebrates provide an initial block to bacteria at epithelial surfaces.
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5

Boulanger, Nathalie, Rebecca J. L. Munks, Joanne V. Hamilton, Françoise Vovelle, Reto Brun, Mike J. Lehane, and Philippe Bulet. "Epithelial Innate Immunity." Journal of Biological Chemistry 277, no. 51 (October 7, 2002): 49921–26. http://dx.doi.org/10.1074/jbc.m206296200.

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The gut epithelium is an essential interface in insects that transmit parasites. We investigated the role that local innate immunity might have on vector competence, takingStomoxys calcitransas a model.S. calcitransis sympatric with tsetse flies, feeds on many of the same vertebrate hosts, and is thus regularly exposed to the trypanosomes that cause African sleeping sickness and nagana. Despite this,S. calcitransis not a cyclical vector of these trypanosomes. Trypanosomes develop exclusively in the lumen of digestive organs, and so epithelial immune mechanisms, and in particular antimicrobial peptides (AMPs), may be the prime determinants of the fate of an infection. To investigate whyS. calcitransis not a cyclical vector of trypanosomes, we have looked in its midgut for AMPs with trypanolytic activity. We have identified a new AMP of 42 amino acids, which we named stomoxyn, constitutively expressed and secreted exclusively in the anterior midgut ofS. calcitrans. It displays an amphipathic helical structure and exhibits a broad activity spectrum affecting the growth of microorganisms. Interestingly, this AMP exhibits trypanolytic activity toTrypanosoma brucei rhodesiense. We argue that stomoxyn may help to explain whyS. calcitransis not a vector of trypanosomes causing African sleeping sickness and nagana.
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6

Shandala, Tetyana, and Doug A. Brooks. "Innate immunity and exocytosis of antimicrobial peptides." Communicative & Integrative Biology 5, no. 2 (March 2012): 214–16. http://dx.doi.org/10.4161/cib.19018.

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7

Shin, Dong-Min, and Eun-Kyeong Jo. "Antimicrobial Peptides in Innate Immunity against Mycobacteria." Immune Network 11, no. 5 (2011): 245. http://dx.doi.org/10.4110/in.2011.11.5.245.

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8

Moosova, Z., O. Adamovsky, M. Pekarova, L. Svihalkova Sindlerova, L. Kubala, and L. Blaha. "Innate immunity response to selected cyanobacterial peptides." Toxicology Letters 238, no. 2 (October 2015): S223. http://dx.doi.org/10.1016/j.toxlet.2015.08.659.

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9

Zasloff, Michael. "Antibiotic peptides as mediators of innate immunity." Current Biology 2, no. 3 (March 1992): 133. http://dx.doi.org/10.1016/0960-9822(92)90251-5.

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10

Zanetti, Margherita. "Cathelicidins, multifunctional peptides of the innate immunity." Journal of Leukocyte Biology 75, no. 1 (July 22, 2003): 39–48. http://dx.doi.org/10.1189/jlb.0403147.

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11

Zasloff, Michael. "Antibiotic peptides as mediators of innate immunity." Current Opinion in Immunology 4, no. 1 (February 1992): 3–7. http://dx.doi.org/10.1016/0952-7915(92)90115-u.

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12

Westwell-Roper, Clara, and C. Bruce Verchere. "Modulation of Innate Immunity by Amyloidogenic Peptides." Trends in Immunology 40, no. 8 (August 2019): 762–80. http://dx.doi.org/10.1016/j.it.2019.06.005.

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13

Pawaria, Sudesh, and Robert Binder. "Role of CD91 in HSP-mediated innate immunity (165.9)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 165.9. http://dx.doi.org/10.4049/jimmunol.186.supp.165.9.

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Abstract The immunogenic HSPs gp96, hsp70 and calreticulin are known to chaperone antigenic peptides and elicit strong immunity against tumors and pathogens. The peptide bound form of the HSP bind to and are endocytosed by CD91 on antigen presenting cells leading to the cross-presentation of the chaperoned peptides. We show here that CD91 gets phosphorylated in response to HSPs and results in activation of downstream signals. By selective mutation of the two phosphorylation sites of CD91, we observed that HSPs appear to utilize different sites resulting in different downstream signaling pathways. As a result the cytokine profiles released from stimulated APCs are different for each HSP leading to priming of differential T helper responses including Th17 cells. These results are important in understanding how T cell responses are initiated when HSPs are released into the extracellular environment from dying tumor or infected cells or introduced via vaccination.
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14

Torshin, I. Yu, T. E. Bogacheva, and O. A. Gromova. "Placenta peptides: antibacterial effects." Pharmacokinetics and Pharmacodynamics, no. 4 (January 22, 2024): 15–22. http://dx.doi.org/10.37489/2587-7836-2023-4-15-22.

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Mass spectrometric sequencing of peptides in Laennec indicated the presence of 5 peptides in the drug, the biological activity of which may determine the antibacterial properties of the drug. The most significant result of this study is the presence in Laennec of a fragment of the antibacterial peptide cathelicidin (LL-37), an important vitamin D-dependent factor of innate immunity. Other Laennec peptides help reduce excess inflammation by inhibiting the activity of the NF-kB protein, which mediates the effects of TNF-α.
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15

Emilio, Jirillo, and Thea Magrone. "Editorial: Antimicrobial Peptides as Mediators of Innate Immunity." Current Pharmaceutical Design 24, no. 10 (May 28, 2018): 1041–42. http://dx.doi.org/10.2174/1381612824666180416113811.

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16

Strominger, Jack L. "Animal Antimicrobial Peptides: Ancient Players in Innate Immunity." Journal of Immunology 182, no. 11 (May 19, 2009): 6633–34. http://dx.doi.org/10.4049/jimmunol.0990038.

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17

Ganz, T. "The Role of Antimicrobial Peptides in Innate Immunity." Integrative and Comparative Biology 43, no. 2 (April 1, 2003): 300–304. http://dx.doi.org/10.1093/icb/43.2.300.

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18

Guryanova, Svetlana V., Sergey V. Balandin, Oksana Yu Belogurova-Ovchinnikova, and Tatiana V. Ovchinnikova. "Marine Invertebrate Antimicrobial Peptides and Their Potential as Novel Peptide Antibiotics." Marine Drugs 21, no. 10 (September 23, 2023): 503. http://dx.doi.org/10.3390/md21100503.

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Marine invertebrates constantly interact with a wide range of microorganisms in their aquatic environment and possess an effective defense system that has enabled their existence for millions of years. Their lack of acquired immunity sets marine invertebrates apart from other marine animals. Invertebrates could rely on their innate immunity, providing the first line of defense, survival, and thriving. The innate immune system of marine invertebrates includes various biologically active compounds, and specifically, antimicrobial peptides. Nowadays, there is a revive of interest in these peptides due to the urgent need to discover novel drugs against antibiotic-resistant bacterial strains, a pressing global concern in modern healthcare. Modern technologies offer extensive possibilities for the development of innovative drugs based on these compounds, which can act against bacteria, fungi, protozoa, and viruses. This review focuses on structural peculiarities, biological functions, gene expression, biosynthesis, mechanisms of antimicrobial action, regulatory activities, and prospects for the therapeutic use of antimicrobial peptides derived from marine invertebrates.
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19

Zorina, Oksana Aleksandrovna, L. V. Gankovskaya, R. A. Balykin, T. P. Ivanyushko, O. A. Svitich, and V. V. Grechenko. "Positive effect of autologous immune peptides applications in the surgical treatment of inflammatory-destructive periodontal lesions." Russian Journal of Dentistry 21, no. 1 (February 15, 2017): 4–7. http://dx.doi.org/10.18821/1728-2802201721(1):4-7.

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Clinical efficacy of autologous complex immune peptides (ACIP) shown in patients with inflammatory and destructive periodontal lesions. The level of gene recognition expression receptors of innate immunity (TLR4) was studied and beta-defensin (hBD-3) periodontal mucosal epithelial cells and TGF b-1 concentration in gingival fluid. Innate immunity factors analysis was spend before and after surgery using osteoplastic material (ACIP) in dynamics. ACIP immune regulatory effect on the performance of innate immunity was shown.
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20

Sorvina, Alexandra, Tetyana Shandala, Shudong Wang, David J. Sharkey, Emma Parkinson-Lawrence, Stavros Selemidis, and Douglas A. Brooks. "CDKI-73 Is a Novel Pharmacological Inhibitor of Rab11 Cargo Delivery and Innate Immune Secretion." Cells 9, no. 2 (February 5, 2020): 372. http://dx.doi.org/10.3390/cells9020372.

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Innate immunity is critical for host defence against pathogen and environmental challenge and this involves the production and secretion of immune mediators, such as antimicrobial peptides and pro-inflammatory cytokines. However, when dysregulated, innate immunity can contribute to multifactorial diseases, including inflammatory rheumatic disorders, type 2 diabetes, cancer, neurodegenerative and cardiovascular diseases and even septic shock. During an innate immune response, antimicrobial peptides and cytokines are trafficked via Rab11 multivesicular endosomes, and then sorted into Rab11 vesicles for traffic to the plasma membrane and secretion. In this study, a cyclin-dependent kinase inhibitor CDKI-73 was used to determine its effect on the innate immune response, based on previously identified targets for this compound. Our results showed that CDKI-73 inhibited the delivery of Rab11 vesicles to the plasma membrane, resulting in the accumulation of large multivesicular Rab11 endosomes near the cell periphery. In addition to the effect on endosome delivery, CDKI-73 down-regulated the amount of innate immune cargo, including the antimicrobial peptide Drosomycin and pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFα). We concluded that CDKI-73 has the potential to regulate the delivery and secretion of certain innate immune cargo, which could be used to control inflammation.
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21

Yuan, Qian, and W. Allan Walker. "Innate Immunity of the Gut: Mucosal Defense in Health and Disease." Journal of Pediatric Gastroenterology and Nutrition 38, no. 5 (May 2004): 463–73. http://dx.doi.org/10.1002/j.1536-4801.2004.tb12203.x.

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ABSTRACTThe intestine is an important immune organ consisting of a complex cellular network, secreted peptides and proteins and other host defenses. Innate immunity plays a central role in intestinal immune defense against invading pathogens. It also serves as a bridge to the activation of the adaptive immune system. Pattern recognition molecules of microorganisms are an essential component for identifying invading pathogens. Toll‐like receptors (TLRs), CARD15/NOD2 and scavenger receptors all serve as the pattern recognition receptors in the innate immune defense system. Secreted bactericidal peptides or defensins produced by the intestinal epithelia represent another crucial element of innate mucosal immune defense. Mutations in pattern recognition receptors and dysfunction of secretory bactericidal peptides may impair host immune defenses leading to an invasion of pathogens resulting in chronic inflammation of the gut. This review updates our current understanding of innate immunity of the gastrointestinal tract.
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22

Kamysz, Wojciech, Marcin Okrój, and Jerzy Łukasiak. "Novel properties of antimicrobial peptides." Acta Biochimica Polonica 50, no. 2 (June 30, 2003): 461–69. http://dx.doi.org/10.18388/abp.2003_3698.

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Endogenous peptide antibiotics are known as evolutionarily old components of innate immunity. Due to interaction with cell membrane these peptides cause permeabilization of the membrane and lysis of invading microbes. However, some studies proved that antimicrobial peptides are universal multifunctional molecules and their functions extend far beyond simple antibiotics. In this review we present an overview of the general mechanism of action of antimicrobial peptides and discuss some of their additional properties, like antitumour activity, mitogenic activity, role in signal transduction pathways and adaptive immune response.
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23

Habets, Michelle G. J. L., and Michael A. Brockhurst. "Therapeutic antimicrobial peptides may compromise natural immunity." Biology Letters 8, no. 3 (January 25, 2012): 416–18. http://dx.doi.org/10.1098/rsbl.2011.1203.

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Antimicrobial peptides (AMPs) have been proposed as a promising new class of antimicrobials despite warnings that therapeutic use could drive the evolution of pathogens resistant to our own immunity peptides. Using experimental evolution, we demonstrate that Staphylococcus aureus rapidly evolved resistance to pexiganan, a drug-candidate for diabetic leg ulcer infections. Evolved resistance was costly in terms of impaired growth rate, but costs-of-resistance were completely ameliorated by compensatory adaptation. Crucially, we show that, in some populations, experimentally evolved resistance to pexiganan provided S. aureus with cross-resistance to human-neutrophil-defensin-1, a key component of the innate immune response to infection. This unintended consequence of therapeutic use could drastically undermine our innate immune system's ability to control and clear microbial infections. Our results therefore highlight grave potential risks of AMP therapies, with implications for their development.
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24

Zilbauer, Matthias, Nick Dorrell, Parjeet K. Boughan, Andrew Harris, Brendan W. Wren, Nigel J. Klein, and Mona Bajaj-Elliott. "Intestinal Innate Immunity to Campylobacter jejuni Results in Induction of Bactericidal Human Beta-Defensins 2 and 3." Infection and Immunity 73, no. 11 (November 2005): 7281–89. http://dx.doi.org/10.1128/iai.73.11.7281-7289.2005.

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ABSTRACT Campylobacter jejuni is the most prevalent cause of bacterial diarrhea worldwide. Despite the serious health problems caused by this bacterium, human innate immune responses to C. jejuni infection remain poorly defined. Human β-defensins, a family of epithelial antimicrobial peptides, are a major component of host innate defense at the gastrointestinal mucosal surface. In this study, the effect of two different C. jejuni wild-type strains on human intestinal epithelial innate responses was investigated. Up-regulation of β-defensin gene and peptide expression during infection was observed and recombinant β-defensins were shown to have a direct bactericidal effect against C. jejuni through disruption of cell wall integrity. Further studies using an isogenic capsule-deficient mutant showed that, surprisingly, the absence of the bacterial polysaccharide capsule did not change the innate immune responses induced by C. jejuni or the ability of C. jejuni to survive exposure to recombinant β-defensins. This study suggests a major role for this family of antimicrobial peptides in the innate immune defense against this human pathogen.
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Bochenska, Oliwia, Maria Rapala-Kozik, Natalia Wolak, Wojciech Kamysz, Daria Grzywacz, Wataru Aoki, Mitsuyoshi Ueda, and Andrzej Kozik. "Inactivation of human kininogen-derived antimicrobial peptides by secreted aspartic proteases produced by the pathogenic yeast Candida albicans." Biological Chemistry 396, no. 12 (December 1, 2015): 1369–75. http://dx.doi.org/10.1515/hsz-2015-0167.

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Abstract Ten secreted aspartic proteases (Saps) of Candida albicans cleave numerous peptides and proteins in the host organism and deregulate its homeostasis. Human kininogens contain two internal antimicrobial peptide sequences, designated NAT26 and HKH20. In our current study, we characterized a Sap-catalyzed cleavage of kininogen-derived antimicrobial peptides that results in the loss of the anticandidal activity of these peptides. The NAT26 peptide was effectively inactivated by all Saps, except Sap10, whereas HKH20 was completely degraded only by Sap9. Proteolytic deactivation of the antifungal potential of human kininogens can help the pathogens to modulate or evade the innate immunity of the host.
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26

Sathyan, Naveen, Rosamma Philip, E. R. Chaithanya, and P. R. Anil Kumar. "Identification and Molecular Characterization of Molluskin, a Histone-H2A-Derived Antimicrobial Peptide from Molluscs." ISRN Molecular Biology 2012 (October 15, 2012): 1–6. http://dx.doi.org/10.5402/2012/219656.

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Antimicrobial peptides are humoral innate immune components of molluscs that provide protection against pathogenic microorganisms. Among these, histone-H2A-derived antimicrobial peptides are known to actively participate in host defense responses of molluscs. Present study deals with identification of putative antimicrobial sequences from the histone-H2A of back-water oyster Crassostrea madrasensis, rock oyster Saccostrea cucullata, grey clam Meretrix casta, fig shell Ficus gracilis, and ribbon bullia Bullia vittata. A 75 bp fragment encoding 25 amino acid residues was amplified from cDNA of these five bivalves and was named “Molluskin.” The 25 amino acid peptide exhibited high similarity to previously reported histone-H2A-derived AMPs from invertebrates indicating the presence of an antimicrobial sequence motif. Physicochemical properties of the peptides are in agreement with the characteristic features of antimicrobial peptides, indicating their potential role in innate immunity of molluscs.
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27

Edfeldt, Kristina, Philip T. Liu, Rene Chun, Stephan R. Krutzik, John S. Adams, Martin Hewison, and Robert L. Modlin. "IFN-γ and IL-4 differentially regulate TLR-triggered induction of antimicrobial peptides by altering vitamin D metabolism (135.49)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 135.49. http://dx.doi.org/10.4049/jimmunol.182.supp.135.49.

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Abstract Innate immunity is important for host defense against microbial infections and vitamin D has been shown to play a role in this response. Vitamin D is required for Toll-like receptor (TLR)-triggered induction of the antimicrobial peptides cathelicidin and DEFB4, but how acquired immunity influences this system is not known. The objective of this study was to assess the role of acquired immune cytokines on TLR-triggered vitamin D-dependent induction of antimicrobial peptides. We showed that acquired immune cytokine responses influence antimicrobial pathways in innate immunity by regulating vitamin D metabolism. The Th1 cytokine IFN-γ induced bioconversion of 25-hydroxyvitamin D3 (25D3) to its active metabolite 1,25-dihydroxyvitamin D3 and resulted in a subsequent increase in cathelicidin mRNA in cells treated with a TLR2/1 ligand. In contrast, the Th2 cytokine IL-4 lead to induction of 25D3 catabolism by inducing 24-hydroxylase enzyme activity and consequently inhibited TLR2/1-triggered induction of the antimicrobial peptides cathelicidin and DEFB4. In conclusion our results support a role for acquired immune cytokines in regulating vitamin D-dependent antimicrobial pathways in innate immunity. KE is a Wenner-Gren Fellow
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28

Huang, Chun-Ming, Justin W. Torpey, Yu-Tseung Liu, Yun-Ru Chen, Katherine E. Williams, Elizabeth A. Komives, and Richard L. Gallo. "A Peptide with a ProGln C Terminus in the Human Saliva Peptidome Exerts Bactericidal Activity against Propionibacterium acnes." Antimicrobial Agents and Chemotherapy 52, no. 5 (February 19, 2008): 1834–36. http://dx.doi.org/10.1128/aac.01347-07.

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ABSTRACT Nine proline-rich peptides ending with a proline-glutamine C terminus in a salivary peptidome were sequenced by matrix-assisted laser desorption ionization time of flight time of flight tandem mass spectrometry. A GPPPQGGRPQ peptide binds gram-positive Propionibacterium acnes and considerably inhibits bacterial growth. The peptide exhibiting innate immunity may be applied for treatment of various P. acnes-associated human diseases.
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29

Matsuzaki, K. "Why and how are peptide-lipid interactions utilized for self defence?" Biochemical Society Transactions 29, no. 4 (August 1, 2001): 598–601. http://dx.doi.org/10.1042/bst0290598.

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Animals defend themselves against invading pathogenic micro-organisms by utilizing cationic anti-microbial peptides, which rapidly kill various micro-organisms without exerting toxicity against the host. Physicochemical peptide-lipid interactions provide attractive mechanisms for innate immunity. Many of these peptides form amphipathic secondary structures (α-helices and β-sheets) which can selectively interact with anionic bacterial membranes by electrostatic interaction. Rapid, peptide-induced membrane permeabilization is an effective mechanism of anti-microbial action. Magainin 2 from frog skin forms a dynamic peptide-lipid supramolecular-complex pore that allows mutually coupled transmembrane transport of ions and lipids. The peptide molecule is internalized upon the disintegration of the pore. Several anti-microbial peptides are known to work synergistically.
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30

Bals, Robert, Daniel J. Weiner, A. David Moscioni, Rupalie L. Meegalla, and James M. Wilson. "Augmentation of Innate Host Defense by Expression of a Cathelicidin Antimicrobial Peptide." Infection and Immunity 67, no. 11 (November 1, 1999): 6084–89. http://dx.doi.org/10.1128/iai.67.11.6084-6089.1999.

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ABSTRACT Antimicrobial peptides, such as defensins or cathelicidins, are effector substances of the innate immune system and are thought to have antimicrobial properties that contribute to host defense. The evidence that vertebrate antimicrobial peptides contribute to innate immunity in vivo is based on their expression pattern and in vitro activity against microorganisms. The goal of this study was to investigate whether the overexpression of an antimicrobial peptide results in augmented protection against bacterial infection. C57BL/6 mice were given an adenovirus vector containing the cDNA for LL-37/hCAP-18, a human cathelicidin antimicrobial peptide. Mice treated with intratracheal LL-37/hCAP-18 vector had a lower bacterial load and a smaller inflammatory response than did untreated mice following pulmonary challenge with Pseudomonas aeruginosa PAO1. Systemic expression of LL-37/hCAP-18 after intravenous injection of recombinant adenovirus resulted in improved survival rates following intravenous injection of lipopolysaccharide with galactosamine or Escherichia coli CP9. In conclusion, the data demonstrate that expression of an antimicrobial peptide by gene transfer results in augmentation of the innate immune response, providing support for the hypothesis that vertebrate antimicrobial peptides protect against microorganisms in vivo.
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31

Shai, Yechiel. "From Innate Immunity to de-Novo Designed Antimicrobial Peptides." Current Pharmaceutical Design 8, no. 9 (April 1, 2002): 715–25. http://dx.doi.org/10.2174/1381612023395367.

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32

Risso, Angela. "Leukocyte antimicrobial peptides: multifunctional effector molecules of innate immunity." Journal of Leukocyte Biology 68, no. 6 (December 2000): 785–92. http://dx.doi.org/10.1189/jlb.68.6.785.

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33

Katzenback, Barbara. "Antimicrobial Peptides as Mediators of Innate Immunity in Teleosts." Biology 4, no. 4 (September 25, 2015): 607–39. http://dx.doi.org/10.3390/biology4040607.

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34

Aslam, R., M. Atindehou, T. Lavaux, Y. Haïkel, F. Schneider, and M. -H. Metz-Boutigue. "Chromogranin A-Derived Peptides Are Involved in Innate Immunity." Current Medicinal Chemistry 19, no. 24 (August 1, 2012): 4115–23. http://dx.doi.org/10.2174/092986712802430063.

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35

West, Nicholas P., David B. Pyne, Gillian Renshaw, and Allan W. Cripps. "Antimicrobial peptides and proteins, exercise and innate mucosal immunity." FEMS Immunology & Medical Microbiology 48, no. 3 (December 2006): 293–304. http://dx.doi.org/10.1111/j.1574-695x.2006.00132.x.

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36

Linde, A., C. R. Ross, E. G. Davis, L. Dib, F. Blecha, and T. Melgarejo. "Innate Immunity and Host Defense Peptides in Veterinary Medicine." Journal of Veterinary Internal Medicine 22, no. 2 (March 2008): 247–65. http://dx.doi.org/10.1111/j.1939-1676.2007.0038.x.

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37

Rosenfeld, Yosef, Niv Papo, and Yechiel Shai. "Endotoxin (Lipopolysaccharide) Neutralization by Innate Immunity Host-Defense Peptides." Journal of Biological Chemistry 281, no. 3 (November 17, 2005): 1636–43. http://dx.doi.org/10.1074/jbc.m504327200.

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38

Hancock, Robert EW. "Cationic peptides: effectors in innate immunity and novel antimicrobials." Lancet Infectious Diseases 1, no. 3 (October 2001): 156–64. http://dx.doi.org/10.1016/s1473-3099(01)00092-5.

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39

Barak, Orr, James R. Treat, and William D. James. "Antimicrobial Peptides: Effectors of Innate Immunity in the Skin." Advances in Dermatology 21 (January 2005): 357–74. http://dx.doi.org/10.1016/j.yadr.2005.07.001.

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40

Mitta, Guillaume, Franck Vandenbulcke, and Philippe Roch. "Original involvement of antimicrobial peptides in mussel innate immunity." FEBS Letters 486, no. 3 (December 12, 2000): 185–90. http://dx.doi.org/10.1016/s0014-5793(00)02192-x.

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41

Otte, Jan-Michel, Karlheinz Kiehne, and Karl-Heinz Herzig. "Antimicrobial peptides in innate immunity of the human intestine." Journal of Gastroenterology 38, no. 8 (August 1, 2003): 717–26. http://dx.doi.org/10.1007/s00535-003-1136-5.

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42

Bevins, C. L. "Paneth cell defensins: key effector molecules of innate immunity." Biochemical Society Transactions 34, no. 2 (March 20, 2006): 263–66. http://dx.doi.org/10.1042/bst0340263.

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Antimicrobial peptides are fundamental effector molecules of innate immunity, utilized in host defence by virtually all organisms studied. These gene-encoded peptides have direct antibiotic activity against a wide range of bacteria and other microbes. In humans and other mammals, defensins are a predominant class of such peptides. In the mammalian small intestine, Paneth cells, specialized secretory epithelial cells located at the base of the crypt invaginations lining the intestinal wall, produce defensins and other antibiotic proteins. Recent investigations in murine models provide compelling support for the hypothesis that enteric defensins play a pivotal role in defence from food- and water-borne pathogens in the intestinal lumen. Investigations by others indicate that intestinal commensal bacteria are key factors in the pathogenesis of IBD (inflammatory bowel disease) in genetically susceptible humans. Recent studies provide evidence that reduced expression of Paneth cell defensins may be a key factor in the pathogenesis of ileal Crohn's disease, a subgroup of IBD. Future studies to further define the function and regulation of Paneth cell defensins will enhance our understanding of normal small bowel physiology, and probably contribute to a better understanding of the pathogenesis of inflammatory and infectious diseases of the bowel. Such knowledge may provide new therapeutic targets and strategies.
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43

Sizyakina, L. P., and A. I. Sergeeva. "Influence of preparations with peptides on innate and adaptive immunity." Medical Herald of the South of Russia 14, no. 3 (September 26, 2023): 101–4. http://dx.doi.org/10.21886/2219-8075-2023-14-2-101-104.

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Objective: to assess the dynamics of the immune system functioning when using mesotherapy with peptide complexes. Materials and methods: the observation group consisted of 26 women (from 35 to 55 years old) who received a course of mesotherapy with preparations containing peptides for the first time. Injections were carried out in a course of 5 procedures with an interval of 14 days. The exclusion criteria were the absence of same manipulations in the past, hormone replacement therapy, combined oral contraceptives, pregnancy, lactation, acute infections, somatic pathologies. The parameters of innate and adaptive immunity were studied before the course of procedures, right after it, 3 and 6 months after the course. Skin quality changes were assessed using the Aramo Smart Lite 300 dermatoscope. Results: improved skin quality, decreased skin creases, increased skin moisture. The obtained clinical improvements last for three months after the end of the course and there is a tendency for the effects to decrease after six months. In the functioning of the immune system, there is a redistribution of lymphocytes population in the peripheral bloodstream immediately after the course of mesotherapy. In addition, an increase in peripheral T-regulatory lymphocytes responsible for intraimmune suppression was documented. The activation of spontaneous oxygen-producing activity was noted. 3 months after the procedure, no significant changes in immunological parameters were found. 6 months after the course of procedures, a decrease in the level of T-lymphocytes with an increase in the expression of markers of early T-cell activation was recorded. In the humoral link, an increase in circulating B-lymphocytes was documented. In the parameters of innate immunity, there is a decrease in the spontaneous oxygen-producing activity of neutrophils. Conclusion: as a result of the study, a positive persistent clinical effect is documented, simultaneously with the mobilization of factors of innate and adaptive immunity. It is important to note the fact that the immune response restores completely within 6 months after a course of mesotherapy with peptide complexes, with still noticeable clinical results.
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44

Ma, Shuhua, Anastasia Nijnik, Laurence Madera, Melissa Elliott, Donna Easton, Matthew Mayer, Jason Kindrachuk, et al. "Innate Defence Regulator Peptides as a Novel Anti-infective Strategy (94.2)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 94.2. http://dx.doi.org/10.4049/jimmunol.184.supp.94.2.

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Abstract The therapy of bacterial infections is under great threat as multiple antibiotic resistance increases and there is a paucity of new antibiotic discovery and development. Synthetic Innate Defence Regulator (IDR) peptides, which mimic natural host defence (antimicrobial) peptides, have been designed as a novel anti-infective strategy, working by selectively boosting innate immune protective mechanisms while dampening potentially harmful inflammation. These peptides can resolve serious infections in animal models. The optimal method of use of these peptides was evaluated here using an animal model infection by one of the highly resistant bacteria (Superbugs) afflicting our society, Staphylococcus aureus. A luminescent version of this bacterium was utilized to follow the kinetics of infection non-invasively using IVIS imaging. Protection was achieved by both prophylactic and therapeutic administration. Investigation of the mechanism of protection by examining cells infiltrating the infection site and cytokines/chemokines revealed remarkable parallels between in vitro action of the peptides in primary human cells and these animal models. System biology approaches such as Microarray and InnateDB are being utilized to decipher the complex. This has revealed several receptors, signaling pathways, transcription factors and effector proteins involved in the modulation by peptides of innate immunity.
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45

Laman, Alexander G., Richard Lathe, Anna O. Shepelyakovskaya, Alexandra Gartseva, Feodor A. Brovko, Svetlana Guryanova, Ludmila Alekseeva, Elena A. Meshcheryakova, and Vadim T. Ivanov. "Muramyl peptides activate innate immunity conjointly via YB1 and NOD2." Innate Immunity 22, no. 8 (September 30, 2016): 666–73. http://dx.doi.org/10.1177/1753425916668982.

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Bacterial cell wall muramyl dipeptide (MDP) and glucosaminyl-MDP (GMDP) are potent activators of innate immunity. Two receptor targets, NOD2 and YB1, have been reported; we investigated potential overlap of NOD2 and YB1 pathways. Separate knockdown of NOD2 and YB1 demonstrates that both contribute to GMDP induction of NF-κB expression, a marker of innate immunity, although excess YB1 led to induction in the absence of NOD2. YB1 and NOD2 co-migrated on sucrose gradient centrifugation, and GMDP addition led to the formation of higher molecular mass complexes containing both YB1 and NOD2. Co-immunoprecipitation demonstrated a direct interaction between YB1 and NOD2, a major recombinant fragment of NOD2 (NACHT–LRR) bound to YB1, and complex formation was stimulated by GMDP. We also report subcellular colocalization of NOD2 and YB1. Although YB1 may have other binding partners in addition to NOD2, maximal innate immunity activation by muramyl peptides is mediated via an interaction between YB1 and NOD2.
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46

Oudhoff, Menno J., Marjolein E. Blaauboer, Kamran Nazmi, Nina Scheres, Jan G. M. Bolscher, and Enno C. I. Veerman. "The role of salivary histatin and the human cathelicidin LL-37 in wound healing and innate immunity." Biological Chemistry 391, no. 5 (May 1, 2010): 541–48. http://dx.doi.org/10.1515/bc.2010.057.

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Abstract Antimicrobial peptides are multifunctional in innate immunity and wound repair of multicellular organisms. We were the first to discover that histatins, a family of salivary antimicrobial peptides, enhance epithelial cell migration, suggesting a role in oral wound healing. It is unknown whether histatins display innate-immunity activities, similar to other antimicrobial peptides such as LL-37. Therefore, we compared the effect of Histatin-2 and LL-37 on several activities within the context of wound healing and innate immunity. We found that Histatin-2 enhances fibroblast migration, but only weakly induces proliferation. LL-37 enhances both fibroblast migration and proliferation, but only at a narrow concentration optimum (approximately 1 μm). At higher concentrations LL-37 causes cell death, whereas Histatin-2 is not cytotoxic. Both peptides do not alter fibroblast-to-myofibroblast differentiation. Histatin-2 does not alter interleukin-8 (IL-8) expression and lipopolysaccharide (LPS)-elevated cytokine and chemokine expression. In contrast, LL-37 induces IL-8 expression, but dampens the LPS-induced immune response. Neither Histatin-2 nor LL-37 affects human-neutrophil migration. Histatins are, unlike other antimicrobial peptides, not cytotoxic or proinflammatory. It seems that they are important for the initial stage of wound healing in which fast wound coverage is important for healing without infection, inflammation, or fibrosis development. Interestingly, these characteristics are more typical for the mouth than for skin.
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47

Sol, Asaf, Guangshun Wang, Edna Blotnick, Radha Golla, Gilad Bachrach, and Andras Muhlrad. "Interaction of the core fragments of the LL-37 host defense peptide with actin." RSC Advances 5, no. 13 (2015): 9361–67. http://dx.doi.org/10.1039/c4ra13007c.

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48

Akahoshi, Doug T., Dean E. Natwick, Sean R. Collins, and Charles L. Bevins. "Can Effector Molecules of Innate Immunity Target Microbial Motility?" Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 227.21. http://dx.doi.org/10.4049/jimmunol.204.supp.227.21.

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Abstract Antimicrobial peptides are key effector molecules throughout nature responsible in part for the defense against microbial pathogens and influencing the composition of colonizing microbes. Defensins are the major antimicrobial peptides produced by Paneth cells in the mammalian small intestine and are essential for maintaining homeostasis between host and microbe. While mature defensin peptides typically have microbicidal activity, human alpha defensin 6 (HD6) lacks such activity yet provides protection from invasion by bacterial pathogens. Using a transgenic mouse model expressing HD6 in Paneth cells, we reported the importance of HD6 in preventing the translocation of pathogenic Salmonella Typhimurium (STM) across the small intestinal epithelium (doi:10.1126/science.1218831); however, the mechanism underlying the inhibition of invasion is not fully understood. We hypothesize HD6 binds to extracellular bacterial protein structures, such as flagella, and inhibits swimming motility through a process of direct binding and self-assembly. Using an agar based motility assay, we show STM radially swim at a slower rate when in the presence of HD6. In ongoing studies using live-microscopy to visualize GFP-expressing STM in the presence of HD6, we observe a decrease in STM motility in a concentration dependent manner with some STM appearing to be completely immobilized, but without changes in bacterial viability. Unexpectedly, it appears the immobilization observed is influenced more by the expression of fimbriae than by the expression of flagella. With these results in mind, we plan to expand our investigation to elucidate key molecular determinants and include other microbes to test the broader relevance of this activity of HD6.
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49

Hinds, Nichole A., and Sylvia L. Smith. "Characterization of constitutive antimicrobial activity associated with leukocyte lysates from the nurse shark, Ginglymostoma cirratum (44.42)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S56. http://dx.doi.org/10.4049/jimmunol.178.supp.44.42.

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Abstract Antimicrobial peptides are mediators of innate immunity. Studies have shown that peptide fragments of histones, proteins primarily involved with DNA packaging, display antimicrobial activity. This project examines the antibacterial activity associated with shark leukocyte lysates and the potential role of histone fragments in constitutive innate immunity. Preliminary studies have demonstrated antimicrobial activity, distinct from that of lysozyme, in crude cell lysates prepared from unstimulated shark blood leukocytes. The antimicrobial activity has been partially purified using a combination of ion exchange, size exclusion and affinity chromatography. SDS PAGE analysis of fractions showed the presence of several low molecular weight (<15 kDa) protein bands. N-terminal amino acid sequence analysis of four peptides identified them as histone fragments with sequence similarity to mammalian histones H2A, H2B and H4. The peptide sequences are also similar to histone fragments described for the catfish and the Asian toad, which exhibit antibacterial activity. The spectrum of antibacterial activity, biochemical characterization and mode of action of shark histone fragments is under investigation. Such information will determine their potential use against clinically significant organisms. The research was supported in part by FIU’s Comparative Immunology Initiative (NIH R25GM061347).
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50

Ouellette, Andre J. "IV. Paneth cell antimicrobial peptides and the biology of the mucosal barrier." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 2 (August 1, 1999): G257—G261. http://dx.doi.org/10.1152/ajpgi.1999.277.2.g257.

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The hypothesis that epithelial cells release preformed antibiotic peptides as components of mucosal innate immunity has gained experimental support in recent years. In the mammalian small intestine, Paneth cells secrete granules that are rich in α-defensins and additional antimicrobial peptides into the lumen of the crypt. The α-defensins are homologues of peptides that function as mediators of nonoxidative microbial cell killing in phagocytic leukocytes, and they are potent microbicidal agents in in vitro assays. Because certain mouse α-defensins stimulate cultured epithelial cells to secrete chloride ion, those peptides appear to be capable of interacting directly with the apical membranes of neighboring cells and perhaps influencing crypt physiology. In instances of crypt disruption or induced Paneth cell deficiency, crypt intermediate cells appear to compensate by accumulating and secreting Paneth cell antimicrobial peptides. Challenges for the future will be to understand the mechanisms of this epithelial plasticity and to show that Paneth cells contribute directly to innate immunity in the crypt microenvironment.
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