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Novel anti-bacterial activities of β-defensin 1 in human platelets: Suppression of pathogen growth and signaling of neutrophil extracellular trap formation
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نویسنده
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kraemer b.f. ,campbell r.a. ,schwertz h. ,cody m.j. ,franks z. ,tolley n.d. ,kahr w.h.a. ,lindemann s. ,seizer p. ,yost c.c. ,zimmerman g.a. ,weyrich a.s.
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منبع
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plos pathogens - 2011 - دوره : 7 - شماره : 11
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چکیده
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Human β-defensins (hbd) are antimicrobial peptides that curb microbial activity. although hbd's are primarily expressed by epithelial cells,we show that human platelets express hbd-1 that has both predicted and novel antibacterial activities. we observed that activated platelets surround staphylococcus aureus (s. aureus),forcing the pathogens into clusters that have a reduced growth rate compared to s. aureus alone. given the microbicidal activity of β-defensins,we determined whether hbd family members were present in platelets and found mrna and protein for hbd-1. we also established that hbd-1 protein resided in extragranular cytoplasmic compartments of platelets. consistent with this localization pattern,agonists that elicit granular secretion by platelets did not readily induce hbd-1 release. nevertheless,platelets released hbd-1 when they were stimulated by α-toxin,a s. aureus product that permeabilizes target cells. platelet-derived hbd-1 significantly impaired the growth of clinical strains of s. aureus. hbd-1 also induced robust neutrophil extracellular trap (net) formation by target polymorphonuclear leukocytes (pmns),which is a novel antimicrobial function of β-defensins that was not previously identified. taken together,these data demonstrate that hbd-1 is a previously-unrecognized component of platelets that displays classic antimicrobial activity and,in addition,signals pmns to extrude dna lattices that capture and kill bacteria. © 2011 kraemer et al.
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آدرس
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molecular medicine program,university of utah,salt lake city,ut,united states,medizinische klinik iii,universitaetsklinikum tuebingen,tuebingen, Germany, molecular medicine program,university of utah,salt lake city,ut, United States, molecular medicine program,university of utah,salt lake city,ut,united states,department of surgery,university of utah,salt lake city,ut, United States, molecular medicine program,university of utah,salt lake city,ut, United States, molecular medicine program,university of utah,salt lake city,ut, United States, molecular medicine program,university of utah,salt lake city,ut, United States, division of haematology/oncology,program in cell biology,department of paediatrics,the hospital for sick children,university of toronto,ontario, Canada, the petri-hospital,warburg, Germany, medizinische klinik iii,universitaetsklinikum tuebingen,tuebingen, Germany, molecular medicine program,university of utah,salt lake city,ut,united states,department of pediatrics,university of utah,salt lake city,ut, United States, department of internal medicine,university of utah,salt lake city,ut, United States, department of internal medicine,university of utah,salt lake city,ut, United States
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Authors
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