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During sepsis there is aberrant activation, migration and sequestration of neutrophils in visceral organsthat leads to widespread
release of pro-inflammatory mediators contributing to multi-organ failure and death. Interaction of cell surface integrins
with their counterpart ligands, results in the adherence of circulating neutrophils and directed migration to infection sites.In
our study, we show that administration of a cyclic analog of RGD peptide (Arg-Gly-Asp) significantly reduced the number
of tissue-invading neutrophils and the degree of sepsis-induced lethality in mice as compared to control peptide. Secondly,
integrin (CD29) and more specifically VLA-3(CD49c/CD29) is dramatically up regulated on a subpopulation of neutrophils
isolated from both human septic patients and mouse sepsis models. Compared with the Gr
cells from septic animals displayed hyper-inflammatory phenotypes.Administration of
VLA-3 antagonist peptides and conditional genetic ablation of VLA(3)/integrin from granulocytes also improved survival and
bacterial clearance in septic animals. Thus, our results indicate that expression of VLA(3)/integrin is important for modulating
neutrophil trafficking during sepsis, and therapeutics specifically targeted against VLA(3)/integrin may be beneficial.
Pranita P. Sarangi is a research fellow at the National Institutes of Health. She is a graduate of the University of Tennessee, with postdoctoral training
at Center for Vaccine Biology and Immunology, University of Rochester Medical Center. She has published 8 first author and 6 co-author papers in
reputed peer reviewed journals including a book chapter.
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