Pranita P. Sarangi

Pranita P. Sarangi

National Institute of Dental and Craniofacial Research, NIH, USA

Title: Tissue homing of infl ammatory neutrophils during sepsis is mediated by integrin VLA-3 (CD49c/CD29)


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.


During sepsis there is aberrant activation, migration and sequestration of neutrophils in visceral organsthat leads to widespread release of pro-infl ammatory 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) signifi cantly reduced the number of tissue-invading neutrophils and the degree of sepsis-induced lethality in mice as compared to control peptide. Secondly, b1 integrin (CD29) and more specifi cally 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 Gr1highCD11bhighVLA-3low granulocyte population, Gr1highCD11bhighVLA-3high cells from septic animals displayed hyper-infl ammatory 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. Th us, our results indicate that expression of VLA(3)/integrin is important for modulating neutrophil traffi cking during sepsis, and therapeutics specifi cally targeted against VLA(3)/integrin may be benefi cial.

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