| First Author | Sarangi PP | Year | 2012 |
| Journal | Shock | Volume | 38 |
| Issue | 3 | Pages | 281-7 |
| PubMed ID | 22683734 | Mgi Jnum | J:237965 |
| Mgi Id | MGI:5817564 | Doi | 10.1097/SHK.0b013e31826136f8 |
| Citation | Sarangi PP, et al. (2012) Role of beta1 integrin in tissue homing of neutrophils during sepsis. Shock 38(3):281-7 |
| abstractText | Aberrant activation of neutrophils during sepsis results in the widespread release of proinflammatory mediators, leading to multiorgan system failure and death. However, aberrant activation of neutrophils during sepsis results in the widespread release of harmful inflammatory mediators causing host tissue injuries that can lead to multiorgan system failure and death. One of the pivotal components of neutrophil migration during inflammation is the expression of surface integrins. In this 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 with control peptide. Second, beta1 integrin (CD29) was highly upregulated on the neutrophils isolated from both septic patients and animals. Finally, conditional genetic ablation of beta1 integrin from granulocytes also improved survival and bacterial clearance in septic animals Thus, our results indicate that expression of beta1 integrin is important for modulating neutrophil trafficking during sepsis and that therapeutics designed against beta1 integrins may be beneficial. |
