Abstract

The functional behavior of polymorphonuclear neutrophils (PMN) in burn injury has been extensively studied, with evidence of upreulation early and downregulation later. The proposal is based on the hypothesis that early burn injury hypersensitizes PMN signaling via burn-related inflammatory mediators, leading to excessive O2- generation and hydroytic enzyme release. Studies are designed to ascertain the involvement of Ca2+ and phosphorylation signaling in these events. Effects of burn-mediated PMN hyperfunction and its blockade on microvascular and parenchymal tissues in intestine will also be examined. A rat scald burn (25%) model will be used, with/without injection of E. coli., studied 1,3,7 and 10 days post burn.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM056865-04
Application #
6386802
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Program Officer
Somers, Scott D
Project Start
1998-07-01
Project End
2002-06-30
Budget Start
2001-07-01
Budget End
2002-06-30
Support Year
4
Fiscal Year
2001
Total Cost
$279,276
Indirect Cost

  Institution

Name
Loyola University Chicago
Department
Physiology
Type
Schools of Medicine
DUNS #
791277940
City
Maywood
State
IL
Country
United States
Zip Code
60153

  Publications

Goto, Masakatsu; Samonte, Victoria; Ravindranath, Thyyar et al. (2006) Burn injury exacerbates hemodynamic and metabolic responses in rats with polymicrobial sepsis. J Burn Care Res 27:50-9
Sayeed, Mohammed M (2005) Inflammatory/cardiovascular-metabolic responses in a rat model of burn injury with superimposed infection. Shock 24 Suppl 1:40-4
Fazal, Nadeem; Choudhry, Mashkoor A; Sayeed, Mohammed M (2005) Inhibition of T cell MAPKs (Erk 1/2, p38) with thermal injury is related to down-regulation of Ca2+ signaling. Biochim Biophys Acta 1741:113-9
Hu, Zhihong; Sayeed, Mohammed M (2005) Activation of PI3-kinase/PKB contributes to delay in neutrophil apoptosis after thermal injury. Am J Physiol Cell Physiol 288:C1171-8
Samonte, Victoria A; Goto, Masakatsu; Ravindranath, Thyyar M et al. (2004) Exacerbation of intestinal permeability in rats after a two-hit injury: burn and Enterococcus faecalis infection. Crit Care Med 32:2267-73
Al-Ghoul, Walid M; Khan, Mehdi; Fazal, Nadeem et al. (2004) Mechanisms of postburn intestinal barrier dysfunction in the rat: roles of epithelial cell renewal, E-cadherin, and neutrophil extravasation. Crit Care Med 32:1730-9
Hu, Zhihong; Sayeed, Mohammed M (2004) Suppression of mitochondria-dependent neutrophil apoptosis with thermal injury. Am J Physiol Cell Physiol 286:C170-8
Dallal, Ousama; Ravindranath, Thyyar M; Choudhry, Mashkoor A et al. (2003) T-cell proliferative responses following sepsis in neonatal rats. Biol Neonate 83:201-7
Choudhry, Mashkoor A; Haque, Farah; Khan, Mehdi et al. (2003) Enteral nutritional supplementation prevents mesenteric lymph node T-cell suppression in burn injury. Crit Care Med 31:1764-70
Choudhry, Mashkoor A; Fazal, Nadeem; Goto, Masakatsu et al. (2002) Gut-associated lymphoid T cell suppression enhances bacterial translocation in alcohol and burn injury. Am J Physiol Gastrointest Liver Physiol 282:G937-47

Showing the most recent 10 out of 26 publications