Mashkoor A. Choudhry

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Protein kinase B (Akt) is known to be involved in proinflammatory and chemotactic events in response to injury. Akt activation also leads to the induction of heme oxygenase (HO)-1. Up-regulation of HO-1 mediates potent, anti-inflammatory effects and attenuates organ injury. Although studies have shown that 17beta-estradiol (E2) prevents organ damage(More)
A significant number of burn and other traumatic injuries are reported to occur under the influence of alcohol (EtOH) intoxication. Despite this overwhelming association between EtOH intoxication and injury, relatively little attention has been paid to determining the role of EtOH in post-injury pathogenesis. This article reviews studies which have(More)
Recent findings from our laboratory have shown that acute alcohol (EtOH) intoxication before burn injury impairs intestinal immunity and barrier functions. To further delineate the mechanism of impaired intestinal barrier function, the present study examined the role of corticosterone (CORT) and interleukin (IL)-18, as CORT and IL-18 are elevated following(More)
miRNA155 has been implicated in normal T cell function and their differentiations into the Th1 subtype. We have shown that acute alcohol (ethanol) intoxication combined with burn injury suppresses T cell IFN-γ release. Herein, we examined whether the decrease in IFN-γ is resulted from altered expression of miRNA155 and transcription factors--NFAT, Tbx21,(More)
Natural killer T (NKT) cells are known to modulate T cell responses during autoimmunity, tolerance, and antitumor immunity; however, their potential role in regulating the immune response to injury has not been reported. Using a murine model of burn injury, we investigated whether CD1d-restricted NKT cells played a role in the T cell suppression that occurs(More)
The increasing prevalence of binge drinking and its association with trauma necessitate accurate animal models to examine the impact of intoxication on the response and outcome to injuries such as burn. While much research has focused on the effect of alcohol dose and duration on the subsequent inflammatory parameters following burn, little evidence exists(More)
Studies have shown that burn patients who are intoxicated at the time of injury are more susceptible to infection and have higher incidence of mortality. A major cause of death in burn and trauma patients regardless of their alcohol (EtOH) exposure is the multiple organ dysfunction; which, in part, is driven by systemic inflammatory response and activated(More)
Recent studies have shown that administration of dehydroepiandrosterone (DHEA) following trauma-hemorrhage (T-H) improves cardiovascular and hepatic function in male animals. Although androstenediol, one of the DHEA metabolites, has been recently reported to produce salutary effects on cardiac function and splanchnic perfusion following T-H, it remains(More)
Sepsis remains one of the leading causes of death in burn patients who survive the initial insult of injury. Disruption of the intestinal epithelial barrier has been shown after burn injury; this can lead to the translocation of bacteria or their products (e.g., endotoxin) from the intestinal lumen to the circulation, thereby increasing the risk for sepsis(More)
The depression in cell-mediated immune function following trauma-hemorrhage is shown to be restored by 17␤-estradiol (E2) administration. However , it remains unknown which of the two estrogen-receptors, (ER)-␣ or ER-␤, plays the predominant role in mediating the beneficial effects of E2. Female B57BL/J6 ER-␤ ؊/؊ transgenic mice [knockout (KO)] and(More)