16-16-dimethylprostaglandin-e2 and Pseudomonas-Infections

Burn injuries have been shown to impair immune function. One of the hypotheses for the etiology of the immunosuppression is that burn injuries result in an elevation of prostaglandin E (PGE) levels which then impair leukocyte function. We evaluated the effect of PGE levels on immune function in multiple animal models utilizing T cell subset levels for our immunologic measurements. Elevations in PGE levels were achieved by administering 16,16-dimethyl-prostaglandin E (dPGE) and reductions by administering indomethacin. The animal models included burned rats, burned-septic rats, and nonburned rats. Neither indomethacin nor dPGE administration resulted in alterations of any of the T cell subset populations in our models.

Topics: 16,16-Dimethylprostaglandin E2; Animals; Burns; Disease Models, Animal; Indomethacin; Leukocyte Count; Male; Prostaglandins E, Synthetic; Pseudomonas Infections; Rats; Rats, Inbred Lew; Spleen; T-Lymphocytes; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory; Wound Infection