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Glutathione Depletion in Rats Impairs T-Cell and Macrophage Immune Function
Malcolm K. Robinson, MD;
Mary L. Rodrick, PhD;
Danny O. Jacobs, MD, MPH;
Jan D. Rounds;
Kathryn H. Collins;
Inna B. Saporoschetz;
John A. Mannick, MD;
Douglas W. Wilmore, MD
Arch Surg. 1993;128(1):29-35.
Abstract
Critical illness is associated with both immunosuppression and glutathione deficiency. We determined if in vivo depletion of glutathione would adversely affect immune status. Rats with normal glutathione levels and those with glutathione stores depleted by diethyl maleate underwent analysis of splenocyte function and mesenteric lymph node lymphocyte function. Lymphocytes of the spleen and mesenteric lymph nodes were tested for concanavalin A proliferative response and interleukin 2 production. Tumor necrosis factor and interleukin 6 secretion by splenic adherent cells was also measured. Glutathione-depleted animals had significantly decreased lymphocyte proliferation and decreased production of tumor necrosis factor and interleukin 6 but unaltered interleukin 2 production. These findings indicate that in vivo glutathione deficiency impairs macrophage and T-cell function. Because glutathione depletion may occur in sepsis, trauma, and shock, treatments that help maintain glutathione levels may enhance immunocompetence and thus improve the ability of patients to recover from critical illness.
(Arch Surg. 1993;128:29-35)
Author Affiliations
From the Laboratories for Surgical Metabolism and Nutrition (Drs Robinson, Jacobs, and Wilmore and Ms Rounds) and Surgical Immunology (Drs Rodrick and Mannick and Mss Collins and Saporoschetz), Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Footnotes
Accepted for publication August 23, 1992.
Presented at the 12th Annual Meeting of the Surgical Infection Society, Los Angeles, Calif, April 9, 1992.
Reprint requests to Laboratory for Surgical Metabolism and Nutrition, Thorn Bldg, 14th Floor, Brigham and Women's Hospital, 20 Shattuck St, Boston, MA 02115 (Dr Wilmore).
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