The provision of glutamine or glutamine 'precursors' (glutamine-containing dipeptides, N-acetylglutamine, 2-oxoglutarate, branched-chain amino acids), usually by the parenteral route, has been used in various catabolic situations in humans. In most cases, the intention was not to support the immune system but rather to maintain nitrogen balance, muscle mass and/or gut integrity (for a review, see Furst et al., 1997). Nevertheless, the maintenance of plasma glutamine concentrations in such a group of patients very much at risk of immunosuppression might have the added benefit of maintaining immune function.
The provision of glutamine intravenously for patients following bone-marrow transplantation resulted in a lower level of infection (12% of patients with clinical infections vs. 42% in the control group) and a shorter stay in hospital (29 ± 1 days vs. 36 ±2 days) than for patients receiving glutamine-free parenteral nutrition (Ziegler et al., 1992). A later report by this group (Ziegler et al., 1998) showed that glutamine treatment resulted in greater numbers of total lymphocytes, T lymphocytes and CD4+ lymphocytes (but not B lymphocytes or natural killer cells) in the bloodstream after the patients were discharged. The authors suggested that glutamine specifically enhances T lymphocyte number and that this might be responsible for the diminished infection rate observed.
Very low-birth-weight babies who received a glutamine-enriched premature feeding formula (providing 0.3 g glutamine kg-1 body weight day-1) had a much lower rate of sepsis (11% vs. 31%) than babies who received a standard formula (Neu et al., 1997). In a study of patients in intensive care, glutamine provision decreased mortality compared with standard parenteral nutrition (43% vs. 67%) and changed the pattern of mortality (Griffiths et al., 1997). Neither of these studies reported immunological outcomes of the treatments. However, another study of patients in intensive care reported that enteral glutamine increased the blood CD4:CD8 ratio (Jensen et al., 1996). In a more recent study, in which patients received enteral glutamine vs. standard enteral feed from within 48 h of the trauma, there was a significant reduction in the 15-day incidence of pneumonia (17% vs. 45% in the control group), bacteraemia (7% vs. 42%) and severe sepsis (4% vs. 26%) in the glutamine group, although this was not associated with reduced mortality (Houdijk et al., 1998). Parenteral administration of glutamine into patients postcolorectal surgery increased mito-gen-stimulated proliferation of blood lymphocytes (O'Riordain et al., 1994), suggesting that glutamine does improve T lymphocyte function in patients at risk of sepsis; glutamine did not affect ex vivo TNF or IL-6 production. In another study, post-operative patients who received alanyl-glutamine parenter-ally had increased blood lymphocyte numbers, increased ex vivo production of cysteinyl leucotrienes by blood neutrophils and a shorter stay in hospital (Morlion et al., 1998). Most recently, infusion of a parenteral mixture containing glycyl-glutamine for 48 h after major abdominal surgery resulted in better maintenance of the human leucocyte antigen (HLA)-DR expression on circulating monocytes than in control patients who received a standard parenteral mixture (Spittler et al., 2001). There was no effect of the glutamine dipeptide on production of TNF-a or IL-6 by LPS-stimulated whole blood (Spittler et al., 2001). Patients with oesophageal cancer being treated with radiochemotherapy had higher blood lymphocyte counts and better lymphocyte proliferative responses if they consumed glutamine (30 g day-1) for 28 days (Yoshida et al., 1998). These studies indicate that glutamine is able to maintain lymphocyte numbers and (some) immune-cell responses in patients normally at risk of immunosuppression and infection.
In addition to a direct immunological effect, glutamine, even provided par-enterally, improves the gut barrier function in patients at risk of infection (van der Hulst et al., 1993). This would have the benefit of decreasing the translocation of bacteria from the gut and so eliminating a key source of infection. Animal studies indicate that providing glutamine does decrease bacterial translocation (Burke et al., 1989).
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