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Reversible Impairment in Monocyte Major Histocompatibility Complex Class II Expression in Malnourished Surgical Patients

Academic Surgical Unit, St James's University Hospital, Leeds, England

Susan M. Farmery, PHD

Academic Surgical Unit, St James's University Hospital, Leeds, England

Carol Ramsden, FIBMS

Academic Surgical Unit, St James's University Hospital, Leeds, England

Pierre J. Guillou, FRCS

Academic Surgical Unit, St James's University Hospital, Leeds, England

John V. Reynolds, FRCSI

Academic Surgical Unit, St James's University Hospital, Leeds, England

Background: Upregulation of major histocompatibility complex (MHC) class II antigen in response to the T-cell lymphokine interferon-gamma (IFN-) is central to T cell-macrophage cooperation and immune homeostasis. We evaluated this property in malnourished surgical patients and assessed the impact of nutrition repletion with total parenteral nutrition (TPN). Methods: Sixty-two patients were studied: 37 malnourished and 25 controls. Whole blood was cultured with or without IFN- (100 U mL^-1), dual-labeled with anti-CD 14 (monocyte) and anti-human leukocyte antigen-DR antibodies and analyzed by flow cytometry. Phagocytosis was measured by flow cytometry. In a second study, 10 severely malnourished patients received 5 days of TPN and MHC class II expression was measured at the end of this period. Results: The magnitude of the increase in monocyte MHC class II expression in response to IFN- was significantly increased in the control group compared with the malnourished group (107% vs 53%; p < .05). This impairment directly correlated with severity of malnutrition, but did not correlate with age or disease type. The number of bacteria phagocytozed per cell was significantly decreased (p <.05) in the malnourished group. In study 2, there was a significant increase in MHC class II induction with IFN- after short-term TPN (58% before vs 173% after; p < .001). Conclusions: MHC class II induction in response to IFN- is significantly impaired in malnourished patients, correlating with the severity of malnutrition. This defect is reversed by short-term TPN. These data identify the reversible loss of a key mechanism, fundamental to host defense, that may enhance the risk of infection in malnourished patients. (Journal of Parenteral and Enteral Nutrition 20:344-348, 1996)

Journal of Parenteral and Enteral Nutrition, Vol. 20, No. 5, 344-348 (1996)
DOI: 10.1177/0148607196020005344


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