REVERSIBLE IMPAIRMENT IN MONOCYTE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II EXPRESSION IN MALNOURISHED SURGICAL PATIENTS

Citation
Fks. Welsh et al., REVERSIBLE IMPAIRMENT IN MONOCYTE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II EXPRESSION IN MALNOURISHED SURGICAL PATIENTS, JPEN. Journal of parenteral and enteral nutrition, 20(5), 1996, pp. 344-348
Citations number
42
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
01486071
Volume
20
Issue
5
Year of publication
1996
Pages
344 - 348
Database
ISI
SICI code
0148-6071(1996)20:5<344:RIIMMH>2.0.ZU;2-4
Abstract
Background: Upregulation of major histocompatibility complex (MHC) cla ss II antigen in response to the T-cell lymphokine interferon-gamma (I FN-gamma) is central to T cell-macrophage cooperation and immune homeo stasis. We evaluated this property in malnourished surgical patients a nd assessed the impact of nutrition repletion with total parenteral nu trition (TPN). Methods: Sixty-two patients were studied: 37 malnourish ed and 25 controls. Whole blood was cultured with or without IFN-gamma (100 U mL(-1)), dual-labeled with anti-CD14 (monocyte) and anti-human leukocyte antigen-DR antibodies and analyzed by flow cytometry Phagoc ytosis was measured by flow cytometry. In a second study, 10 severely malnourished patients received 5 days of TPN and MHC class Ii expressi on was measured at the end of this period. Results: The magnitude of t he increase in monocyte MHC class II expression in response to IFN-gam ma was significantly increased in the control group compared with the malnourished group(107% us 53%; P <.05). This impairment directly corr elated with severity of malnutrition, but did not correlate with age o r disease type. The number of bacteria phagocytozed per cell was signi ficantly decreased (p < .05) in the malnourished group. In study 2, th ere was a significant increase in MHC class II induction with IFN-gamm a after short-term TPN (58% before us 173% after; P < .001). Conclusio ns: MNC class LI induction in response to IFN-gamma is significantly i mpaired in malnourished patients, correlating with the severity of mal nutrition. This defect is reversed by short-term TPN. These data ident ify the reversible loss of a key mechanism, fundamental to host defens e, that may enhance the risk of infection in malnourished patients.