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
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.