Dietary restriction impairs neutrophil exudation by reducing CD11b/CD18 expression and chemokine production

Hypothesis: Patients with malnutrition are susceptible to infection. Polymo rphonuclear neutrophils (PMNs) are the major effector of the nonspecific im mune response in host resistance to infection. Dietary restriction may impa ir PMN-mediated immunity in the peritoneal cavity by reducing PMN exudation , adhesion molecule expression on PMNs, and chemokine production. Design: Randomized study of murine glycogen-induced peritonitis with dietar y restriction. Setting: University research laboratory. Materials: Male C57BL/6J mice. Interventions: Mice (N=204) were assigned to ad libitum, moderate, and seve re diet-restricted groups receiving mouse chow adlibitum (132 g/kg, 66 g/kg , and 33 g/kg daily for 7 days, respectively). After dietary restriction wi th or without 1 day of refeeding, mice were administered glycogen intraperi toneally to induce cell exudation. Main Outcome Measures: CD11b, CD18, and CD62L expressions on circulating PM Ns, phagocytosis, and reactive oxygen intermediate production by exudative PMNs were measured after glycogen installation. The levels of PMN-specific chemokine, macrophage inflammatory protein 2 (MIP-2), in peritoneal lavage fluid were also measured. These parameters were measured after glycogen ins tallation in the refeeding experiment. Results: Seven days of dietary restriction decreased CD11B/CD18 expression on circulating PMNs, MIP-2 levels in peritoneal lavage fluid, and subsequen t PMN exudation into the peritoneal cavity early in peritonitis. Both CD11b and CD18 expression on circulating PMNs and MIP-2 levels correlated signif icantly with numbers of exudative PMNs. Seven days of dietary restriction a lso impaired phagocytosis, while up-regulating reactive oxygen intermediate production by exudative PMNs. Only 1 day of ad libitum refeeding normalize d CD11b/CD18 expression with PMN exudation into the peritoneal cavity. Conclusions: Short-term dietary restriction impairs PMN exudation into loca l inflammatory sites in murine peritonitis by reducing CD11B/CD18 expressio n and MIP-2. production. Even brief nutritional replenishment in diet-restr icted patients may improve host defense via restoring these PMN functions a nd chemokine production at local inflammatory sites.