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Dietary restriction impairs neutrophil exudation by reducing CD11b/CD18 expression and chemokine production
1Department of Surgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Hypothesis:
Patients with malnutrition are susceptible to infection. Polymorphonuclear neutrophils (PMNs) are the major effector of the nonspecific immune response in host resistance to infection. Dietary restriction may impair 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 dietary restriction.
Setting:
University research laboratory.
Materials:
Male C57BL/6J mice.
Interventions:
Mice (N = 204) were assigned to ad libitum, moderate, and severe diet-restricted groups receiving mouse chow ad libitum (132 g/kg, 66 g/kg, and 33 g/kg daily for 7 days, respectively). After dietary restriction with or without 1 day of refeeding, mice were administered glycogen intraperitoneally to induce cell exudation.
Main Outcome Measures:
CD11b, CD18, and CD62L expressions on circulating PMNs, 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 installation 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 subsequent PMN exudation into the peritoneal cavity early in peritonitis. Both CD11b and CD18 expression on circulating PMNs and MIP-2 levels correlated significantly with numbers of exudative PMNs. Seven days of dietary restriction also impaired phagocytosis, while up-regulating reactive oxygen intermediate production by exudative PMNs. Only 1 day of ad libitum refeeding normalized CD11b/CD18 expression with PMN exudation into the peritoneal cavity.
Conclusions:
Short-term dietary restriction impairs PMN exudation into local inflammatory sites in murine peritonitis by reducing CD11b/CD18 expression and MIP-2 production. Even brief nutritional replenishment in diet-restricted patients may improve host defense via restoring these PMN functions and chemokine production at local inflammatory sites.
Insights
Short-term dietary restriction impairs immune cell function and migration, increasing infection susceptibility. Brief nutritional refeeding can restore these polymorphonuclear neutrophil functions and improve host defense.
Area of Science:
- Immunology
- Nutrition Science
- Infectious Disease
Background:
- Malnourished patients exhibit increased susceptibility to infections.
- Polymorphonuclear neutrophils (PMNs) are crucial for non-specific immunity against pathogens.
- Dietary restriction can compromise PMN-mediated immunity, affecting their function and migration.
Purpose of the Study:
- To investigate the impact of short-term dietary restriction on PMN function and peritoneal exudation in a murine model.
- To determine if nutritional refeeding can restore PMN functions and improve host defense mechanisms.
Main Methods:
- A randomized study involving murine glycogen-induced peritonitis was conducted.
- Mice were subjected to ad libitum, moderate, or severe dietary restriction for 7 days.
- PMN adhesion molecule expression (CD11b, CD18, CD62L), phagocytosis, reactive oxygen intermediate production, and chemokine (MIP-2) levels were measured.
Main Results:
- Dietary restriction reduced CD11b/CD18 expression on PMNs, MIP-2 levels, and subsequent PMN exudation into the peritoneal cavity.
- Impaired phagocytosis and increased reactive oxygen intermediate production were observed in diet-restricted mice.
- One day of refeeding normalized PMN exudation and CD11b/CD18 expression.
Conclusions:
- Short-term dietary restriction impairs PMN exudation by reducing CD11b/CD18 expression and MIP-2 production.
- Nutritional replenishment can restore PMN functions and enhance host defense in diet-restricted individuals.