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Elemental diet alters macrophage function in mice
1Harrison Department of Surgical Research, University of Pennsylvania, School of Medicine, Philadelphia 19104.
Abstract:
Administration of a chemically defined liquid elemental diet (ED) induces spontaneous bacterial translocation to mesenteric lymph nodes (MLN) in animal models. The influence of this process on host immunity is unclear. This study evaluated the effects of ED on peritoneal macrophage (PM phi) antimicrobial functions. Conventional C57/BL6 mice and endotoxin-resistant C3H/HeJ mice (n = 60) were randomized to be pair-fed either an ED or regular chow diet (RD) for 14 days. Blood, spleen, liver, and MLN were cultured for bacteria. PM phi were harvested for: percentage Candida albicans (CA) phagocytosis, percentage killing of CA, PM phi superoxide anion (O2-) production, and TNF-dependent macrophage cytotoxicity. Enteral feeding of ED in conventional C57/BL6 mice caused significant bacterial translocation to MLN but not other organs. Significant impairment of CA killing by PM phi occurred in the ED group and was associated with reduced O2- production. Tumor necrosis factor (TNF)-dependent cytotoxicity of PM phi was also decreased. In endotoxin-resistant C3H/HeJ mice, bacterial translocation was not observed and PM phi antifungal functions remained similar in both RD and ED groups. Thus, enteral feeding of an elemental diet downregulates host oxidative and antimicrobial mechanisms and TNF-dependent cytotoxicity in conventional mice which may be secondary to elemental diet-induced bacterial translocation.
Insights
Elemental diets (ED) can cause bacterial translocation in mice, impairing macrophage antimicrobial functions and reducing TNF-dependent cytotoxicity. This suggests ED may suppress host immunity, possibly due to gut bacteria translocation.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- Chemically defined liquid elemental diets (ED) induce bacterial translocation to mesenteric lymph nodes (MLN) in animal models.
- The impact of ED-induced bacterial translocation on host immune function remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of ED administration on peritoneal macrophage (PM phi) antimicrobial functions in conventional and endotoxin-resistant mice.
- To determine if ED-induced changes in PM phi function are linked to bacterial translocation.
Main Methods:
- Conventional C57/BL6 and endotoxin-resistant C3H/HeJ mice were pair-fed either ED or regular chow (RD) for 14 days.
- Bacterial cultures were performed on blood, spleen, liver, and MLN.
- Peritoneal macrophages were assessed for phagocytosis and killing of Candida albicans (CA), superoxide anion (O2-) production, and TNF-dependent cytotoxicity.
Main Results:
- ED induced significant bacterial translocation to MLN in conventional mice, but not in endotoxin-resistant mice.
- Conventional mice on ED showed impaired CA killing by PM phi, reduced O2- production, and decreased TNF-dependent cytotoxicity.
- PM phi function in endotoxin-resistant mice remained unaffected by ED.
Conclusions:
- Enteral feeding of ED downregulates host oxidative and antimicrobial mechanisms and TNF-dependent cytotoxicity in conventional mice.
- These immune alterations may be a consequence of ED-induced bacterial translocation.
- The findings highlight a potential link between elemental diet composition, gut microbiota, and host immune responses.