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Impaired recovery from peritoneal inflammation in a mouse model of mild dietary zinc restriction
Author(s) -
Phillips Brett E.,
Geletzke Abby K.,
Smith Philip B.,
Podany Abigail B.,
Chacon Alexander,
Kelleher Shan L.,
Patterson Andrew D.,
Soybel David I.
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201500688
Subject(s) - inflammation , immune system , zinc deficiency (plant disorder) , endocrinology , medicine , cytokine , splenocyte , zinc , phagocytosis , peritonitis , macrophage , peritoneum , immunology , chemistry , biology , biochemistry , pathology , in vitro , organic chemistry
Scope Mild dietary zinc (Zn) deficiency is wide‐spread in human populations, but the effect on Zn‐dependent processes of immune function and healing are not well understood. The consequences of mild dietary Zn restriction were examined in two mouse models of inflammation and recovery. Methods and results Male C57BL/6 mice were fed a Zn adequate diet (ZA, 30 mg Zn/kg diet), or diets containing sub‐optimal Zn levels (ZM, 15 mg Zn/kg diet; ZD, 10 mg Zn/kg diet) for 30 days before a thioglycollate peritonitis challenge. Plasma lipid profiles were distinct, with greater Zn restriction resulting in a greater impact on metabolites. The milder ZM diet was selected for immune studies. Peritoneal macrophages from ZM mice displayed increased phagocytosis and amplified pro‐inflammatory cytokine (IL‐1β, IL‐6, and TNFα) release compared to ZA, at baseline and after a secondary LPS challenge. Splenocytes isolated from ZM mice displayed an increase in IL‐6 and a reduction in anti‐inflammatory IL‐4 compared to ZA. Cytokine levels in plasma were unaltered. Following mechanical manipulation of the intestines to induce ileus, ZM mice had delayed intestinal transit compared to ZA. Conclusion Mild Zn deficiency enhances local inflammatory responses, amplifying macrophage functions and delaying recovery from acute insults within the peritoneum.