Abstract

Acute stressor exposure induces a sterile inflammatory response marked by shifts in circulating and white adipose tissue (WAT) cytokines. Although the sterile inflammatory response occurs in healthy/non-obese WAT and varies in magnitude relative to the WAT depot, the mechanisms which regulate stress-induced WAT cytokines remain unclear. Because the gut microbiota modulates visceral WAT inflammation and stress-induced systemic cytokines, we hypothesized that changes to the normal microbiota environment would also affect stress-induced WAT cytokines. To test this hypothesis 8 week old male Fischer 344 rats were treated for four days with antibiotics (4 mg/mL streptomycin and 2 mg/mL penicillin G) administered via drinking water prior to receiving 100 tail-shocks (1.5 mA, 5s, every 60 s ± 25 s). Immediately before or following stress rats were sacrificed and subcutaneous, retroperitoneal, epididymal, omental, and mesenteric WAT were harvested for cytokine analyses via ELISA. Stress differentially increased interleukin-1beta (IL-1beta) in all WAT depots, decreased interleukin-10 (IL-10) in subcutaneous and mesenteric WAT and tumor necrosis factor-alpha in omental WAT. Antibiotic treatment reduced fecal colony forming units, dampened the stress-induced increase in IL-1beta in subcutaneous and retroperitoneal WAT and the stress-induced decrease in IL-10 in subcutaneous and mesenteric WAT. These data demonstrate that the gut microbiota directly affects stress-induced shifts in WAT cytokine concentrations in a depot specific manner suggesting a novel mechanism through which pro-inflammatory cytokine concentrations are regulated in healthy, stressed non-obese WAT. NSF-1022451.

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