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Effects of IL‐6 on intestinal damage and cytokine profiles during recovery from heat stroke
Author(s) -
Phillips Neil Andre,
Richards Jennifer,
Clanton Thomas
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.949.11
Subject(s) - cytokine , medicine , stroke (engine) , duodenum , tumor necrosis factor alpha , endocrinology , interleukin 6 , inflammation , immunology , mechanical engineering , engineering
Interleukin‐6 is expressed at high levels during and after heat stroke. Previous studies have shown that IL‐6 deficient mice are intolerant of heat. The mechanisms for the apparent protective effects of IL‐6 are unknown. We hypothesized that IL‐6 reduces the severity of the pro‐inflammatory cytokine response and intestinal damage associated with heat stroke. Circulating cytokines and small intestine (SI) histology were evaluated in anesthetized mice 30 and 120 min following a progressive heat treatment to 42.4°C. Thirty min following HS, IL‐6, KC, IL‐10, MCP‐1, IL‐12, IP‐10, TNF‐α, IP‐10, and MIP‐1α were significantly elevated (P<0.05). All remained elevated at 2h, except TNF‐α and MIP‐1α. Pre‐treatment with IL‐6 failed to alter the circulating cytokine profile. HS induced marked injury to the proximal SI (duodenum) at 30 min (P<0.05), but at 2h into recovery, injury levels resembled those of control sham animals. IL‐6 pre‐treatment significantly attenuated the heat‐induced increases in injury and villus width (swelling) seen in the proximal SI (P<0.05), 30 min into recovery. No differences were seen at 120 min. We conclude: IL‐6 pre‐treatment is effective in protecting the proximal SI. The mechanism for protection does not appear to involve attenuation of the circulating inflammatory cytokine response. AHA #11GRNT7990119