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Heat stroke decreases cytokine and chemokine gene expression in the hypothalamus of rats (1104.15)
Author(s) -
Audet Gerald,
Ramon Jose,
Dineen Shauna,
Leon Lisa
Publication year - 2014
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.28.1_supplement.1104.15
Subject(s) - chemokine , cytokine , hypothalamus , medicine , endocrinology , cx3cl1 , biology , immunology , chemistry , inflammation , chemokine receptor
We showed previously that rats display ~1°C core temperature (T c ) increase during ~4 days of heat stroke (HS) recovery; however, the mechanisms mediating this response remain unidentified. It was suggested that hypothalamic damage mediates this T c response, but there is a lack of histological evidence in support of this. We hypothesized that local hypothalamic cytokines and/or chemokines, which are known regulators of T c , may be mediating the elevation in T c during HS recovery. The hypothalamus of Fischer 344 rats was examined for 83 cytokine/chemokine genes (real‐time PCR) at T c,Max (41.8°C), 1, 3, and 10 days of HS recovery (3‐8 rats/group). IL‐1β was elevated ~14‐fold at T c,Max and returned to baseline by 24 hours; IFNγ and IL‐10 were decreased ~3‐fold at 24 hours. All cytokines returned to baseline by 3 days. Most chemokines were downregulated ~2‐ to 4‐fold through 24 hours, but shifted towards increased expression by 3 days. Despite normal T c at 10 days of recovery, some chemokine changes persisted. Contrary to our hypothesis, most cytokines/chemokines showed significant down regulation during HS recovery, which may indicate increased translation in our model. Importantly, resumption of normal T c at 10 days with persistent alteration in the hypothalamic cytokine/chemokine profile may indicate greater susceptibility to a subsequent HS event. Author views not official US Army or DoD policy.