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IL‐6 Immunoreactivity is increased in mouse liver during heat strain recovery
Author(s) -
Blaha Michael,
Leon Lisa
Publication year - 2007
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.21.6.a1139-b
Subject(s) - spleen , kidney , staining , immunohistochemistry , hypothermia , pathology , endocrinology , knockout mouse , histopathology , medicine , biology , receptor
High plasma levels of interleukin (IL)‐6 correlate with morbidity/mortality in heat stroke patients and animal models, yet IL‐6 knockout mice show higher heat strain mortality than wildtype controls. These data suggest that high IL‐6 levels may be a marker of heat injury, while basal levels are required for recovery. This study tested the hypothesis that IL‐6 immunoreactivity correlates with liver, kidney and spleen damage in heat strained mice. C57BL/6J mice were exposed to ambient temperature (T a ) of 39.5±0.2°C until maximum core temperature (T c,Max ) of 42.7°C was reached (biotelemetry; ±0.1°C). At T c,Max , mice were removed from the heat to recover at T a of 25.0±2°C until hypothermia developed (29.4±0.4°C); then liver, kidney and spleen were collected for histopathology (H&E) and IL‐6 staining (immunohistochemistry). Kidney and spleen of heat strained mice showed damage compared to nonheated controls, yet IL‐6 staining was absent. Despite no damage, IL‐6 staining was elevated in liver of heat strained mice compared to controls. Staining was confined to the centrolobular region, an area associated with acute‐phase protein synthesis. These data suggest that IL‐6 synthesis by the liver, kidney and spleen of heat‐strained mice does not correlate to tissue damage, but IL‐6 may be serving a protective function in the liver via its known role as a regulator of the acute phase response. Research supported by MRMC.