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Monocyte chemoattractant protein‐1 expression in the lung and kidney is a marker of severity during heat stroke recovery in rats
Author(s) -
Plamper Mark L,
Ward Jermaine A,
Leon Lisa R,
Audet Gerald N
Publication year - 2017
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.31.1_supplement.1018.5
Subject(s) - monocyte , chemokine , lung , kidney , infiltration (hvac) , medicine , stroke (engine) , blood pressure , pathology , chemotaxis , ccl2 , inflammation , mean arterial pressure , endocrinology , chemistry , heart rate , receptor , physics , engineering , thermodynamics , mechanical engineering
Heat Stroke (HS) is a common environmental threat to both civilian and war fighter populations. Building on previous studies, our aim is to determine the course of HS associated organ damage and find new molecular pathways that will help in HS treatment and diagnosis. Monocyte chemoattractant protein‐1 (MCP‐1) is one of the key chemokines that regulate migration and infiltration of monocyte/macrophages, into organ tissues, which may be a key component of HS pathology. In this study, we used conscious passively heated Fisher 344 rats (Tc 42 ±0.1°C) with implantable radio telemetric devices that could gather data before, during and after heating. Data obtained included core temperature (Tc), heart rate (HR) and mean arterial blood pressure. Tissues and blood samples were collected at 24h for molecular and histological analysis. Using results from physiological data and histological sectioning, rats were divided into the categories of mild (MLD), moderate (MOD) and severe (SEV). In the lung, MCP‐1 showed significantly (P<0.001) higher content in the SEV rats (mean 28.51 ±2.34 pg/ml), with proportionate decreasing amounts in MOD (12.03 ±1.56 pg/ml) and MLD (6.66 ±2.34 pg/ml) rats. The control animals showed a lack of response of MCP‐1 (0.0 pg/ml). In the kidney, MCP‐1 results suggest a useful general marker of HS, where SEV (mean 85.54 ±12.60 pg/ml), MOD (89.05 ±10.62 pg/ml) and MLD (97.34 ±12.74 pg/ml) rats were equally elevated compared to the control animals (28.27 ±12.74 pg/ml). Protease‐activated receptor 1 (PAR1), was also tested for a potential marker for HS. Western blot results in lung samples showed significantly (P<0.017) increased intensity of SEV (mean 0.49 ±0.12 au) rats compared with control animals (0.20 ±0.01 au). However, PAR1 was unable to differentiate between MOD and MLD rats versus control animals. Several other molecular markers were also examined, including Matrix metalloproteinases (MMP9), Tissue factor (TF) and Vascular endothelial growth factor (VEGF); none showed elevated levels in lung or kidney tissues at 24h of recovery. In conclusion, the increase in MCP‐1 suggests immune cell infiltration into the lung and kidney and points to MCP‐1 as potential marker for determining overall HS severity during recovery. Author views not official US Army or DoD policy