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Prior Viral Illness Exacerbates the Severity of Lung Injury in a Mice Heat Stroke Model
Author(s) -
Plamper Mark l.,
Dineen Shauna M.,
King Michelle A.,
Leon Lisa R.
Publication year - 2018
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.2018.32.1_supplement.590.8
Subject(s) - ards , eotaxin , heat illness , medicine , saline , inflammation , lung , monocyte , immunology , gastroenterology , endocrinology , chemokine , physics , meteorology
Heat Stroke (HS) is a common threatto both civilian and warfighter populations, however the mechanisms underlying tissueinjury are unknown. Acute respiratory distress syndrome (ARDS) is often seen with the adverse sequelae that follows HS, and correlates with mortality. Further, anecdotal evidence suggests that prior illness can increase the severity of multi‐organ injury in HS. To examine the effect of a recent viral illness on the severity of ARDS following HS, male C57BL/6J mice (body weight 23.0 ± 0.3g)were intraperitoneally injected with Polyinosinic: Polycytidylic acid (PIC; 100μg) or saline (SAL; 100 μl) 48‐h prior to heat exposure (HE; 39.5 ±0.1°C). Miceremained in HE until core temperature (Tc; ±0.1°C; radio telemetry) reached Tc Max of 42.4°C. Control mice were injected with saline or PIC, but never exposed to the heat. Lung tissue was collected for analysis of inflammatory biomarkers indicative of ARDS and cell death at Tc Max and at 1 day post HE (1d). Monocyte chemoattractant protein‐1 (MCP‐1; a predictor of ARDS severity) was upregulated in control mice injected with PIC alone (P=0.003 at Tc Max; P<0.001 at 1d)and HE exacerbated this response at both Tc Max and 1d (P<0.001 and P=0.029 respectively). Interestingly, eotaxin (an eosinophil‐specific chemoattractant)was suppressed at Tc Max following HE in both PIC and SAL groups (P<0.001). PIC in the absence of HE did not alter expression at Tc Max, however eotaxin was significantly upregulated in this group at 1d (P=0.041). To determine the extent of lung injury, a cell death assay was conducted. Unexpectedly, at Tc Max no differences in cell death were seen between groups; however, at 1d cell death was significantly augmented in those that received PIC alone (P=0.001) and those that received PIC prior to HE (P=0.002). In conclusion, PIC injection 48‐h prior to HE increases severity of lung tissue injury with the magnitude and time course of inflammatory changes was unique to each biomarker. Author views not official US Army or DOD policy. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .