Prior viral illness increases heat stroke severity in mice
Autor: | Shauna M. Dineen, Jermaine A. Ward, Lisa R. Leon |
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Rok vydání: | 2020 |
Předmět: |
Male
Hyperthermia Chemokine medicine.medical_specialty Hot Temperature Fever Lipopolysaccharide Physiology Heat Stroke medicine.medical_treatment Inflammation Hypothermia 030204 cardiovascular system & hematology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Physiology (medical) Internal medicine medicine Animals Platelet Saline Stroke Nutrition and Dietetics biology business.industry General Medicine medicine.disease Mice Inbred C57BL Disease Models Animal Endocrinology chemistry biology.protein Cytokines Chemokines medicine.symptom business 030217 neurology & neurosurgery Body Temperature Regulation |
Zdroj: | Experimental Physiology. 106:244-257 |
ISSN: | 1469-445X 0958-0670 |
Popis: | NEW FINDINGS What is the central question of this study? We hypothesized that prior illness would increase the susceptibility to and severity of heat stroke (HS). What is the main finding and its importance? We provide the first experimental evidence, using a mouse model of HS, that recent viral illness increases the severity of HS. Our data indicate that this effect is not attributable to the exacerbation of hyperthermia but is a consequence of ongoing coagulation and systemic inflammatory reactions. Our data suggest that measurement of platelets, cytokines and chemokines before heat exposure might be indicative of susceptibility to HS, with coagulation and inflammation being potential targets for intervention that could improve recovery. ABSTRACT It is hypothesized that prior illness exacerbates heat stroke (HS) in otherwise healthy organisms by augmenting hyperthermia during heat exposure or deactivating cellular pathways that protect against organ injury. To test these hypotheses, we injected telemetered male C57BL/6J mice with lipopolysaccharide (LPS; 50 µg kg-1 i.p.) or polyinosinic:polycytidylic acid (PIC; 100 µg i.p.) as a bacterial or a viral mimic, respectively, with saline (SAL; equivalent volume) as a control. Mice recovered for 48 or 72 h before HS (maximal core temperature = 42.4°C). Platelet counts, cytokines, chemokines and organ injury were determined 48 or 72 h after injection (without heating) or at maximal core temperature and at 1 day of recovery from HS. In the absence of heat, PIC induced more robust signs of sickness and increased cytokines and chemokines (TNF-α, RANTES, IP-10 and MIP-1β) at 48 h, which was not observed with LPS (P |
Databáze: | OpenAIRE |
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