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Whole Body Hyperthermia Ameliorates Inflammation via Regulating Pro‐inflammatory but not Anti‐inflammatory Macrophages in Tenotomized Rat Skeletal Muscle
Author(s) -
Hirunsai Muthita,
Srikuea Ratchakrit
Publication year - 2019
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.2019.33.1_supplement.868.4
Subject(s) - tenotomy , inflammation , cytokine , medicine , macrophage , tumor necrosis factor alpha , skeletal muscle , soleus muscle , hyperthermia , muscle atrophy , proinflammatory cytokine , endocrinology , pathology , chemistry , tendon , biochemistry , in vitro
Following disuse condition, macrophages play significant role in inflammatory responses during muscle degeneration and repairing processes. Pro‐inflammatory (M1 phenotype) macrophage becomes classically activated during an initial phase of muscle degeneration. Contrariwise, anti‐inflammatory (M2 phenotype) macrophage abrogates inflammation by deactivating M1 macrophage and promotes muscle growth in repairing stage. Previously, we demonstrated that heat treatment alleviates the loss of muscle mass via enhancing intramuscular capillarization and remodeling extracellular matrix in disuse muscle. Of these, the effect of heat stress on inflammatory responses in tenotomy‐induced atrophy is currently unknown. In this study, the effect of hyperthermia on M1 and M2 macrophage populations as well as the responses of inflammatory cytokine protein expression in the soleus muscle following Achilles tendon transection (tenotomy) were examined. Male Wistar rats were designed into sedentary control (CON), tenotomy without heat treatment (TEN), and tenotomy plus heat treatment (TEN+HEAT) groups. Whole body hyperthermia was maintained in TEN+HEAT group with animal core body temperature at 40.5–41.5°C, 30 min for 7 days. After 8 days of tenotomy, soleus muscle demonstrated a reduction in fiber size and tremendous infiltration of inflammatory macrophages. These occurrences coincided with an increase in pro‐inflammatory cytokine, particularly tumor necrosis factor‐alpha (TNF‐α). Whilst tenotomy had no effect on interleukin‐10 (IL‐10) which is an anti‐inflammatory cytokine. Interestingly, whole body hyperthermia diminished accumulation of M1 macrophages and associated with reduction of TNF‐α protein expression in tenotomized muscle. Nevertheless, heat stress affected neither M2 macrophage phenotype invasion nor IL‐10 protein level following tenotomy. Collectively, heat stress relieved tenotomy‐induced inflammatory response, partly by inhibiting M1 macrophage invasion. Our findings provide a foundation for therapeutic strategy of heat stress on fiber inflammation during skeletal muscle atrophy. Support or Funding Information The research was supported by the grant from Srinakharinwirot University (to MH). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .