['Hypothermia is a well-known risk factor for postoperative complications because it prolongs the monocyte inflammatory response. The purpose of this study was to investigate whether temperature-activated ion channels (transient receptor protein channels [TRP] A1 and V1) mediate the effects of temperature on monocytes.', 'Primary human monocytes were isolated and stimulated with lipopolysaccharide at 32°C or 39°C. RNA was isolated for analysis of microRNA (miR)-155 expression, and cytokines in the supernatant were measured with an enzyme-linked immunosorbent assay. Specific inhibitors of TRPA1 (HC- 030031) and a specific activator of TRPV1 (capsaicin) were used to block or activate TRPA1 and TRPV1, respectively. Statistical analysis was performed using the Wilcoxon signed-rank test.', 'TRPM8 mRNA was not expressed in primary human monocytes, whereas TRPA1 and TRPV1 were expressed. TRPV1 mRNA expression was suppressed at 32°C but not at 39°C. TRPA1 was induced strongly at 32°C and 39°C. Immunofluorescence microscopy confirmed that monocytes express TRPA1 and TRPV1 on their cell surface. Interleukin-10 secretion was increased by blocking TRPA1 (77.8\xa0±\xa03 2.8 pg/mL) and activating TRPA1 (79.4\xa0±\xa016.1 pg/mL) after 24\xa0hours at 32°C (control 37.4\xa0±\xa017.1 pg/mL, P\xa0<\xa0.05). At 36\xa0hours, tumor necrosis factor secretion was decreased after TRPA1 blockade (2,321\xa0±\xa0439 pg/mL) and TRPV1 activation (2,137\xa0±\xa0411 pg/mL) compared with control (2,567\xa0±\xa0495 pg/mL, P\xa0<\xa0.05). Furthermore, miR-155 expression also was suppressed at 24\xa0hours by TRPA1 blockade and TRPV1 activation (both P\xa0<\xa0.05). Silencing of TRPA1 normalized monocyte IL-10 secretion at 32°C.'] Does tRPA1 mediate the effects of hypothermia on the monocyte inflammatory response?