PMID- 34648662 OWN - NLM STAT- MEDLINE DCOM- 20220504 LR - 20220504 IS - 1097-4652 (Electronic) IS - 0021-9541 (Linking) VI - 237 IP - 1 DP - 2022 Jan TI - Hyperthermia alters interleukin-6 production in response to lipopolysaccharide via endoplasmic reticulum stress in bovine endometrial cells. PG - 1087-1099 LID - 10.1002/jcp.30604 [doi] AB - In the postpartum period, cows experience the uterine bacterial infection and develop the endometritis. To eliminate bacteria and recover from endometritis, endometrial epithelial and stromal cells secrete the cytokine and chemokine, such as interleukin 6 (IL-6), IL-8, and monocyte chemotactic protein 1 (MCP1), to recruit immune cells. Moreover, the symptom of endometritis is prolonged in summer and we have recently indicated that hyperthermia suppresses and enhances the IL-6 production in response to lipopolysaccharide (LPS) challenge in endometrial epithelial and stromal cells, respectively. However, the mechanisms for the opposite reaction of IL-6 secretion in response to LPS challenge in both types of endometrial cells under hyperthermia conditions were still unclear. To reveal these mechanisms, both types of endometrial cells were cultured with LPS under the control (38.5 degrees C) or hyperthermia (40.5 degrees C) conditions and comprehensively analyzed differential gene expressions of them by RNA-seq. In addition, based on these results, we examined the effect of endoplasmic reticulum (ER) stress on the IL-6 production in both types of endometrial cells cultured with LPS under hyperthermia conditions. In comprehensive analysis, hyperthermia induced the ER stress in the endometrial stromal cells but not in the endometrial epithelial cells. Actually, we confirmed that hyperthermia increased the gene expression of BiP, ATF4, and sXBP1 and protein expression of BiP and phosphorylated inositol requiring 1, ER stress marker, in the endometrial stromal cells but not in the endometrial epithelial cells. Moreover, in the endometrial stromal cells exposed to LPS, activation and inhibition of ER stress enhanced the IL-6 production under control conditions and suppressed it under hyperthermia conditions, respectively. In this study, we could uncover the one of causes for the disruption of IL-6 production in response to LPS challenge in the endometrial cells under hyperthermia conditions. This finding might be a clue for the improvement of the symptom of endometritis in cows during summer. CI - (c) 2021 Wiley Periodicals LLC. FAU - Sakai, Shunsuke AU - Sakai S AD - Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan. FAU - Inoue, Yuki AU - Inoue Y AD - Laboratory of Animal Reproduction, Department of Animal Science, Tokyo University of Agriculture, Kanagawa, Japan. FAU - Tanaka, Keisuke AU - Tanaka K AD - NODAI Genome Research Center, Tokyo University of Agriculture, Tokyo, Japan. FAU - Yamamoto, Yuki AU - Yamamoto Y AD - Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan. FAU - Iwata, Hisataka AU - Iwata H AD - Laboratory of Animal Reproduction, Department of Animal Science, Tokyo University of Agriculture, Kanagawa, Japan. FAU - Kimura, Koji AU - Kimura K AUID- ORCID: 0000-0001-6153-6384 AD - Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20211014 PL - United States TA - J Cell Physiol JT - Journal of cellular physiology JID - 0050222 RN - 0 (Interleukin-6) RN - 0 (Lipopolysaccharides) SB - IM MH - Animals MH - Cattle MH - *Endometritis/genetics MH - Endometrium/metabolism MH - Endoplasmic Reticulum Stress MH - Female MH - Gene Expression MH - Humans MH - *Hyperthermia, Induced MH - Interleukin-6/metabolism MH - Lipopolysaccharides/metabolism/pharmacology OTO - NOTNLM OT - IL-6 OT - cattle OT - endometrial cells OT - endoplasmic reticulum stress OT - heat stress OT - hyperthermia EDAT- 2021/10/15 06:00 MHDA- 2022/05/06 06:00 CRDT- 2021/10/14 17:26 PHST- 2021/09/12 00:00 [revised] PHST- 2021/04/26 00:00 [received] PHST- 2021/09/15 00:00 [accepted] PHST- 2021/10/15 06:00 [pubmed] PHST- 2022/05/06 06:00 [medline] PHST- 2021/10/14 17:26 [entrez] AID - 10.1002/jcp.30604 [doi] PST - ppublish SO - J Cell Physiol. 2022 Jan;237(1):1087-1099. doi: 10.1002/jcp.30604. Epub 2021 Oct 14.