In Vitro Effects of Short-Term and Long-Term Heat Exposures on the Immune Response and Prostaglandin Biosynthesis in Bovine Endometrial Cells

SIMPLE SUMMARY: The bovine endometrium is a major contributor to the regulation of reproduction and participates in several processes of producing offspring, including the resumption of estrus cyclicity, implantation and placenta formation. Heat stress is one of the underlying factors contributing to low fertility in cattle. The most significant elements of heat stress are increased temperature and humidity, which cause an economic loss in the dairy industry from decreased milk production, reduced reproductive performance and increased culling. The current study aimed to investigate the effect of elevated temperature (short-term or long-term) on bovine endometrial cell cultures. Our findings suggest that heat exposure compromised the endometrial immune response and prostaglandin synthesis in different ways based on elevated temperature duration, which could reduce subsequent fertility. This research provides data regarding the impact of thermal stress on uterine functions in cattle to further improve reproductive management strategies and prevent uterine infection in cattle experiencing heat stress during the current climate change era. ABSTRACT: Worldwide heat stress (HS) conditions have a negative impact on dairy cow fertility. However, understanding of the effect of heat stress on endometrial functions is still unclear. The present study aimed to investigate the effects of differential heat exposure conditions on the immune response and prostaglandin biosynthesis of bovine endometrium challenged with bacterial lipopolysaccharide (LPS). Cultures of endometrial cells were grown to confluence at 37 °C (control) and 40.4 °C for 24 h after confluence (short-term heat exposure) and 40.4 °C for 8 days from the beginning of the culture (long-term heat exposure), prior to a challenge by 100 ng/mL LPS for 12 h. LPS altered ALOX12, IL8, IL1B, S100A8, PTGES and AKR1B1 expressions, as well as secretory IL8 and PGF2α. Short-term heat exposure decreased S100A8, IL8 and PGF2α compared with the control temperature, while long-term heat exposure decreased S100A8 and PGF2α. In contrast, HSPA5 expression was not altered by heat exposure or LPS. Indeed, the short-term heat treatment was insufficient for accomplishing the responses of the endometrium to LPS treatment for IL8, S100A8 and PTGES expressions when compared with other temperature conditions. Our findings showed that heat exposure could compromise endometrium immune response and prostaglandin biosynthesis in different ways based on elevated temperature duration, which could reduce subsequent fertility.