Chicken embryo thermal manipulation alleviates postnatal heat stress-induced jejunal inflammation by inhibiting Transient Receptor Potential V4

Abstract

Intestinal inflammation induced by heat stress is an important factor restricting the healthy growth of broilers. The aim of this study was to evaluate the effect of chicken embryo thermal manipulation (39.5 ℃ and 65 % RH for 3 h daily during 16–18 th embryonic age) on intestinal inflammation in broilers under postnatal heat stress and to investigate whether transient receptor potential V4 (TRPV4) plays a role in this process. Our results suggest that broilers with embryo thermal manipulation experience could delay the rising of rectal temperature during postnatal heat stress (P < 0.05), and had better production performance (P < 0.05), intestinal morphological parameters (P < 0.05) and higher expression of tight junction related genes (P < 0.05). The increased serum lipopolysaccharide (LPS) content, activation of nuclear factor-kappa B (NF-κB) signaling pathway and the increased expression of pro-inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor alpha (TNF-α) in jejunum during postnatal heat stress were alleviated by embryo thermal manipulation (P < 0.05). Postnatal heat stress induced an increase in mRNA and protein expression of TRPV4 in jejunum (P < 0.05), but had no effect on broilers which experienced embryo thermal manipulation (P > 0.05). Inhibition of TRPV4 reduced LPS-induced Ca2+ influx and restrained the activation of NF-κB signaling pathway and the expression of downstream pro-inflammatory cytokines (P < 0.05). The expression of DNA methyltransferase (DNMT) in the jejunum of broilers exposed to postnatal heat stress was increased by embryo thermal manipulation (P < 0.05). The DNA methylation level of TRPV4 promoter region was detected, and the results showed that embryo thermal manipulation increased the DNA methylation level of TRPV4 promoter region (P < 0.05). In conclusion, Chicken embryo thermal manipulation can alleviate jejunal inflammation in broilers under postnatal heat stress. This may be due to the decreased circulating LPS or the increased DNA methylation level in the promoter region of TRPV4, which inhibits TRPV4 expression, thereby reducing Ca2+ influx, and finally alleviating inflammation by affecting NF-κB signaling pathway. The work is an attempt to understand the mechanism involved in alleviation of adverse effects of heat stress during postnatal life through prenatal thermal manipulation and to reveal the important role of epigenetics.