Heat shock protein 70 protects the quail cecum against oxidant stress, inflammatory injury, and microbiota imbalance induced by cold stress.

The intent of this study was to investigate the effects of cold stress on oxidative indexes, inflammatory factors, and microbiota in the quail cecum. A total of 192 male quails (15-day-old) were randomly divided into 12 groups (16 in each group) and were exposed to acute (up to 12 h) and chronic (up to 20 D) cold stress at 12 ± 1°C. After cold stress treatment, we examined morphological damage, oxidative stress indexes, inflammatory factors, and intestinal microbiota. Results of morphological examination showed that both acute and chronic cold stress can lead to cecal tissue injury. In addition, both acute and chronic cold stress, especially chronic cold stress can influence the activity of oxidative stress mediators. Glutathione (GSH) and glutathione peroxidase (GSH-Px) activities decreased significantly (p < 0.05), while the nitric oxide (NO) content and inducible nitric oxide synthase (iNOS) activity increased significantly (p < 0.05). Moreover, mRNA levels of inflammatory factors cyclooxygenase-2 (COX-2), prostaglandin E synthase (PTGES), and heat shock protein 70 (Hsp70) were higher in both acute and chronic cold stress groups when compared with the control group (p < 0.05). Furthermore, the intestinal microbiota was changed in both the acute and chronic cold stress groups. These results suggested that cold stress caused oxidative stress and inflammatory injury in cecal tissues, influenced cecal microbiota, and increased expression of Hsp70, which may contribute in protecting the cecum against cold stress in quails.