Dietary cysteamine hydrochloride protects against oxidation, inflammation, and mucosal barrier disruption of broiler chickens challenged with Clostridium perfringens.

This study aimed to investigate the effect of dietary cysteamine hydrochloride (CSH) on the growth performance, oxidation, inflammation, and gene expression of cytoskeleton and tight junction in the intestinal mucosa of broiler chickens challenged with Clostridium perfringens (C. perfringens). A total of 360 one-day-old broiler chicks were randomly distributed into 5 groups for a negative control (NC, without C. perfringens challenge), a positive control (PC, with C. perfringens challenge), and PC plus CSH at 100, 150, or 200 mg/kg of diet. The results showed that average daily gain, gain:feed, cecal population and enterotoxin of C. perfringens were negatively affected (P < 0.05) by the C. perfringens challenge, but were conversely affected (P < 0.05) by the CSH supplementation, and G:F reached to the level of NC group. The PC group increased (P < 0.05) serum diamine oxidase, malondialdehyde, protein carbonyl, interleukin-6, interleukin-1β, and tumor necrosis factor-α, whereas the supplementation of CSH decreased (P < 0.05) these parameters. Moreover, the C. perfringens challenge worsened the disruption of intestinal mucosal cytoskeleton and tight junction by downregulating (P < 0.05) the mRNA levels of actin protein of muscle Z-line alpha, syncoilin, synemin, tubulin, claudin-1, and zona occludens protein-2, while these parameters were partially compensated (P < 0.05) by CSH supplementation. For the dose trends of CSH, there were linear and quadratic (P < 0.05) effects on gain:feed, enterotoxins, tumor necrosis factor-α, tubulin alpha 1c, syncoilin, and synemin. In conclusion, the CSH can be an alternative against C. perfringens infection by beneficially regulating gut pathogenic bacteria and enterotoxins, oxidation, inflammation, cytoskeleton, and tight junction in broiler chickens.