Chlorogenic acid mitigates avian pathogenic Escherichia coli-induced intestinal barrier damage in broiler chickens via anti-inflammatory and antioxidant effects

This study was conducted to investigate the protective effects of chlorogenic acid (CGA) on intestinal health in broilers challenged with avian pathogenic Escherichia coli (APEC). One hundred and eighty one-day-old male broiler chicks were divided into three groups with six replicates of ten chicks each for a 21-day trial. The birds in the control and APEC groups were fed a basal diet, while birds in the CGA-treated group received a basal diet supplemented with 1000 mg/kg of CGA. At 14 days, birds in the APEC and CGA groups were administered with an APEC suspension Compared with the APEC group, CGA incorporation decreased mortality and cecal Escherichia coli colonies in bacterially challenged broilers (P < 0.05). Additionally, CGA reduced the relative weight of the heart, liver, kidney, gizzard, proventriculus, and intestine, as well as serum triglyceride level and alanine aminotransferase activity in APEC-challenged broilers (P < 0.05). Supplementing CGA reduced the concentrations of interferon-γ, tumor necrosis factor-α, interleukin-1β, and/or interleukin-6 in serum, duodenum, jejunum, and/or ileum in APEC-challenged broilers presumably through the inactivation of the toll-like receptor 4/myeloid differentiation factor 88 pathway (P < 0.05). CGA administration reduced serum diamine oxidase activity and d-lactate and endotoxin concentrations, but increased the ratio between villus height and crypt depth in duodenum and jejunum of APEC-infected chickens, accompanied by the restored intestinal expression of tight junction proteins (claudin-1, claudin-2, occludin, and zonula occludens-1) and genes involved in apoptosis (B cell lymphoma-2 associated X protein, B cell lymphoma-2, and cysteine-requiring aspartate protease 9) (P < 0.05). Additionally, CGA increased superoxide dismutase, glutathione peroxidase, and catalase activities, and glutathione levels in serum and intestinal mucosa, but inhibited the accumulation of intestinal malondialdehyde in APEC-challenged broilers possibly via activating the nuclear factor-erythroid 2-related factor-2/heme oxygenase-1 pathway (P < 0.05). The results suggested that CGA alleviated APEC-induced intestinal damage in broilers by inhibiting inflammation and oxidative stress. However, its potential application in practical poultry production is contingent upon both its efficacy and cost-effectiveness.