Poultry Science最新文献

Campylobacter jejuni (C. jejuni) is a leading foodborne pathogen, and cecal colonization in broilers is a major source of carcass contamination at processing. Understanding how colonization relates to immune activity in systemic and B cell-rich lymphoid tissues is needed to identify immune markers and guide practical strategies to mitigate C. jejuni persistence. We used a chick challenge model to relate treatment group- and time-dependent colonization to gene expression in the spleen and bursa of Fabricius. Seventy-two 1-day-old male broilers were orally inoculated at 7 days of age (negative control, low dose 10⁴ CFU/mL, high dose 10⁶ CFU/mL; six cages per group). At 7 and 14 days post inoculation (DPI), one bird per cage was sampled (n = 6 per group per time point). Cecal and intestinal loads were enumerated, and a 10-gene cytokine panel (IFN-γ, IL-1β, TNF-α, SOCS3, IL-6, IL-10, TGF-β1, BAFF, CD40, TLR-21) was quantified in spleen and bursa by RT-qPCR. Cecal colonization showed a clear group × DPI interaction (P = 0.005) and was more consistent than intestinal recovery. Cecal counts were similar at 7 DPI, but by 14 DPI the high-dose group had higher counts than low-dose and control birds (P < 0.05). Intestinal counts were variable and frequently at or below the detection limit. Splenic responses were largely time-driven, with strong DPI effects but few significant group differences or group × DPI interactions. In contrast, bursal profiles showed marked group × DPI interactions (P < 0.05). At 7 DPI, only CD40 differed among groups, whereas by 14 DPI the high-dose group exhibited significantly higher expression than controls of pro-inflammatory mediators, B cell-associated markers, and regulatory cytokines. Overall, sustained high cecal colonization was associated with a delayed, B cell-centered bursal inflammatory and regulatory signature, while splenic profiles remained primarily time-driven. Cecal load and bursal B cell-related pathways at 14 DPI are promising endpoints for future vaccine and intervention studies in young broilers.

To unravel the differences between host- and pathogen-mediated responses, this study compared the efficacy and mechanisms of a novel phytochemical mixture and monensin in enhancing growth performance, intestinal health, and modulating gut microbiota in broiler chickens infected with Eimeria maxima (E. maxima). A total of 280 one-day-old male broiler chickens were randomly assigned using a randomized complete block design based on initial body weight (BW) and distributed into four dietary treatments with five chickens per cage: non-challenged control (NC), challenged control (PC), monensin-supplemented (MO), and phytochemical mixture (CPG)-supplemented groups. All chickens, except those in NC, were orally challenged with 10,000 E. maxima oocysts on day 15, and body weights were recorded on days 1, 8, 15, 21, and 23. Fourteen chickens per treatment were euthanized at 6 and 8 days post-infection for jejunal mucosa collection to analyze gene expression of cytokines, tight junction proteins (TJPs), nutrient transporters, TLR4 signaling, and antioxidant enzymes. Jejunal lesion scores, fecal oocyst shedding, and microbial composition were also assessed. Compared with the PC group, supplementation with both MO and CPG significantly reduced jejunal lesion scores and fecal oocyst shedding; however, the magnitude of reduction was greater with MO, resulting in more pronounced improvements in BW and feed conversion ratio. In E. maxima-infected broiler chickens, both treatments alleviated jejunal inflammation by modulating pro-inflammatory cytokine expression and TLR4 signaling; however, CPG was more actively involved in host-mediated responses through restoration of nutrient transporter and TJPs expression, maintenance of intestinal barrier integrity, and enhancement of antioxidant defenses. In contrast, MO acted more effectively on pathogen-related outcomes, such as reductions in oocyst shedding and lesion severity, and also induced distinct alterations in the jejunal microbiota based on microbial community and PICRUSt-based predictive functional analyses. Collectively, this study demonstrates that CPG contributes to the control of E. maxima infection in broiler chickens by simultaneously supporting host intestinal function and gut microbial balance through a mode of action distinct from the pathogen-targeted strategy of monensin.