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Updated: Feb 9, 2026

Subtyping of Campylobacter jejuni ssp. doylei Isolates Using Mass Spectrometry-based PhyloProteomics MSPP
Published on: October 30, 2016
Research note: Temporal and tissue-specific immune responses to Campylobacter jejuni colonization in broiler chickens
Xin Ye1, Hailey Fugate2, Chrysta N Beck1
1Department of Poultry Science, Mississippi State University, Mississippi State, MS, 39762, USA.
Abstract:
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.
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