Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
Avian Pathol. 2023 Apr;52(2):108-118. doi: 10.1080/03079457.2022.2154195. Epub 2023 Jan 23.
Necrotic enteritis (NE), caused by , is an economically important disease of chickens. Although NE pathogenesis is moderately well studied, the host immune responses against are poorly understood. The present study used an experimental NE model to characterize lymphoid immune responses in the caecal tonsils (CT), bursa of Fabricius, Harderian gland (HG) and spleen tissues of broiler chickens infected with four + strains (CP1, CP5, CP18, and CP26), of which CP18 and CP26 strains also carried the gene. The gross and histopathological lesions in chickens revealed CP5 to be avirulent, while CP1, CP18, and CP26 strains were virulent with CP26 being "very virulent". Gene expression analysis showed that, while the virulent strains induced a significantly upregulated expression of pro-inflammatory IL-1β gene in CT, the CP26-infected birds had significantly higher CT transcription of IFNγ and IL-6 pro-inflammatory genes compared to CP5-infected or uninfected chickens. Furthermore, CP26 infection also led to significantly increased bursal and HG expression of the anti-inflammatory/regulatory genes, IL-10 or TGFβ, compared to control, CP5 and CP1 groups. Additionally, the splenic pro- and anti-inflammatory transcriptional changes were observed only in the CP26-infected chickens. An antibody-mediated response, as characterized by increased IL-4 and/or IL-13 transcription and elevated IgM levels in birds infected with virulent strains, particularly in the CP26-infected group compared to uninfected controls, was also evident. Collectively, our findings suggest that lymphoid immune responses during NE in chickens are spatially regulated such that the inflammatory responses against depend on the virulence of the strain.
坏死性肠炎（NE）由 引起，是一种对鸡具有重要经济意义的疾病。尽管 NE 的发病机制得到了一定程度的研究，但宿主对 的免疫反应仍知之甚少。本研究使用实验性 NE 模型，研究了感染 4 种 + 菌株（CP1、CP5、CP18 和 CP26）的肉鸡盲肠扁桃体（CT）、法氏囊、哈德腺（HG）和脾脏组织中的淋巴免疫反应，其中 CP18 和 CP26 株还携带 基因。鸡的大体和组织病理学病变表明 CP5 为无毒株，而 CP1、CP18 和 CP26 株为有毒株，其中 CP26 株为“非常毒”株。基因表达分析显示，虽然有毒株在 CT 中诱导了促炎细胞因子 IL-1β 基因的显著上调表达，但 CP26 感染的鸡 CT 中转录的 IFNγ 和 IL-6 促炎基因显著高于 CP5 感染或未感染的鸡。此外，与对照组、CP5 组和 CP1 组相比，CP26 感染还导致法氏囊和 HG 中抗炎/调节基因 IL-10 或 TGFβ 的表达显著增加。此外，仅在 CP26 感染的鸡中观察到脾脏的促炎和抗炎转录变化。抗体介导的反应，表现为感染毒力株的鸡中 IL-4 和/或 IL-13 转录增加和 IgM 水平升高，特别是与未感染对照组相比 CP26 感染组更为明显。综上所述，我们的研究结果表明，鸡坏死性肠炎期间的淋巴免疫反应是空间调节的，针对 的炎症反应取决于菌株的毒力。
