背景:艾美球虫属属于尖顶丛寄生虫门,是球虫病的原因,对家禽生产具有重大经济影响的肠道疾病。柔嫩艾美耳球虫是鸡中毒性最强的物种之一。在之前的研究中,我们发现盲肠微生物群对这种感染的病理生理学有负面影响.然而,微生物群导致病理生理学的机制仍未确定。巨噬细胞在炎症过程中起关键作用,并且它们在E.tenella感染期间与微生物群的相互作用从未被研究过。因此,我们检查了在E.tenella感染期间微生物群对巨噬细胞的影响。通过用KUL01抗体免疫荧光染色在未感染和感染的无菌鸡和常规鸡的盲肠组织中监测巨噬细胞。分离盲肠细胞,染色,使用高通量qPCR进行分析和分选以检查其基因表达。
结果:我们证明了微生物群是E.tenella感染中盲肠巨噬细胞募集所必需的。此外,微生物群促进了巨噬细胞的促炎转录组学谱,其特征是NOS2,ACOD1,PTGS2,TNFα的基因表达增加,IL1β,感染鸡的IL6、IL8L1、IL8L2和CCL20。从常规鸡对无菌感染鸡的盲肠微生物群的施用部分恢复了巨噬细胞募集和反应。
结论:综合来看,这些结果表明,微生物群通过巨噬细胞募集和激活增强了这种感染的病理生理学.因此,涉及肠道菌群调节的策略可能导致巨噬细胞介导的炎症反应的减弱,从而限制了该疾病的负面临床结果。
BACKGROUND: Eimeria genus belongs to the apicomplexan parasite phylum and is responsible for coccidiosis, an intestinal disease with a major economic impact on poultry production. Eimeria tenella is one of the most virulent species in chickens. In a previous study, we showed a negative impact of caecal microbiota on the physiopathology of this infection. However, the mechanism by which microbiota leads to the physiopathology remained undetermined. Macrophages play a key role in inflammatory processes and their interaction with the microbiota during E. tenella infection have never been investigated. We therefore examined the impact of microbiota on macrophages during E. tenella infection. Macrophages were monitored in caecal tissues by immunofluorescence staining with KUL01 antibody in non-infected and infected germ-free and conventional chickens. Caecal cells were isolated, stained, analyzed and sorted to examine their gene expression using high-throughput qPCR.
RESULTS: We demonstrated that microbiota was essential for caecal macrophage recruitment in E. tenella infection. Furthermore, microbiota promoted a pro-inflammatory transcriptomic profile of macrophages characterized by increased gene expression of NOS2, ACOD1, PTGS2, TNFα, IL1β, IL6, IL8L1, IL8L2 and CCL20 in infected chickens. Administration of caecal microbiota from conventional chickens to germ-free infected chickens partially restored macrophage recruitment and response.
CONCLUSIONS: Taken together, these results suggest that the microbiota enhances the physiopathology of this infection through macrophage recruitment and activation. Consequently, strategies involving modulation of the gut microbiota may lead to attenuation of the macrophage-mediated inflammatory response, thereby limiting the negative clinical outcome of the disease.