Coccidiosis progression and its effect on skeletal muscle yield and jejunal mucosa proteome profiles of broiler chickens

Abstract

Coccidiosis is a prevalent and economically significant enteric disease in poultry, caused by protozoan parasites of the genus Eimeria. The parasite employs a diverse array of proteins to facilitate host invasion, with proteomic variation across species and even strains complicating effective control. Infected birds often exhibit reduced growth performance, increased susceptibility to opportunistic pathogens, and mortality. Despite the availability of nutritional, pharmaceutical, and management strategies, coccidiosis remains one of the most relevant enteric diseases in broiler production. While transcriptomic and microbiome studies have advanced our understanding of host responses during infection, tissue-specific proteomic investigations are limited. Moreover, the systemic effects of coccidiosis, particularly on tissues such as skeletal muscle, remain largely unexplored. This study combined performance parameters, muscle yield data, and temporal proteomic analyses to characterize the progression and systemic impact of coccidiosis infection. In a randomized complete block design experiment, 432 broilers were orally challenged with 30,000 sporulated E. maxima (EM) oocysts or given saline only, and samples were collected at 1-, 2-, 4-, 6-, 8-, and 10-d post-inoculation (dpi). Performance parameters, muscle yields, and Wooden Breast (WB) scores were recorded, while jejunal mucosa was analyzed using label-free LC-MS/MS proteomics and fluorescent Western Blot. Broilers in the EM group maintained performance until 4 dpi; however, from 6 to 10 dpi, they exhibited lower body weight (BW), reduced BW gain and feed efficiency, and higher mortality compared to controls. In EM broilers, Bicep femoris muscle yield relative to live BW tended to be lower at 2, 8, and 10 dpi, while Pectoralis major muscle yield was lower at 10 dpi. Jejunal proteomic analysis revealed 12 differentially abundant proteins (DAP) at 1 dpi, peaking at 256 DAP by 6 dpi, and declining to 58 by 10 dpi. Notably, MHC class I was downregulated in EM broilers early, while proteins involved in fatty acid metabolism and oxidative stress were suppressed from 4 to 8 dpi. In EM broilers, STAT1, IFI6, annexin 2, and heat shock proteins were upregulated at 6 dpi, aligning with elevated IL-10 relative protein abundance detected by Western Blot at 4 and 6 dpi. Greater IL-17 protein abundance was observed in EM broilers at 4 dpi, whereas annexins 4 and 13 were downregulated. Functional enrichment analysis showed early activation of biosynthetic and metabolic pathways, followed by shifts toward lipid metabolism, nitrogen utilization, and steroid biosynthesis by 10 dpi. Immune-related pathways, including PPAR signaling and neutrophil degranulation were also temporally enriched. These findings demonstrate that EM infection induces a dynamic and coordinated host response involving immune activation, metabolic reprogramming, and tissue remodeling. The integration of performance outcomes and mucosal proteomic changes highlights how coccidiosis extends beyond localized intestinal damage to affect systemic physiology and muscle accretion throughout the disease cycle.