# Tissue-specific transcriptomic adaptation in three strains of chickens during coinfections with parasites

## TL;DR

This study explores how different chicken strains adapt at the gene level in specific tissues when infected with multiple parasites.

## Contribution

The study reveals tissue-specific and strain-dependent transcriptomic responses to coinfections in chickens.

## Key findings

- The caecum showed the most significant immune pathway activation and metabolic inhibition.
- Slower-growing chicken strains showed better tissue repair and worm expulsion responses.
- High-performing strains exhibited stronger inflammatory responses in the liver and caecum.

## Abstract

The widespread adoption of non-caged production systems contributes to the pathogenesis of coinfections with gastrointestinal nematodes and Histomonas meleagridis, triggering local and systemic immune and metabolic responses in chickens. This study investigated transcriptomic adaptation of tissues two weeks after experimental coinfections with Ascaridia galli, Heterakis gallinarum, and H. meleagridis in Lohmann Brown (LB), Lohmann Dual (LD), and Ross-308 (R) male chickens, which differ in growth rates (R > LD > LB).

RNA sequencing of the jejunum, caecum, and liver tissues revealed tissue-specific, strain-dependent transcriptional responses. Coinfection was confirmed during necropsy, and Ascaris-specific antibodies as well as alpha-1-acid glycoprotein were significantly higher in infected birds (p < 0.01). The caecum exhibited the highest unique differentially expressed genes, DEGs (n = 4,094), corresponding to significant activation of complex immune pathways and inhibition of metabolic pathways (p < 0.01). Jejunum DEGs (n = 760) primarily related to muscle contraction, collagen metabolism notably in LB and LD strains. The liver displayed fewer unique DEGs (n = 266) but prominently activated immune responses, especially in R chickens.

In general, slower-performing strains effectively initiated responses favouring worm expulsion and tissue repair in the jejunum, whereas high-performing strains predominantly showed inflammatory responses in the caecum and liver. These findings highlight tissue-specific adaptations underlying strain-dependent tolerance to coinfections with mixed parasites.

The online version contains supplementary material available at 10.1186/s13099-025-00716-1.