# Genome-wide transcriptional profiling and functional analysis of long noncoding RNAs and mRNAs in chicken macrophages associated with the infection of avian pathogenic E. coli

## TL;DR

This study explores how chicken macrophages respond to E. coli infection by analyzing gene activity, revealing new roles for noncoding RNAs in immune response.

## Contribution

The study identifies a novel lncRNA, TCONS_00007391, that regulates inflammation during APEC infection by targeting CD86.

## Key findings

- 816 differentially expressed lncRNAs and 1,798 mRNAs were identified in APEC-infected chicken macrophages.
- The lncRNA TCONS_00007391 was found to regulate inflammatory responses by targeting CD86.
- DE lncRNAs and mRNAs were linked to immune-related pathways like Toll-like receptor and VEGF signaling.

## Abstract

Avian pathogenic E. coli (APEC) can cause localized or systemic infections, collectively known as avian colibacillosis, resulting in huge economic losses to poultry industry globally per year. In addition, increasing evidence indicates that long non-coding RNAs (lncRNAs) play a critical role in regulating host inflammation in response to bacterial infection. However, the role of lncRNAs in the host response to APEC infection remains unclear.

Here, we found 816 differentially expressed (DE) lncRNAs and 1,798 DE mRNAs in APEC infected chicken macrophages by RNAseq. The identified DE lncRNA-mRNAs were involved in Toll like receptor signaling pathway, VEGF signaling pathway, fatty acid metabolism, phosphatidylinositol signaling system, and other types of O-glycan biosynthesis. Furthermore, we found the novel lncRNA TCONS_00007391 as an important immune regulator in APEC infection was able to regulate the inflammatory response by directly targeting CD86.

These findings provided a better understanding of host response to APEC infection and also offered the potential drug targets for therapy development against APEC infection.

The online version contains supplementary material available at 10.1186/s12917-024-03890-7.