# Integrated Transcriptome Analysis Reveals the Lung miRNA–mRNA Regulatory Network Associated with Avian Pathogenic E. coli Infection

**Authors:** Huan Li, Jishuang Tan, Xiaoyi Li, Susan J. Lamont, Hongyan Sun

PMC · DOI: 10.3390/vetsci12020095 · 2025-01-26

## TL;DR

This study identifies miRNA–mRNA regulatory interactions in chicken lungs infected with avian pathogenic E. coli, offering insights into immune responses.

## Contribution

The study reveals novel miRNA–mRNA regulatory pairs in chicken lungs during APEC infection, including gga-miR-214 targeting RAB37.

## Key findings

- APEC infection caused lung lesions and increased inflammatory cytokine expression in chickens.
- 22 differentially expressed miRNAs and 608 differentially expressed mRNAs were identified in infected chickens.
- 23 miRNA–mRNA regulatory pairs were discovered, with gga-miR-214 targeting RAB37 to modulate inflammation.

## Abstract

The economic impact of colibacillosis, a disease caused by avian pathogenic E. coli (APEC), is significant for the global poultry industry. The investigation of APEC–host interactions is important for understanding the host in response to APEC infection and developing effective antibacterial strategies. The aim of this study was to determine the transcriptome (mRNAs and miRNAs) regulation in chicken lungs in response to APEC infection. We found 22 and 608 differentially expressed miRNAs and mRNAs, respectively, between APEC-infected and non-infected chickens, in addition to 23 potential miRNA–mRNA interactions. These data will prove invaluable in elucidating the role of miRNA–mRNA interactions in the defense of chicken lungs against APEC.

Avian pathogenic E. coli (APEC), one of the most common pathogens, can cause localized or systemic infections and lead to significant economic losses in the poultry industry annually. Recently, evidence suggests that microRNAs (miRNAs) play important roles in the host immune response to bacterial infection by targeting mRNAs. However, few studies have examined the immune mechanisms of miRNAs and mRNAs in chicken lungs following APEC infection. Herein, hematoxylin–eosin staining and qRT-PCR were employed to investigate APEC-induced lung inflammation in chickens. RNAseq was used to identify the miRNAs and mRNAs expression profile between the APEC infection group (APEC) vs. the Control group (Control). The results show that APEC can induce lung lesions in chickens and increase the expression levels of inflammatory cytokines (IL1β, IL8, IL6, and TNFα). High-quality sequencing data were obtained, of which more than 93% of the reads can be mapped to the chicken genome. A total of 22 differentially expressed (DE) miRNAs and 608 DE mRNAs were detected in the APEC vs. the Control. Remarkably, 23 regulatory pairs of miRNA–mRNA interactions were identified in chicken lungs upon APEC infection. Further validation revealed that gga-miR-214 could directly target the RAB37 gene upon APEC infection to modulate the expression of inflammatory cytokine response. This study provides new insights into the host immune response to APEC infection.

## Linked entities

- **Genes:** RAB37 (RAB37, member RAS oncogene family) [NCBI Gene 326624]
- **Diseases:** colibacillosis (MONDO:0020920)
- **Species:** Gallus gallus (taxon 9031)

## Full-text entities

- **Genes:** LITAF (lipopolysaccharide induced TNF factor) [NCBI Gene 374125] {aka TNF-alpha}, IL8L2 (interleukin 8 like 2) [NCBI Gene 396495] {aka CEF4, CXCL8, CXCLi2, EMF-1, EMF1, IL8}, IL1B (interleukin 1, beta) [NCBI Gene 395196] {aka IL-1BETA, IL1beta}, IL6 (interleukin 6) [NCBI Gene 395337] {aka CHIL-6, IL-6, interleukin-6}, MIR214 (microRNA 214) [NCBI Gene 100315861] {aka gga-mir-214}
- **Diseases:** infections (MESH:D007239), lung lesions (MESH:D008171), APEC infection (MESH:D004927), inflammatory (MESH:D007249), bacterial infection (MESH:D001424), lung inflammation (MESH:D011014)
- **Species:** Escherichia coli (E. coli, species) [taxon 562], Gallus gallus (bantam, species) [taxon 9031]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11860573/full.md

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Source: https://tomesphere.com/paper/PMC11860573