Escherichia coli O88 induces intestinal damage and inflammatory response through the oxidative phosphorylation and ribosome pathway in Pekin ducks

Abstract

Colibacillosis is one of the major health threats in the poultry industry worldwide. Understanding the pathogenic mechanisms involved in Escherichia coli-induced inflammatory response may lead to the development of new therapies to combat the disease. To address this, a total of 96 1-day-old male lean Pekin ducklings were employed and randomly allocated to two treatments, each with six replicates of eight ducks. Ducks in the experiment group (EG) and the control group (CG) were separately orally administered with 0.2 ml of pathogenic E. coli O88 (3 × 109 CFU/ml) or equivalent volumes of 0.9% sterile saline solution on day 7, two times with an 8-h interval. Serum and intestinal samples were collected on days 9, 14, and 28. Results showed that ducks challenged with E. coli had lower average daily gain and higher feed intake/weight gain during days 9–14 and overall (P < 0.05). Histopathological examination showed that E. coli decreased the villus height and the ratio of villus height/crypt depth in the jejunum (P < 0.05) on days 9 and 14. The intestinal barrier was disrupted, presenting in E. coli ducks having higher serum DAO and D-LA on days 9 and 14 (P < 0.05) and greater content of serum LPS on day 9 (P < 0.05). Escherichia coli infection also triggered a systemic inflammatory response including the decrease of the serum IgA, IgM, and jejunal sIgA on day 14 (P < 0.05). In addition to these, 1,062 differentially expressed genes were detected in the jejunum tissues of ducks by RNA-seq, consisting of 491 upregulated and 571 downregulated genes. Based on the KEGG database, oxidative phosphorylation and the ribosome pathway were the most enriched. These findings reveal the candidate pathways and genes that may be involved in E. coli infection, allow a better understanding of the molecular mechanisms of inflammation progression and may facilitate the genetic improvement of ducks, and provide further insights to tackle the drug sensitivity and animal welfare issues.

A comparative study on histopathological features of duodenum, jejunum, and ileum from broiler chicken with avian pathogenic Escherichia coli infection

“…The heterophils are the fastest to E. coli within 6 hours postinfection response, contributing to the clearance mechanism by degranulation and antibacterial compounds (Mol et al, 2019). Besides, the macrophage is a key component to contribute to tissue self-repair inflammation (Li et al, 2022). Thus, when there is either a localized or systemic infection, the organ will be changed functionally, resulting in poor performance of the chicken.…”

Bacillus subtilis Protects the Ducks from Oxidative Stress Induced by Escherichia coli: Efficacy and Molecular Mechanism

“…It has been demonstrated that E. coli infection can damage the intestinal barrier and trigger mucosal inflammatory responses subsequently in ducks, which is an energy-consuming process [ 58 ]. In the previous study, ducks infected with E. coli impaired the growth performance of ducks through an interfering energy metabolism pathway, down-regulating gene expression related to the ribosome and oxidative phosphorylation [ 59 ]. In the present study, B. subtilis reduced intestinal oxidative stress through interfering with ribosome and energy metabolism by up-regulating the expression of genes that encode mitochondrial ribosome proteins, ribosome biogenesis and translation factors.…”