The influence on oxidative stress markers, inflammatory factors and intestinal injury-related molecules in Wahui pigeon induced by lipopolysaccharide.

Fei Wang,Xu Yuan,Feng Wen,Xiaofen Hu,Yong Li,Shanshan Yang,Jin Liu,Zuohong Zhou,Shengwei Zhong,Xiaoen Tang,Youbao Zhong,Rosanna Di Paola

doi:10.1371/journal.pone.0251462

Abstract

IntroductionThe intestinal structure is the foundation for various activities and functions in poultry. An important question concerns the changes in the intestinal status under endotoxin stimulation. This study aimed to investigate the mechanism of intestinal injury induced by lipopolysaccharide (LPS) in Wahui pigeons.MethodsThirty-six 28-day-old healthy Wahui pigeons were randomly divided into two groups. The experimental group was injected with LPS (100 μg/kg) once per day for five days, and the control group was treated with the same amount of sterile saline. Blood and the ileum were collected from pigeons on the first, third, and fifth days of the experiment and used for oxidative stress assessment, inflammatory factor detection, histopathological examination, and positive cell localization. In addition, intestinal injury indices and mRNA expression levels (tight junction proteins, inflammatory cytokines, and factors related to autophagy and apoptosis) were evaluated.ResultsVilli in the ileum were shorter in the LPS group than in the control group, and D-lactic acid levels in the serum were significantly increased. Glutathione and catalase levels significantly decreased, but the malondialdehyde content in the serum increased. TNF-α and IL-10 were detected at higher levels in the serum, with stronger positive signals and higher mRNA expression levels, in the LPS group than in the control group. In addition, the levels of TLR4, MyD88, NF-κB, and HMGB1 in the inflammatory signaling pathway were also upregulated. Finally, the mRNA expression of Claudin3, Occludin, and ZO-1 was significantly decreased; however, that of Beclin1 and Atg5 was increased in the LPS group.ConclusionIleal pathological changes and oxidative stress were caused by LPS challenge; it is proposed that this triggering regulates the inflammatory response, causing excessive autophagy and apoptosis, promoting intestinal permeability, and leading to intestinal injury in Wahui pigeons.

Highlights

The intestinal structure is the foundation for various activities and functions in poultry
Ileal pathological changes and oxidative stress were caused by LPS challenge; it is proposed that this triggering regulates the inflammatory response, causing excessive autophagy and apoptosis, promoting intestinal permeability, and leading to intestinal injury in Wahui pigeons
The current study explored the dynamic changes in the intestinal microstructure, degree of oxidative stress, expression of inflammatory factors, and activity of autophagy, apoptosis in Wahui pigeons induced by Salmonella LPS

Summary

Introduction

The intestinal structure is the foundation for various activities and functions in poultry. This study aimed to investigate the mechanism of intestinal injury induced by lipopolysaccharide (LPS) in Wahui pigeons. It is well known that poultry meat is very popular owing to its competitive price, lack of religious and geographical restrictions, and high nutritional value [1]. In pigeons bred for meat, salmonellosis frequently occurs. This disease can lead to fever, dysentery, arthritis, neurological symptoms, or acute septicemia in later stages, with high mortality in squabs. Stimulation with LPS has extensively been employed in many endotoxic models for the understanding of underlying complex molecular mechanisms of endotoxin-mediated acute intestine tissue damage [4,5,6,7]

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