Details

Autor(en) / Beteiligte

• Peng, Lu-Yuan
• Shi, Hai-Tao
• Gong, Zi-Xuan
• Yi, Peng-Fei
• Tang, Bo
• Shen, Hai-Qing
• Fu, Ben-Dong

Titel

Protective effects of gut microbiota and gut microbiota-derived acetate on chicken colibacillosis induced by avian pathogenic Escherichia coli

Ist Teil von

• Veterinary microbiology, 2021-10, Vol.261, p.109187-109187, Article 109187

Ort / Verlag

Amsterdam: Elsevier B.V

Erscheinungsjahr

2021

Quelle

Elsevier ScienceDirect Journals

Beschreibungen/Notizen

• •Chicken colibacillosis, caused by avian pathogenic Escherichia coli (APEC), leads to huge economic losses to the poultry industry.•Gut microbiota depletion exacerbated the lung inflammation and the damage to air-blood barrier induced by APEC.•Feeding acetate derived from gut microbiota inhibited the APEC-induced lung injury and the damages to air-blood barrier.•Novel therapeutic targets that focus on the gut microbiota and its metabolites may be effective in the control of colibacillosis. Chicken colibacillosis is caused by avian pathogenic Escherichia coli (APEC), and results in huge economic losses to the poultry industry. With the investigation of the gut-lung axis, more studies have demonstrated the important role of gut microbiota in lung inflammation. The precise role of the gut microbiota in chickens-associated colibacillosis, however, is unknown. Thus, this study assessed the function of the gut microbiota in the chicken defense against APEC infection. Chicken gut microbiota was depleted by drinking water with a mixture of antibiotics (Abx), and subsequently, a model of colibacillosis was established by the intranasal perfusion of APEC. The results showed that gut microbiota protects the chicken challenge by APEC from aggravated lung histopathologic injury, up-regulated pro-inflammatory cytokine production, and increased bacterial load in lung tissues compared with controls. In addition, the air-blood barrier permeability was significantly increased in gut microbiota-depleted chickens compared to the control chickens after challenge with APEC. Furthermore, feeding acetate significantly inhibited the lung inflammatory response and the reduced air-blood permeability induced by APEC infection. The expression of free fatty acid receptor 2 (FFAR2), a receptor for acetate, was also increased in the lung after treatment with acetate. In conclusion, depletion of the gut microbiota resulted in increased susceptibility of chickens to APEC challenge, and gut microbiota derived acetate acted as a protective mediator during the APEC challenge. Novel therapeutic targets that focus on the gut microbiota may be effective in controlling colibacillosis in poultry.