Abstract
Fowl cholera is a serious, highly contagious disease caused by the bacterium Pasteurella multocida (P. multocida) in a range of avian species and is characterized by an acute form of septicaemia. The pathogenic mechanism of chicken lung injury caused by the bacterium is unclear. Therefore, P. multocida Q (a reference standard strain isolated from chicken) and 1G1 (a clinic isolated strain from duck) were selected to infect chickens, establishing fowl cholera-induced laying hen models. Several important proteins involved in the process of lung injury were identified and quantified using immunohistochemistry and WB. The results showed that chicken lungs infected with bacteria for 24 h showed congestion and edema. The inflammatory factors HMGB1 and IL-6, intercellular matrix MMP, the cell apoptosis-associated caspase-3 and necrotic apoptosis signal molecules RIPK1 and RIPK3 were widely expressed in the lungs of group Q and were significantly different compared with those of 1G1 group and uninfected group (P < 0.05). The results indicated that RIPK1 and RIPK3 are involved in the injury process of chicken lungs after infection with P. multocida, and the mechanisms of lung injury induced by different strains are different.
Highlights
Lung inflammation is the major pathological change observed in fowl cholera
We evaluated the histopathological changes in chickens infected with P. multocida and found that pathological changes in the infected group were mainly associated with inflammation
We found that the proteins studied were all expressed in heterophilic granulocytes
Summary
Lung inflammation is the major pathological change observed in fowl cholera. Heterophils are important in this process, initially causing tissue damage and removing the bacteria to control infection[10]. Apoptosis is a caspase-dependent cell death signalling pathway, and caspase-3 is a key enzyme involved in this process. Necroptosis is a form of regulated necrosis that is executed by receptor-interacting serine/threonine kinase (RIPK) 1 and/or RIPK3 when caspases are inhibited. Lipopolysaccharide (LPS) is a toxin produced by P. multocida that can induce RIPK1 and RIPK3 kinase-dependent inflammation[24], and high mobility group box 1 (HMGB1) is an important pro-inflammatory factor that promotes both early and late inflammation and modulates non-physiological cell death[25,26]. We established a chicken model of P. multocida infection to examine the mechanism by which the host resists infection, focusing on the type of cell death that causes lung tissue lesions in chickens and the inflammatory process in the lungs of chickens with cholera
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