2. Academic Validation
  3. Actinobacillus pleuropneumoniae infection activates IL-1β expression in porcine alveolar macrophages via β-amyloid production

Actinobacillus pleuropneumoniae infection activates IL-1β expression in porcine alveolar macrophages via β-amyloid production

  • Microb Pathog. 2025 Jul:204:107559. doi: 10.1016/j.micpath.2025.107559.
Kang Yan 1,  Qiyun He 1,  Jia Tang 1,  Wei Peng 1,  Beibei Dou 2,  Huanchun Chen 3,  Weicheng Bei 4
Affiliations

Affiliations

  • 1 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China; The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, Hubei, China.
  • 2 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
  • 3 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China; The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, Hubei, China; Hubei Hongshan Laboratory, Wuhan, China.
  • 4 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China; The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, Hubei, China; Hubei Hongshan Laboratory, Wuhan, China. Electronic address: beiweic@163.com.
PMID: 40220800 DOI: 10.1016/j.micpath.2025.107559
Abstract

Actinobacillus pleuropneumoniae (A. pleuropneumoniae), a porcine respiratory tract pathogen, causes porcine pleuropneumonia. Porcine alveolar macrophages (PAMs) play a crucial role during A. pleuropneumoniae Infection. Amyloid precursor protein (APP) can be cleaved by β- and γ-secretase to produce β-amyloid (Aβ). APP and Aβ are associated with the inflammatory response. They activate microglia and astrocytes to secrete IL-1β, IL-6, and Other cytokines. In this study, we found that during the interaction between A. pleuropneumoniae and PAMs, the two-component system CpxAR upregulates wecA expression, increasing lipopolysaccharide (LPS) production. LPS promotes APP production and cleavage to generate Aβ. The Aβ activates NF-κB, leading to increased IL-1β expression. We hypothesize that A. pleuropneumoniae Infection of PAMs regulates APP production and cleavage to control Aβ levels. Different quantities of Aβ induce PAMs to produce varying amounts of cytokines, leading to different pathological processes in porcine pleuropneumonia.

Keywords

Actinobacillus pleuropneumoniae; Amyloid precursor protein; CpxAR; IL-1β; Lipopolysaccharide; Porcine alveolar macrophage; β-Amyloid.

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