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Peer-reviewedCC BY 4.0Veterinary Research

Cooperation between Adh and OR5M11 contributes to the lung pathogenicity of Actinobacillus pleuropneumoniae by facilitating the NLRP3-mediated inflammatory response

7 more authors

Abstract

Actinobacillus pleuropneumoniae (A. pleuropneumoniae) is the etiologic agent of porcine pleuropneumonia, a severe respiratory disease characterized by hemorrhagic, necrotizing lung lesions that cause significant economic losses on the global swine industry. However, the molecular mechanisms underlying the lung pathogenicity of A. pleuropneumoniae remain unclear. Here we demonstrate that A. pleuropneumoniae infection induces lung injury through activating the NLRP3-mediated inflammatory response mediated by the YadA-like head region (Adh) of Apa1, a bacterial adhesin that mediates attachment to host cells. Importantly, we show that Adh triggers the NLRP3-mediated inflammatory response by engaging olfactory receptor family 5 subfamily M member 11 (OR5M11), a host receptor previously shown to interact with Adh. Furthermore, OR5M11 contributes to the Adh-activated inflammatory response by promoting mitochondrial DNA release. Taken together, our results provide new insights into the pathogenesis of A. pleuropneumoniae, particularly regarding NLRP3-mediated inflammatory pathology.

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BibTeX
@article{wen2026cooperation,
  title = {{Cooperation between Adh and OR5M11 contributes to the lung pathogenicity of Actinobacillus pleuropneumoniae by facilitating the NLRP3-mediated inflammatory response}},
  author = {Bo Wen and Xiaoli Yin and Xinhe Zhang and Chunling Zhu and Xiaofeng Li and Yilin Bai and Huarun Sun and Zhiyi Liu and Shuwen Ji and Ruibiao Wang and Chenru Yu and Jiaqi Wang and Longfei Zhang and Jiyuan Shen and Jianhe Hu and Yueyu Bai and Huihui Zhang and Ke Ding and Lei Wang},
  journal = {Veterinary Research},
  year = {2026},
  month = oct,
  doi = {10.1186/s13567-026-01845-4},
  url = {https://hal.science/hal-05777451v1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Cooperation between Adh and OR5M11 contributes to the lung pathogenicity of Actinobacillus pleuropneumoniae by facilitating the NLRP3-mediated inflammatory response
AU  - Bo Wen
AU  - Xiaoli Yin
AU  - Xinhe Zhang
AU  - Chunling Zhu
AU  - Xiaofeng Li
AU  - Yilin Bai
AU  - Huarun Sun
AU  - Zhiyi Liu
AU  - Shuwen Ji
AU  - Ruibiao Wang
AU  - Chenru Yu
AU  - Jiaqi Wang
AU  - Longfei Zhang
AU  - Jiyuan Shen
AU  - Jianhe Hu
AU  - Yueyu Bai
AU  - Huihui Zhang
AU  - Ke Ding
AU  - Lei Wang
PY  - 2026
DA  - 2026/10/05
JO  - Veterinary Research
DO  - 10.1186/s13567-026-01845-4
UR  - https://hal.science/hal-05777451v1
AB  - Actinobacillus pleuropneumoniae (A. pleuropneumoniae) is the etiologic agent of porcine pleuropneumonia, a severe respiratory disease characterized by hemorrhagic, necrotizing lung lesions that cause significant economic losses on the global swine industry. However, the molecular mechanisms underlying the lung pathogenicity of A. pleuropneumoniae remain unclear. Here we demonstrate that A. pleuropneumoniae infection induces lung injury through activating the NLRP3-mediated inflammatory response mediated by the YadA-like head region (Adh) of Apa1, a bacterial adhesin that mediates attachment to host cells. Importantly, we show that Adh triggers the NLRP3-mediated inflammatory response by engaging olfactory receptor family 5 subfamily M member 11 (OR5M11), a host receptor previously shown to interact with Adh. Furthermore, OR5M11 contributes to the Adh-activated inflammatory response by promoting mitochondrial DNA release. Taken together, our results provide new insights into the pathogenesis of A. pleuropneumoniae, particularly regarding NLRP3-mediated inflammatory pathology.
SN  - 0928-4249
SN  - 1297-9716
ER  -