What question did this study set out to answer?

To examine how WWC1 deficiency affects lung injury in sepsis and its underlying mechanisms involving inflammation and cell death.

April 19, 2026Journal of InflammationOpen Access

WWC1 deficiency exacerbates sepsis-induced lung injury by promoting NETosis, M1 and M2b macrophage recruitment, and pyroptosis via YAP1 and STING pathways

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Investigations reveal WWC1 deficiency worsens lung injury during sepsis by activating inflammatory responses.

To examine how WWC1 deficiency affects lung injury in sepsis and its underlying mechanisms involving inflammation and cell death.
Used wild-type and WWC1 knockout/knock-in mice for sepsis modeling via cecal ligation and puncture.
Analyzed lung tissues for NETosis and pyroptosis markers using immunofluorescence and western blot.
Utilized flow cytometry to measure neutrophil and macrophage proportions in bronchoalveolar lavage fluid.
Applied histological staining to assess lung inflammatory responses.
Tested effects of YAP1 and STING antagonists and agonists on inflammatory responses.
WWC1 knockout mice exhibited heightened NETosis and increased recruitment of M1 and M2b macrophages in the lungs.
Enhanced pyroptosis activation was observed in WWC1 knockout mice.
Administration of specific antagonists reduced pyroptosis and NETosis, alleviating inflammatory lung damage.
WWC1 knock-in mice were more resistant to inflammation, effects diminished by artificial activation of YAP1 or STING.

Chen et al. (2026) studied this question.

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April 19, 2026Journal of InflammationOpen Access

View Full Paper

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Authors

Investigations reveal WWC1 deficiency worsens lung injury during sepsis by activating inflammatory responses.

To examine how WWC1 deficiency affects lung injury in sepsis and its underlying mechanisms involving inflammation and cell death.
Used wild-type and WWC1 knockout/knock-in mice for sepsis modeling via cecal ligation and puncture.
Analyzed lung tissues for NETosis and pyroptosis markers using immunofluorescence and western blot.
Utilized flow cytometry to measure neutrophil and macrophage proportions in bronchoalveolar lavage fluid.
Applied histological staining to assess lung inflammatory responses.
Tested effects of YAP1 and STING antagonists and agonists on inflammatory responses.
WWC1 knockout mice exhibited heightened NETosis and increased recruitment of M1 and M2b macrophages in the lungs.
Enhanced pyroptosis activation was observed in WWC1 knockout mice.
Administration of specific antagonists reduced pyroptosis and NETosis, alleviating inflammatory lung damage.
WWC1 knock-in mice were more resistant to inflammation, effects diminished by artificial activation of YAP1 or STING.

Chen et al. (2026) studied this question.

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