Polydatin alleviates mycoplasma pneumoniae-induced injury via inhibition of Caspase-1/GSDMD-dependent pyroptosis

  • Int J Med Microbiol. 2023 Sep 26;313(5):151586. doi: 10.1016/j.ijmm.2023.151586.
Yiliu Chen  1 ,  Yonghong Jiang  2 ,  Xiuxiu Liu  3 ,  Xiufeng Chen  4 ,  Qiuyue Fan  5 ,  Zhen Xiao  6
Affiliations
  • 1. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
  • 2. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
  • 3. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
  • 4. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
  • 5. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
  • 6. Department of Pediatric, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: [email protected].
PMID: 37776814 DOI: 10.1016/j.ijmm.2023.151586
Abstract

Mycoplasma pneumoniae (MP) is one of the main pathogens causing community acquired pneumonia (CAP) in children and adults. Previous pharmacological and clinical studies have shown that Polydatin (PD) exerts anti-inflammatory action by conferring protective benefit in MP pneumonia. However, the mechanism underlying the of PD on MP Infection remains unclear. It was found that PD alleviated MP-induced injury by inhibiting Caspase-1/gasdermin D (GSDMD)-mediated epithelial Pyroptosis. The results demonstrated that PD inhibited the transformation of GSDMD to N-terminal gasdermin-N (GSDMD-N) by decreasing Caspase-1 activation, as well as suppressed the formation and secretion of interleukin-1β (IL-1β) and interleukin-18 (IL-18), reversed Na, K-ATPase reduction, and suppressed LDH release both in vitro and vivo. Taken together, epithelial Pyroptosis in BEAS-2B cells and lung injury in mice were prevented by PD. In conclusion, PD suppressed pulmonary injury triggered by MP Infection, by inhibiting the Caspase-1/GSDMD-mediated epithelial Pyroptosis signaling pathway. Thus, PD may be regarded as a potential therapy for MP-induced inflammation.

Keywords
Epithelial pyroptosis; GSDMD; MP; Pneumonia; Polydatin.
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