Forsythia suspensa Ethanolic Extract Alleviates Mycoplasma pneumoniae-induced Lung Inflammation via Inhibition of NF-κB Signaling

ABSTRACT

Background/Objectives: Mycoplasma pneumoniae is a significant contributor to respiratory tract infections, notably community-acquired pneumonia (CAP), bronchitis, and exacerbations of chronic lung diseases. Its epidemiology varies across regions and time periods, and while often presenting as a mild illness known as “walking pneumonia,” it can be severe in high-risk populations, with mortality reaching 30% in some cases. The increasing emergence of antibiotic-resistant M. pneumoniae strains presents a significant challenge, highlighting the need for deeper insights into its pathogenicity to develop more effective treatment strategies. Materials and Methods: BALB/c mice were challenged with M. pneumoniae and administered with an ethanolic extract of Forsythia suspensa ethanolic extract (FSEE). Survival rate and pulmonary index inhibitory rate were assessed. Nitric oxide, myeloperoxidase, C-reactive protein, and immunoglobulin M levels were measured. Total cell counts and M. pneumoniae deoxyribonucleic acid (DNA) content were quantified. Anti-inflammatory potential was evaluated through cytokine measurements. Regulatory effects on inflammation-associated signaling pathways were examined by assessing extracellular signal-regulated protein kinases 1/2 (ERK1/2), c-Jun N-terminal protein kinase 1/2 (JNK1/2), and nuclear factor kappa-lightchain-enhancer of activated B cells (NF-κB) expression levels. Results: FSEE treatment significantly improved survival rates and reduced pulmonary index scores. It effectively attenuated excessive immune responses induced by M. pneumoniae infection, leading to a marked reduction in total cell count and M. pneumoniae DNA content. Pro-inflammatory cytokines and NF-κB levels were downregulated, while JNK1/2 expression was notably enhanced following FSEE treatment. Conclusion: These findings indicate that FSEE mitigates M. pneumoniae-induced lung inflammation by modulating immune responses and inflammatory mediators, suggesting its potential as a therapeutic agent for M. pneumoniae-associated pneumonia.

KEYWORDS

• Pneumonia
• Mycoplasma pneumoniae
• inflammation
• phytomedicine
• ERK/JNK/NF-κB pathway

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• DOI10.1177/09731296251346353Copy

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