Authors
Long Gao, Nara Davtyan, Ruiyong Zhang
Published in
Iranian journal of immunology : IJI. Volume 23. Issue 2. Pages 6. Jun 28, 2026. Epub Jun 28, 2026.
Abstract
Streptococcus pneumoniae remains a leading cause of community-acquired pneumonia. Severe pulmonary inflammation and subsequent tissue damage are driven significantly by the overexpression of both the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Mitogen-Activated Protein Kinase (MAPK) signaling pathways.
To investigate the immunomodulatory effects of rhein in a mouse model of Streptococcus pneumoniae-induced pneumonia.
Forty male C57BL/6 mice were randomly assigned to four experimental groups: healthy control, S. pneumoniae infected control, and two rhein-treatment groups (10 mg/kg and 30 mg/kg). Expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-10, transforming growth factor (TGF)-β, monocyte chemoattractant protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in lung tissues and bronchoalveolar lavage fluid (BALF) were quantified using reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Additionally, ELISA and Western blotting were employed to assess the phosphorylation profiles of MAPK and NF-κB.
Rhein significantly decreased the lung wet/dry weight ratio, reduced bacterial load, and downregulated COX-2 and iNOS expression. Cytokine analysis revealed marked reductions in pro-inflammatory mediators (IL-6, IL-1β, TNF-α, and MCP-1) alongside elevated levels of the anti-inflammatory cytokine IL-10 in both lung tissues and BALF. Furthermore, ELISA and Western blotting confirmed that rhein significantly inhibited the phosphorylation of MAPK and NF-κB.
Rhein attenuates S. pneumoniae-induced pulmonary inflammation and injury by modulating the MAPK/NF-κB signaling pathways. These findings highlight Rhein as a promising potential therapeutic agent for pneumococcal pneumonia and related inflammatory lung diseases.
PMID:
42365475
Bibliographic data and abstract were imported from PubMed on 28 Jun 2026.
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