Effects of azithromycin on lung oxidative injury and immune function in mice infected with Mycoplasma pneumoniae based on the Nrf2/ARE signaling pathway.

INTRODUCTION

To explore the mechanism of action of azithromycin on lung oxidative injury and immune function in mice infected with Mycoplasma pneumoniae (MP) based on the nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway.

MATERIAL AND

METHODS

The lung index, dry/wet weight ratio, inflammatory factor levels in alveolar lavage fluid, serum contents of interferon-γ (IFN-γ) and immunoglobulin G (IgG), oxidative stress markers, peripheral blood levels of T-lymphocyte subsets, pathological changes, and Nrf2, HO-1, and NQO1 expression were assessed.

RESULTS

Compared to the control group, the MP group exhibited elevated lung index, reduced lung dry/wet weight ratio, elevated tumor necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 contents, reduced IL-10 levels, raised IFN-γ, IgG and peripheral blood CD8+ levels, reduced CD3+ and CD4+ levels, CD4+/CD8+ ratio, and superoxide dismutase (SOD) and glutathione (GSH) activity, elevated malondialdehyde (MDA) contents, destruction of lung tissue structure, elevated pathological scores, and diminished Nrf2, HO-1, and NQO1 levels. Compared with MP and MP + DMSO groups, MP + azithromycin (AZI) and MP + sulforaphane (SFN) groups displayed a reduced lung index, elevated lung dry/wet weight ratio, reduced TNF-α, IL-1β, and IL-6 contents, raised IL-10 content, decreased IFN-γ, IgG, and peripheral blood CD8+ levels, increased CD3+ and CD4+ levels and CD4+/CD8+ ratio, raised SOD and GSH activity, and diminished MDA content. HE staining demonstrated improved lung tissue structure, diminished pathological scores, and upregulated Nrf2, HO-1, and NQO1 levels after azithromycin and SFN intervention compared to the MP group (all p < 0.05).

CONCLUSIONS

Azithromycin ameliorates MP infection-induced lung injury and oxidative stress and strengthens immune function in mice, which may be achieved by activating the Nrf2/ARE signaling pathway.