Attenuated efficacy of Streptococcus salivarius K12 against Mycoplasma pneumoniae infection in mice.

The respiratory microbiota plays a crucial role in modulating pulmonary immune responses; however, the mechanisms by which commensal microbiota influence Mycoplasma pneumoniae pneumonia (MPP) pathogenesis remain incompletely understood. This study investigated the impact of Streptococcus salivarius K12 (K12) on pulmonary responses in mice infected with Mycoplasma pneumoniae (Mp). Twenty-four male BALB/c mice were randomly divided into three groups: a normal control group (Control), an Mp + PBS group, and an Mp+K12 group, with eight mice per group. After establishing the Mp infection model, mice were orally administered either K12 probiotic suspension or PBS for 14 consecutive days. Bronchoalveolar lavage fluid (BALF) was collected to assess Mp load and inflammatory cell counts. Inflammatory and pathological changes in serum, BALF, and lung tissue were evaluated. The lower respiratory tract (LRT) microbiota was characterized by 16S rRNA sequencing of BALF samples. No significant intergroup differences were observed in P1 protein or CARDS toxin mRNA levels. Hematoxylin and eosin staining of lung tissue demonstrated no discernible histopathological differences among groups. However, the Mp+K12 group showed a significant reduction in total white blood cell counts in BALF compared to the Mp + PBS group. Serum levels of TNF-α and IL-6 were notably lower in the Mp+K12 group than in the Mp + PBS group. TNF-α mRNA expression in lung tissue was also markedly reduced in the Mp+K12 group. Both the Mp + PBS and Mp+K12 groups exhibited reduced expression of the airway remodeling factor Col3A1 mRNA relative to the Control group, though Col3A1 mRNA expression was higher in the Mp+K12 group than in the Mp + PBS group. Shannon index analysis indicated no significant differences in species richness among the groups, with the Mp+K12 group displaying a microbial community structure most similar to the Control group. The probiotic K12 attenuated the effects of Mp infection in mice, primarily by mitigating inflammatory responses and shifting the lung microbiota toward a more balanced composition. These findings provide valuable insights into potential mechanisms and therapeutic strategies for Mp infections.