Histopathological changes and inflammatory and cell death pathways in the lungs of Balb/c mice with pneumonia induced by different concentrations of Staphylococcus aureus.

Abstract

Pneumonia is often triggered by a bacterial infection, in many cases Staphylococcus aureus. Although this bacterium is found in the microbiota of healthy individuals, it can proliferate and release toxins in the respiratory tract, causing tissue damage by activating the inflammatory process and cell death pathways and resulting in serious complications. In this study, pneumonia was induced in Balb/c mice using different concentrations of S. aureus to evaluate histopathological changes and progression with increasing concentrations of colony forming units (CFUs) as well as their interactions with inflammatory and cell death markers. Hematoxylin and eosin histological techniques and peroxidase immunohistochemistry were utilized to investigate outcomes that included edema and disruption of the bronchiole and blood vessel walls. Alveolar collapse and bronchiolar hyperplasia were also analyzed and were statistically significant, but only hyperplasia varied between the two groups that received intermediate concentrations of CFU (10⁷ and 10⁸, respectively) to induce pneumonia. In the immunohistochemical analysis, progression of apoptosis was observed in groups that received up to 10⁸ CFU, along with a probable predominance of autophagy and reduction in IL-6 in the group that received the highest concentration (10⁹ CFU). These characteristics appear to indicate an attempt to preserve and reuse cells when high CFU concentrations are present and eliminate infected cells at lower concentrations. The data from this present study contribute to understanding crosstalk between cell death pathways and the inflammatory response in S. aureus-induced pneumonia, and may assist in future intervention strategies.