Streptococcus pneumoniae exerts oxidative stress, subverts antioxidant signaling and autophagy in human corneal epithelial cells that is alleviated by tert-Butylhydroquinone

AbstractStreptococcus pneumoniae is one of the leading causes of bacterial keratitis in the developing world and globally. In the current study, we have determined oxidative stress as pathogenesis ofS. pneumoniae infection in corneal tissues and human corneal epithelial cells (HCEC) and explored host immune response of HCEC towardsS. pneumoniae. We also determined whether treatment with tert-Butylhydroquinone (tBHQ), a Nrf2 inducer, could alleviate oxidative stress and reduce bacterial cytotoxicity in these cells. Oxidative stress was determined in corneal tissues of patients and HCEC by immunohistochemistry and immunofluorescence analysis, respectively. The expression of antioxidant genes, cytokines and antimicrobial peptides was determined by quantitative PCR. Infection of HCEC byS. pneumoniae was determined by colony-forming units. The autophagy and cell death were determined by fluorescence microscopy. The phosphorylation of signaling proteins was evaluated by immunoblot analysis.S. pneumoniae induced oxidative stress during corneal infections and inhibited antioxidant signaling pathways and immune responses like autophagy. tBHQ aided in restoring Nrf2 activation, reduced reactive oxygen species generation and prevented cytotoxicity and cell death inS. pneumoniae-infected HCEC. tBHQ also induced autophagy in a Nrf2-dependent manner and reduced bacterial survival in HCEC. Increased expression of antimicrobial peptides by tBHQ might have contributed to a reduction of bacter...

Source: Medical Microbiology and Immunology - March 24, 2022 Category: Microbiology Source Type: research