Open AccessImportance of superoxide dismutases A and M for protection of Staphylococcus aureus in the oxidative stressful environment of cystic fibrosis airways
Author(s) -
Treffon Janina,
ChavesMoreno Diego,
Niemann Silke,
Pieper Dietmar Helmut,
Vogl Thomas,
Roth Johannes,
Kahl Barbara C.
Publication year - 2020
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.13158
Subject(s) - staphylococcus aureus , microbiology and biotechnology , biology , superoxide dismutase , cystic fibrosis , virulence , oxidative stress , sputum , staphylococcal infections , bacteria , immunology , gene , medicine , biochemistry , pathology , genetics , tuberculosis
Staphylococcus aureus is one of the earliest pathogens that persists the airways of cystic fibrosis (CF) patients and contributes to increased inflammation and decreased lung function. In contrast to other staphylococci, S. aureus possesses two superoxide dismutases (SODs), SodA and SodM, with SodM being unique to S. aureus . Both SODs arm S. aureus for its fight against oxidative stress, a by‐product of inflammatory reactions. Despite complex investigations, it is still unclear if both enzymes are crucial for the special pathogenicity of S. aureus . To investigate the role of both SODs during staphylococcal persistence in CF airways, we analysed survival and gene expression of S. aureus CF isolates and laboratory strains in different CF‐related in vitro and ex vivo settings. Bacteria located in inflammatory and oxidised CF sputum transcribed high levels of sodA and sodM . Especially expression values of sodM were remarkably higher in CF sputum than in bacterial in vitro cultures. Interestingly, also S. aureus located in airway epithelial cells expressed elevated transcript numbers of both SODs, indicating that S. aureus is exposed to oxidative stress at various sites within CF airways. Both enzymes promoted survival of S. aureus during polymorphonuclear leukocyte killing and seem to act compensatory, thereby giving evidence that the interwoven interaction of SodA and SodM contributes to S. aureus virulence and facilitates S. aureus persistence within CF airways.