STREPTOCOCCUS PNEUMONIAE ADHESION TO A549 EPITHELIAL CELL UNDER NOREPINEPHRINE REGULATION OF SPXB
Marisa Gonzales, Cody Blackstone, Xavier Gonzales.
Texas A&M University-Corpus Christi, Corpus Christi, TX.
Streptococcus pneumoniae, also known as the pneumococcus, is the primary cause of bacterial pneumonia in children. Pneumococcus can exist asymptomatically in the nasopharyngeal cavity, however, in some individuals it can invade the lungs and the blood. Systemic release of norepinephrine (NE) is a component of the acute host response to infection and studies in the field of microbial endocrinology generally indicate that NE increases bacterial growth rate and promotes invasive disease. However, NE attenuates experimental invasive pneumococcal disease by decreasing its capabilities to adhere to epithelial cells. The NE regulation of pneumococcal adherence to lung epithelial cells is associated with the bacterial iron uptake mechanisms. We propose that NE inhibits pneumococcal adhesion through regulation of the iron associated surface protein that participates in adhesion, SpxB (pyruvate oxidase). In this study, we utilize proteomic analysis through 2D and 1D gel electrophoresis along with antibodies raised toward SpxB protein. Further, in vitro adhesion assays with A549 lung epithelial cells and spxB mutant pneumococcus with and without NE treatment are performed. Currently, 2D gel assessment suggest that NE decreases pneumococcal production of the SpxB protein. Further, assessment of adhesion assays will provide evidence for acceptance or rejection of the proposed hypothesis. We conclude that pneumococcal SpxB is regulated by NE.