F0F1 H+ Atpase is involved in the invasion process of Streptococcus pneumoniae into pneumocytes

CIAN M*, CORTES PR*, PIÑAS GE, DA SILVA MA, ECHENIQUE J

POTRERO DE LOS FUNES

Encuentro; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2011

SAIB

S. pneumoniae must overcome adverse conditions to cause human diseases, such as acidic stress in inflammatory niches, for which it has developed survival mechanisms such as Acid Tolerance Response (ATR). It was described that F0F1 H+ ATPase is a major contributor of bacterial ATR because of the tight regulation of intracellular concentration of protons. We have previously identified and characterized different point mutations in the atpC gene that encodes the C-subunit of the F0F1 H+-ATPase. Here, we found that these atpCmutants lost the ATR mechanism, suggesting a restriction to survive intracellularly in acidic endosomes. To assess intracellular survival, we exposed A549 cells (cell line of type II pneumocytes) to atpCmutants, and we could not recover bacterial live cells inside the pneumocytes at different incubation times. By confocal microscopy, we observed that the atpCmutants failed to invade A549 cells, in contrast to the wildtype strain. By co-localization experiments, we found that atpCcells adhered to pneumocytes via PAF receptor as described, indicating that metabolic changes caused by atp mutations altered the pneumococcal ability to invade A549 cells, but not their + adherence capacity. These results suggested that the F0F1 H - ATPase is involved in the invasion process of S. pneumoniae into pneumocytes.