F0F1 H+-ATPase of Streptococcus pneumoniae is involved in the invasion process of pneumocytes

CIAN M; CORTES P; PIÑAS G; DA SILVA, MA; ECHENIQUE J

Potrero de Funes, San Luis

Congreso; SAIB; 2011

SAIB

F0F1 H+-ATPase of Streptococcus pneumoniae is involved in the invasion process of pneumocytes Streptococcus pneumoniae must overcome adverse conditions to cause human diseases. One of these challenges is the acidic stress in specific 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 ATR because of the tight regulation of intracellular concentration of protons. We have previously characterized different point mutations in the C-subunit (atpC A49T, G47V and V48L) obtained from optochin-resistant pneumococcal strains. We found that these atpC mutants lost the ATR mechanism, but conserved a normal growth rate. These results suggested that atpC mutants could present limitations to survive intracellularly in acidic endosomes, as described for wild-type cells. With the purpose to evaluate the intracellular survival of these mutants, we exposed A549 cells (cell line of type II pneumocytes) to atp mutants, but we could not recovered bacterial live cells at different incubation times. By confocal microscopy, we observed that the atp mutants were not able to invade A549 cells. However, atp cells adhered to pneumocytes via PAF receptor as described, indicating that metabolic changes caused by atp mutants altered the ability to invade A549 cells. These results suggested that the F0F1 H+ ATPase of Streptococcus pneumoniae is involved in the invasion process of pneumocytes.