Roles of virulence genes (PsaA and CpsA) on the invasion of Streptococcus pneumoniae into blood system

Abstract

BackgroundStreptococcus pneumoniae (SP) is the major cause of childhood mortality worldwide, we need to understand virulence genes of SP so can better target the treatment.We investigated the expression of virulence genes PsaA and CpsA in different strains of SP interacting with monocyte cell line (THP-1) or pneumocyte cell line (A549) and the possible mechanism of SP invasion of the blood system.MethodsA total of 23 strains of SP were collected from hospitalized patients (blood-derived and sputum-derived) in the Second Affiliated Hospital of Wenzhou Medical College. The strains and ATCC 49619 were cultured, and RNAs were extracted. THP-1 and A549 cells were stimulated by different SP and ATCC 49619 for 4 h and 8 h, respectively. Quantitative real-time PCR was used to analyze the mRNA expression of PsaA and CpsA. The data were analyzed by SPSS 17.0.ResultsThe mRNA level of PsaA and CpsA were all significantly increased in clinical SP strains when compared to ATCC49619 after tedTHP-1 and A549 cells were stimulated. Clinical SPs showed higher virulence compared with ATCC49619.ConclusionsThe expression of CpsA is the basis of the pathogenicity of SP. The expression of virulence gene PsaA may be helpful to the invasion of SP to the blood system.

Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

“…The concentrations of such interleukins and adhesin were equal between sd-SP and bd-SP groups, while our previous study proved sd-SP is less virulent than bd-SP. 8,9 The data in this study were some different from those in our previous study, 33 which was due to the different concentrations of S pneumoniae and THP-1 cells. In this study, the ratio of S pneumoniae and THP-1 cells was much lower, which resulted in the faster clearance of S pneumoniae.…”

“…ATCC49619 is a standard S pneumoniae strain, which is less virulent than clinical ones as shown in our previous study. 8,9,33 The intriguing difference among clinical S pneumoniae groups lies in sICAM-1 except IL-1β, IL-6, IL-10, and IL-8.…”

“…We previously verified that certain S pneumoniae virulence factors such as pneumolysin (Ply) may facilitate S pneumoniae's invading blood system. 8,9 However, other differences remain still uncertain among different S pneumoniae strains responsible for the former three types of infections. Dendritic cells, monocytes, and neutrophils are all primary guards for host's fighting S pneumoniae, the former two of which were used for research more often.…”

Genome-Wide Identification of Genes Essential for the Survival of Streptococcus pneumoniae in Human Saliva

“…Manganese could thus be an important cue by which the immediate environment is sensed and the transitioning to internal body sites is experienced. Indeed, in clinical S. pneumoniae strains from Chinese patients, psaA expression was significantly higher in blood-derived than in sputum-derived S. pneumoniae [34]. Expression of psaA may thus be involved in invasion of the blood system by S. pneumoniae , making this gene a potentially interesting target for the development of new classes of antimicrobials.…”

Polyanhydride nanovaccine platform against bacterial pathogens

“…Unlike many circulating diseases, humans provide the main reservoir for S. pneumoniae, making person to person transmission a crucial step in the survival and spread of the pathogen 65 79 . Additionally the cell surface protein pneumococcal adherence and virulence factor A (PavA), important in bacterial binding to fibronectin, has been shown to play an important role in the establishment of a septicemia in a murine model 80 .…”