ArticleJournal of immunology (Baltimore, Md. : 1950)2016
PcpA Promotes Higher Levels of Infection and Modulates Recruitment of Myeloid-Derived Suppressor Cells during Pneumococcal Pneumonia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- The global transcriptional regulator MgaSpn affects the virulence of Streptococcus pneumoniae by regulating PcpA.BMC microbiology · 2025Article
- Increased Proportions of Invasive Pneumococcal Disease Cases Among Adults Experiencing Homelessness Sets the Stage for New Serotype 4 Capsular-Switch Recombinants.The Journal of infectious diseases · 2025Article
- Neutrophil reduction attenuates the severity of lung injury in the early phase of pneumococcal pneumonia in mice.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The Two-Component System YesMN Promotes Pneumococcal Host-to-Host Transmission and Regulates Genes Involved in Zinc Homeostasis.Infection and immunity · 2023Article
- Advances in the study of myeloid-derived suppressor cells in infectious lung diseases.Frontiers in immunology · 2023Review
- Streptococcus pneumoniae binds to host GAPDH on dying lung epithelial cells worsening secondary infection following influenza.Cell reports · 2021Article
- Comparison of specific in-vitro virulence gene expression and innate host response in locally invasive vs colonizer strains of Streptococcus pneumoniae.Medical microbiology and immunology · 2021Article
- Multi-Valent Protein Hybrid Pneumococcal Vaccines: A Strategy for the Next Generation of Vaccines.Vaccines · 2021Review
- Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.Frontiers in immunology · 2020Review
- Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
We used two different infection models to investigate the kinetics of the PcpA-dependent pneumococcal disease in mice. In a bacteremic pneumonia model, we observed a PcpA-dependent increase in bacterial burden in the lungs, blood, liver, bronchoalveolar lavage, and spleens of mice at 24 h postinfection. This PcpA-dependent effect on bacterial burden appeared earlier (within 12 h) in the focal pneumonia model, which lacks bacteremia or sepsis. Histological changes show that the ability of pneumococci to make PcpA was associated with unresolved inflammation in both models of infection. Using our bacteremic pneumonia model we further investigated the effects of PcpA on recruitment of innate immune regulatory cells. The presence of PcpA was associated with increased IL-6 levels, suppressed production of TRAIL, and reduced infiltration of polymorphonuclear cells. The ability of pneumococci to make PcpA negatively modulated both the infiltration and apoptosis of macrophages and the recruitment of myeloid-derived suppressor-like cells. The latter have been shown to facilitate the clearance and control of bacterial pneumonia. Taken together, the ability to make PcpA was strongly associated with increased bacterial burden, inflammation, and negative regulation of innate immune cell recruitment to the lung tissue during bacteremic pneumonia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.