ArticlePloS one2013
Streptococcus pneumoniae serine protease HtrA, but not SFP or PrtA, is a major virulence factor in pneumonia.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Circulating alpha-1 antitrypsin and its c-terminal peptides differentiate bacterial from viral community-acquired pneumonia.Journal of translational medicine · 2026Article
- Streptococcus pneumoniae HtrA is a dynamic and monomeric virulence factor capable of forming larger oligomeric complexes.Protein science : a publication of the Protein Society · 2026Article
- Article
- Airway proteolytic control of pneumococcal competence.PLoS pathogens · 2023Article
- The involvement of CiaR and the CiaR-regulated serine protease HtrA in thermal adaptation ofMicrobiology (Reading, England) · 2023Article
- The Role of Streptococcal Cell-Envelope Proteases in Bacterial Evasion of the Innate Immune System.Journal of innate immunity · 2022Review
- Pathogenicity and virulence ofVirulence · 2021Review
- Article
- Pneumococcal Extracellular Serine Proteases: Molecular Analysis and Impact on Colonization and Disease.Frontiers in cellular and infection microbiology · 2021Review
- The serine protease HtrA plays a key role in heat-induced dispersal of pneumococcal biofilms.Scientific reports · 2020Article
- Extracellular Pneumococcal Serine Proteases Affect Nasopharyngeal Colonization.Frontiers in cellular and infection microbiology · 2020Article
- Article
- Protease Activity ofFrontiers in cellular and infection microbiology · 2019Article
- Function of Serine Protease HtrA in the Lifecycle of the Foodborne PathogenEuropean journal of microbiology & immunology · 2018Review
- PrtA immunization fails to protect against pulmonary and invasive infection by Streptococcus pneumoniae.Respiratory research · 2018Article
- Stress Physiology of Lactic Acid Bacteria.Microbiology and molecular biology reviews : MMBR · 2016Review
- HtrA Is Important for Stress Resistance and Virulence in Haemophilus parasuis.Infection and immunity · 2016Article
- Comparative Proteomic Analyses of Avirulent, Virulent, and Clinical Strains of Mycobacterium tuberculosis Identify Strain-specific Patterns.The Journal of biological chemistry · 2016Article
- Characterization of Pneumococcal Genes Involved in Bloodstream Invasion in a Mouse Model.PloS one · 2015Article
- The role of serine protease HtrA in acute ulcerative enterocolitis and extra-intestinal immune responses during Campylobacter jejuni infection of gnotobiotic IL-10 deficient mice.Frontiers in cellular and infection microbiology · 2014Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus (S.) pneumoniae is a common causative pathogen in pneumonia. Serine protease orthologs expressed by a variety of bacteria have been found of importance for virulence. Previous studies have identified two serine proteases in S. pneumoniae, HtrA (high-temperature requirement A) and PrtA (cell wall-associated serine protease A), that contributed to virulence in models of pneumonia and intraperitoneal infection respectively. We here sought to identify additional S. pneumoniae serine proteases and determine their role in virulence. The S. pneumoniae D39 genome contains five putative serine proteases, of which HtrA, Subtilase Family Protein (SFP) and PrtA were selected for insertional mutagenesis because they are predicted to be secreted and surface exposed. Mutant D39 strains lacking serine proteases were constructed by in-frame insertion deletion mutagenesis. Pneumonia was induced by intranasal infection of mice with wild-type or mutant D39. After high dose infection, only D39ΔhtrA showed reduced virulence, as reflected by strongly reduced bacterial loads, diminished dissemination and decreased lung inflammation. D39ΔprtA induced significantly less lung inflammation together with smaller infiltrated lung surface, but without influencing bacterial loads. After low dose infection, D39ΔhtrA again showed strongly reduced bacterial loads; notably, pneumococcal burdens were also modestly lower in lungs after infection with D39Δsfp. These data confirm the important role for HtrA in S. pneumoniae virulence. PrtA contributes to lung damage in high dose pneumonia; it does not however contribute to bacterial outgrowth in pneumococcal pneumonia. SFP may facilitate S. pneumoniae growth after low dose infection.
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