ArticleInfection and immunity2011
Cathepsin G and neutrophil elastase play critical and nonredundant roles in lung-protective immunity against Streptococcus pneumoniae in mice.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 104 citations in OpenAlex.
- Human inborn errors of the phagocyte respiratory burst: Chronic granulomatous disease and beyond.Journal of human immunity · 2026Article
- Myeloid cell reprogramming drives enhanced defense againstProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immunomodulatory role and therapeutic potential of thrombospondin-1 during infectious diseases and autoimmunity.BMC biology · 2026Review
- By dawn or dusk-how circadian timing rewrites bacterial infection outcomes.FEBS letters · 2026Review
- Extracellular adenosine released by mesenchymal stromal cells from young hosts boosts the antimicrobial activity of neutrophils from aged hosts againstImmunotherapy advances · 2026Article
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Genetic Evidence for Causal Relationships Between Circulating Cathepsin Levels and Chronic Obstructive Pulmonary Disease: A Mendelian Randomization Study.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2025Article
- Neutrophil Elastase Limits Spread of Staphylococcus aureus during Skin Infection.The Journal of infectious diseases · 2025Article
- Exploring the roles of airway dipeptidyl peptidase 1 in obstructive airway disease.ERJ open research · 2025Article
- Article
- Executioner caspases degrade essential mediators of pathogen-host interactions to inhibit growth of intracellular Listeria monocytogenes.Cell death & disease · 2025Article
- Blocking HXAmBio · 2024Article
- Blocking HXAbioRxiv : the preprint server for biology · 2024Article
- Activating A1 adenosine receptor signaling boosts early pulmonary neutrophil recruitment in aged mice in response to Streptococcus pneumoniae infection.Immunity & ageing : I & A · 2024Article
- Neutrophil responsiveness to IL-10 impairs clearance of Streptococcus pneumoniae from the lungs.Journal of leukocyte biology · 2024Article
- Age-related lung changes linked to altered lysosomal protease profile, histology, and ultrastructure.PloS one · 2024Article
- Article
- S100A9 is indispensable for survival of pneumococcal pneumonia in mice.PLoS pathogens · 2023Article
- Advances in immune response to pulmonary infection: Nonspecificity, specificity and memory.Chronic diseases and translational medicine · 2023Review
- Chronic ethanol exposure impairs alveolar leukocyte infiltration during pneumococcal pneumonia, leading to an increased bacterial burden despite increased CXCL1 and nitric oxide levels.Frontiers in immunology · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil serine proteases cathepsin G (CG), neutrophil elastase (NE), and proteinase 3 (PR3) have recently been shown to contribute to killing of Streptococcus pneumoniae in vitro. However, their relevance in lung-protective immunity against different serotypes of S. pneumoniae in vivo has not been determined so far. Here, we examined the effect of CG and CG/NE deficiency on the lung host defense against S. pneumoniae in mice. Despite similar neutrophil recruitment, both CG knockout (KO) mice and CG/NE double-KO mice infected with focal pneumonia-inducing serotype 19 S. pneumoniae demonstrated a severely impaired bacterial clearance, which was accompanied by lack of CG and NE but not PR3 proteolytic activity in recruited neutrophils, as determined using fluorescence resonance energy transfer (FRET) substrates. Moreover, both CG and CG/NE KO mice but not wild-type mice responded with increased lung permeability to infection with S. pneumoniae, resulting in severe respiratory distress and progressive mortality. Both neutrophil depletion and ablation of hematopoietic CG/NE in bone marrow chimeras abolished intra-alveolar CG and NE immunoreactivity and led to bacterial outgrowth in the lungs of mice, thereby identifying recruited neutrophils as the primary cellular source of intra-alveolar CG and NE. This is the first study showing a contribution of neutrophil-derived neutral serine proteases CG and NE to lung-protective immunity against focal pneumonia-inducing serotype 19 S. pneumoniae in mice. These data may be important for the development of novel intervention strategies to improve lung-protective immune mechanisms in critically ill patients suffering from severe pneumococcal pneumonia.
Indexed as
Identifiers
What OpenQuestion holds
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.