ArticleThe Journal of clinical investigation2020
S100A8/A9 regulates CD11b expression and neutrophil recruitment during chronic tuberculosis.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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
99 citing papers in PubMed, 142 citations in OpenAlex.
- The Cyclooxygenase 2 Inhibitor Etoricoxib as Adjunctive Therapy in Tuberculosis Impairs Macrophage Control of Mycobacterial Growth.The Journal of infectious diseases · 2024Trial
- The Proteome of Plasma Extracellular Vesicles in Latent and Active Tuberculosis Reveals Phase-Specific Composition and Immunometabolic Insights.FASEB bioAdvances · 2026Article
- Lonicera japonica-Derived Nanovesicles Ameliorate Acute Lung Injury by Suppressing Neutrophil Extracellular Traps Formation in Mice.Advanced healthcare materials · 2026Article
- Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- The study of immunological markers in tuberculosis across animal models and its translation to human research.Lab animal · 2026Review
- Galectin-9Aging cell · 2026Article
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Conserved neutrophil degranulation transcripts in HIV-TB coinfected children across East and Southern Africa.Communications medicine · 2026Article
- Downregulation ofMolecular therapy. Nucleic acids · 2026Article
- Article
- Membrane atg8ylation and autophagy in protection against Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Article
- S100A8/A9 as a biomarker for differentiating pulmonary tuberculosis from community-acquired pneumonia in children: a multicenter cohort study in China.Frontiers in pediatrics · 2026Article
- Immunopathological signatures in congenital tuberculosis-a case-matched study.Frontiers in immunology · 2026Article
- Concurrent TB and HIV therapies control TB reactivation during co-infection but not chronic immune activation.Nature communications · 2025Article
- Article
- Early and opposing neutrophil and CD4 T cell responses shape pulmonary tuberculosis pathology.The Journal of experimental medicine · 2025Article
- Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8bioRxiv : the preprint server for biology · 2025Article
- Mast cells promote pathology and susceptibility in tuberculosis.bioRxiv : the preprint server for biology · 2025Article
39 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
22 authors at 8 institutions in 6 countries.
Funding
Abstract
Neutrophil accumulation is associated with lung pathology during active tuberculosis (ATB). However, the molecular mechanism or mechanisms by which neutrophils accumulate in the lung and contribute to TB immunopathology are not fully delineated. Using the well-established mouse model of TB, our new data provide evidence that the alarmin S100A8/A9 mediates neutrophil accumulation during progression to chronic TB. Depletion of neutrophils or S100A8/A9 deficiency resulted in improved Mycobacterium tuberculosis (Mtb) control during chronic but not acute TB. Mechanistically, we demonstrate that, following Mtb infection, S100A8/A9 expression is required for upregulation of the integrin molecule CD11b specifically on neutrophils, mediating their accumulation during chronic TB disease. These findings are further substantiated by increased expression of S100A8 and S100A9 mRNA in whole blood in human TB progressors when compared with nonprogressors and rapidly decreased S100A8/A9 protein levels in the serum upon TB treatment. Furthermore, we demonstrate that S100A8/A9 serum levels along with chemokines are useful in distinguishing between ATB and asymptomatic Mtb-infected latent individuals. Thus, our results support targeting S100A8/A9 pathways as host-directed therapy for TB.
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.