ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Importance of TLR2 in early innate immune response to acute pulmonary infection with Porphyromonas gingivalis in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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.
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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.
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Who cites it
49 citing papers in PubMed, 82 citations in OpenAlex.
- A critical review on the roles of natural products in shaping oral microbiota and preventing chronic diseases.Natural products and bioprospecting · 2026Review
- Bridging oral and systemic health: exploring pathogenesis, biomarkers, and diagnostic innovations in periodontal disease.Infection · 2025Review
- Review
- Exploring the Mechanisms and Association between Oral Microflora and Systemic Diseases.Diagnostics (Basel, Switzerland) · 2022Review
- Periodontitis and Its Inflammatory Changes Linked to Various Systemic Diseases: A Review of Its Underlying Mechanisms.Biomedicines · 2022Review
- Oral Lesions Associated with COVID-19 and the Participation of the Buccal Cavity as a Key Player for Establishment of Immunity against SARS-CoV-2.International journal of environmental research and public health · 2022Review
- The Association betweenInternational journal of environmental research and public health · 2022Article
- Macrophage cytokine responses to commensal Gram-positive Lactobacillus salivarius strains are TLR2-independent and Myd88-dependent.Scientific reports · 2021Article
- Severe COVID-19 Lung Infection in Older People and Periodontitis.Journal of clinical medicine · 2021Review
- Review
- Erythromycin inhibits neutrophilic inflammation and mucosal disease by upregulating DEL-1.JCI insight · 2020Article
- Self-Reported Oral Health Related Behaviour and Gum Bleeding of Adolescents in Slovakia in Relation to Socioeconomic Status of Their Parents: Cross-Sectional Study Based on Representative Data Collection.International journal of environmental research and public health · 2019Article
- Association between periodontal pathogens and systemic disease.Biomedical journal · 2019Review
- Effect ofBioMed research international · 2019Article
- Disruption of Immune Homeostasis in Human Dendritic Cells via Regulation of Autophagy and Apoptosis byFrontiers in immunology · 2019Article
- Neutrophil Elastase Subverts the Immune Response by Cleaving Toll-Like Receptors and Cytokines in Pneumococcal Pneumonia.Frontiers in immunology · 2018Article
- Oral Biofilms from Symbiotic to Pathogenic Interactions and Associated Disease -Connection of Periodontitis and Rheumatic Arthritis by Peptidylarginine Deiminase.Frontiers in microbiology · 2018Review
- Article
- Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?Journal of immunology research · 2018Review
- Host response to pulmonary fungal infections: A highlight on cell-driven immunity toCurrent pharmacology reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The periodontal pathogen Porphyromonas gingivalis is implicated in certain systemic diseases including atherosclerosis and aspiration pneumonia. This organism induces innate responses predominantly through TLR2, which also mediates its ability to induce experimental periodontitis and accelerate atherosclerosis. Using a validated mouse model of intratracheal challenge, we investigated the role of TLR2 in the control of P. gingivalis acute pulmonary infection. TLR2-deficient mice elicited reduced proinflammatory or antimicrobial responses (KC, MIP-1alpha, TNF-alpha, IL-6, IL-12p70, and NO) in the lung and exhibited impaired clearance of P. gingivalis compared with normal controls. However, the influx of polymorphonuclear leukocytes into the lung and the numbers of resident alveolar macrophages (AM) were comparable between the two groups. TLR2 signaling was important for in vitro killing of P. gingivalis by polymorphonuclear leukocytes or AM and, moreover, the AM bactericidal activity required NO production. Strikingly, AM were more potent than peritoneal or splenic macrophages in P. gingivalis killing, attributed to diminished AM expression of complement receptor-3 (CR3), which is exploited by P. gingivalis to promote its survival. The selective expression of CR3 by tissue macrophages and the requirement of TLR2 inside-out signaling for CR3 exploitation by P. gingivalis suggest that the role of TLR2 in host protection may be contextual. Thus, although TLR2 may mediate destructive effects, as seen in models of experimental periodontitis and atherosclerosis, we have now shown that the same receptor confers protection against P. gingivalis in acute lung infection.
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Registered trials
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