ArticleInfection and immunity2011
Lipoxin A₄ inhibits porphyromonas gingivalis-induced aggregation and reactive oxygen species production by modulating neutrophil-platelet interaction and CD11b expression.
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 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- Lipoxins modulate neutrophil oxidative burst, integrin expression and lymphatic transmigration differentially in human health and atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Trial
- Safety and Preliminary Efficacy of a Novel Host-Modulatory Therapy for Reducing Gingival Inflammation.Frontiers in immunology · 2021Trial
- Specialized Pro-Resolving Mediators MaR1 and LXAThe American journal of pathology · 2026Article
- Inflammation and resolution in obesity.Nature reviews. Endocrinology · 2025 · on this mapReview
- Lipoxin AFrontiers in immunology · 2024Article
- Immunomodulation of periodontitis with SPMs.Frontiers in oral health · 2023Review
- Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Resolution of Inflammation after Skeletal Muscle Ischemia-Reperfusion Injury: A Focus on the Lipid Mediators Lipoxins, Resolvins, Protectins and Maresins.Antioxidants (Basel, Switzerland) · 2022Review
- Specialized Pro-Resolving Lipid Mediators: New Therapeutic Approaches for Vascular Remodeling.International journal of molecular sciences · 2022Review
- Oral Microbiota-Driven Cell Migration in Carcinogenesis and Metastasis.Frontiers in cellular and infection microbiology · 2022Review
- PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- Lipid mediator lipoxin A4 and its analog BML-111 exert antitumor effects in melanoma.Annals of translational medicine · 2021Article
- Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases.Frontiers in immunology · 2021Review
- Platelet plug formation in whole blood is enhanced in the presence of Porphyromonas gingivalis.Molecular oral microbiology · 2020Article
- The role of serum lipoxin A4 levels in the association between periodontal disease and metabolic syndrome.Journal of periodontal & implant science · 2019Article
- Modified lipoproteins in periodontitis: a link to cardiovascular disease?Bioscience reports · 2019Article
- Lipoprotein modifications by gingipains of Porphyromonas gingivalis.Journal of periodontal research · 2018Article
- Resolution of inflammation in periodontitis: a review.International journal of clinical and experimental pathology · 2018Review
- Infectious Agents in Atherosclerotic Cardiovascular Diseases through Oxidative Stress.International journal of molecular sciences · 2017Review
- Reduced platelet hyper-reactivity and platelet-leukocyte aggregation after periodontal therapy.Thrombosis journal · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porphyromonas gingivalis is an etiological agent that is strongly associated with periodontal disease, and it correlates with numerous inflammatory disorders, such as cardiovascular disease. Circulating bacteria may contribute to atherogenesis by promoting CD11b/CD18-mediated interactions between neutrophils and platelets, causing reactive oxygen species (ROS) production and aggregation. Lipoxin A₄ (LXA₄) is an endogenous anti-inflammatory and proresolving mediator that is protective of inflammatory disorders. The aim of this study was to investigate the effect of LXA₄ on the P. gingivalis-induced activation of neutrophils and platelets and the possible involvement of Rho GTPases and CD11b/CD18 integrins. Platelet/leukocyte aggregation and ROS production was examined by lumiaggregometry and fluorescence microscopy. Integrin activity was studied by flow cytometry, detecting the surface expression of CD11b/CD18 as well as the exposure of the high-affinity integrin epitope, whereas the activation of Rac2/Cdc42 was examined using a glutathione S-transferase pulldown assay. The study shows that P. gingivalis activates Rac2 and Cdc42 and upregulates CD11b/CD18 and its high-affinity epitope on neutrophils, and that these effects are diminished by LXA₄. Furthermore, we found that LXA₄ significantly inhibits P. gingivalis-induced aggregation and ROS generation in whole blood. However, in platelet-depleted blood and in isolated neutrophils and platelets, LXA₄ was unable to inhibit either aggregation or ROS production, respectively. In conclusion, this study suggests that LXA₄ antagonizes P. gingivalis-induced cell activation in a manner that is dependent on leukocyte-platelet interaction, likely via the inhibition of Rho GTPase signaling and the downregulation of CD11b/CD18. These findings may contribute to new strategies in the prevention and treatment of periodontitis-induced inflammatory disorders, such as atherosclerosis.
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Registered trials
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