ArticleCellular microbiology2016
Moraxella catarrhalis induces CEACAM3-Syk-CARD9-dependent activation of human granulocytes.
Article in Cellular microbiology, 2016. 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, 31 citations in OpenAlex.
- Bridging Rare to Common Diseases: Precision Medicine and the Transforming Landscape of Pediatric Allergy and Immunology.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Review
- Expression of Human CEACAM Receptors Promotes Inflammation and Organ Damage During SystemicCells · 2026Article
- Neutrophil CEACAMs and the Inflammatory Response toJournal of innate immunity · 2026Review
- Structural basis for immune cell binding ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The role of CEACAMs in neutrophil function.European journal of clinical investigation · 2024Review
- The Role of Indoor Microbiome and Metabolites in Shaping Children's Nasal and Oral Microbiota: A Pilot Multi-Omic Analysis.Metabolites · 2023Article
- Update on metabolomic findings in COPD patients.ERJ open research · 2023Review
- Microbiome, Metabolism, and Immunoregulation of Asthma: An American Thoracic Society and National Institute of Allergy and Infectious Diseases Workshop Report.American journal of respiratory cell and molecular biology · 2022Article
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- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
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- Article
- The Role of CARD9 Deficiency in Neutrophils.Mediators of inflammation · 2021Review
- Article
- Unaltered Fungal Burden and Lethality in Human CEACAM1-Transgenic Mice DuringFrontiers in microbiology · 2019Article
- CEACAM3-A Prim(at)e Invention for Opsonin-Independent Phagocytosis of Bacteria.Frontiers in immunology · 2019Review
- Molecular and physiological roles of the adaptor protein CARD9 in immunity.Cell death & disease · 2018Review
- Binding ofmBio · 2017Article
- Coevolution of paired receptors in Xenopus carcinoembryonic antigen-related cell adhesion molecule families suggests appropriation as pathogen receptors.BMC genomics · 2016Article
- Moraxella catarrhalis induces CEACAM3-Syk-CARD9-dependent activation of human granulocytes.Cellular microbiology · 2016Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human restricted pathogen Moraxella catarrhalis is an important causal agent for exacerbations in chronic obstructive lung disease in adults. In such patients, increased numbers of granulocytes are present in the airways, which correlate with bacteria-induced exacerbations and severity of the disease. Our study investigated whether the interaction of M. catarrhalis with the human granulocyte-specific carcinoembryonic antigen-related cell adhesion molecule (CEACAM)-3 is linked to NF-κB activation, resulting in chemokine production. Granulocytes from healthy donors and NB4 cells were infected with M. catarrhalis in the presence of different inhibitors, blocking antibodies and siRNA. The supernatants were analysed by enzyme-linked immunosorbent assay for chemokines. NF-κB activation was determined using a luciferase reporter gene assay and chromatin-immunoprecipitation. We found evidence that the specific engagement of CEACAM3 by M. catarrhalis ubiquitous surface protein A1 (UspA1) results in the activation of pro-inflammatory events, such as degranulation of neutrophils, ROS production and chemokine secretion. The interaction of UspA1 with CEACAM3 induced the activation of the NF-κB pathway via Syk and the CARD9 pathway and was dependent on the phosphorylation of the CEACAM3 ITAM-like motif. These findings suggest that the CEACAM3 signalling in neutrophils is able to specifically modulate airway inflammation caused by infection with M. catarrhalis.
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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.