ArticleScientific reports2016
Lysophosphatidylcholine plays critical role in allergic airway disease manifestation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Plasma Metabolomes Identify Distinct Asthma Metabotypes: Findings From the COREA Cohort.Allergy · 2026Article
- Sodium intake and asthma pathophysiology: time to unravel an old mystery?ERJ open research · 2026Article
- Roles of Metabolomics in Allergic Rhinitis: From Cell to Bedside Investigations.International journal of molecular sciences · 2026Review
- Lp-PLA2-derived LysoPC drives dendritic cell immunogenic activation and Th17 inflammation in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Metabolomics discover distinct metabolite profiles in children with different airway allergic diseases.Frontiers in immunology · 2026Article
- Microbial Metabolites in Allergic Diseases: Beyond Short-Chain Fatty Acids.Current allergy and asthma reports · 2025Review
- Multi-omics analysis reveals inhibition of osteosarcoma progression by sporoderm-removed Ganoderma lucidum spores via targeting glycerophospholipid and fatty acid metabolism.Scientific reports · 2025Article
- The Lipid Composition of the Exo-Metabolome fromMetabolites · 2025Article
- Possible Involvement of Lysophospholipids in Severe Asthma as Novel Lipid Mediators.Biomolecules · 2025Review
- Lysophosphatidylcholines Promote Influenza Virus Reproduction through the MAPK/JNK Pathway in PMA-Differentiated THP-1 Macrophages.International journal of molecular sciences · 2024Article
- Review
- CD1-mediated immune responses in mucosal tissues: molecular mechanisms underlying lipid antigen presentation system.Experimental & molecular medicine · 2023Review
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- Lipidomic landscape of lipokines in adipose tissue derived extracellular vesicles.Frontiers in molecular biosciences · 2023Article
- Metabolomic analysis reveals potential biomarkers and the underlying pathogenesis involved inEmerging microbes & infections · 2022Article
- Modulation of gut microbiota, blood metabolites, and disease resistance by dietary β-glucan in rainbow trout (Oncorhynchus mykiss).Animal microbiome · 2022Article
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- Gut Microbiota, Plasma Metabolomic Profiles, and Carotid Artery Atherosclerosis in HIV Infection.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Development of a Novel Targeted Metabolomic LC-QqQ-MS Method in Allergic Inflammation.Metabolites · 2022Article
- Lipids as Regulators of Cellular Senescence.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase A2 (sPLA2), pivotal for allergic and inflammatory response, hydrolyses phosphatidylcholine (PC) to lysophosphatidylcholine (LPC). In present study, the role of LPC in allergic airway disease manifestation was studied using mouse model. Balb/c mice were immunized using cockroach extract (CE) and LPC release was blocked by sPLA2 inhibitor. Airway hyperresponse (AHR), lung-histology, total and differential leukocyte count (TLC&DLC), Th2 type cytokines, sPLA2 activity and LPC levels in bronchoalveolar lavage fluid (BALF) were measured. Exogenous LPC was given to the mice with or without CE sensitization, to demonstrate its role in allergic airway disease manifestation. Anti-CD1d antibody was given to study the involvement of natural killer T (NKT) cells in LPC induced response. AHR, lung-inflammation, TLC, DLC, Th2 type cytokines, sPLA2 activity and LPC levels were increased on CE challenge. sPLA2 activity and LPC release was blocked by sPLA2-inhibitor, which decreased AHR, and inflammatory parameters. Exogenous LPC with or without CE sensitization increased above parameters. CE challenge or LPC exposure increased LY49C(+)TCRβ(+) NKT cells in BALF and spleen, which was reduced by anti-CD1d antibody, accompanied with reduction in AHR and allergic airway inflammation parameters. Conclusively, LPC induces allergic airway disease manifestation and it does so probably via CD1d-restricted LY49C(+)TCRβ(+) NKT cells.
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