Lysophosphatidylcholine plays critical role in allergic airway disease manifestation

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...

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Bibliographic Details
Published in:Scientific reports 2016-06, Vol.6 (1), p.27430-27430, Article 27430
Main Authors: Bansal, Preeti, Gaur, Shailendera Nath, Arora, Naveen
Format: Article
Language:English
Subjects:
Allergens
Allergies
Animals
Antigens, CD1d - immunology
Asthma
Asthma - immunology
Bronchoalveolar Lavage Fluid - immunology
Cockroaches - immunology
Cytokines
Cytokines - immunology
Female
Histology
Immunization
Inflammation - immunology
Killer Cells, Natural - immunology
Lavage
Leukocyte Count - methods
Leukocytes
Lipids
Lung - immunology
Lung - metabolism
Lysophosphatidylcholines - immunology
Mice
Mice, Inbred BALB C
Phospholipases A2 - immunology
Respiratory Hypersensitivity - immunology
Th2 Cells - immunology
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Summary: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.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep27430