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Role of Lysophosphatidylcholine in Allergic Airway Disease Manifestation
Sunday, March 6, 2016: 4:45 PM
Concourse Foyer (Convention Center)
Preeti Bansal, Shailendra N. Gaur, MD FAAAAI, Naveen Arora, PhD
Rationale:

Secretory phospholipase A2 (sPLA2) is involved in allergic and inflammatory response and hydrolyses phosphatidylcholine (PC) to lysophosphatidylcholine (LPC). LPC levels increase in BALF and sera of asthma and rhinitis patients. In the present study the role of LPC was studied in mouse model of allergic airway disease.

Methods: Mice were immunized with cockroach extract (CE) and sPLA2 inhibitor was given to block LPC release. AHR, TLC, DLC, lung inflammation, Th2 type cytokines, sPLA2 activity and LPC were analysed. Mice were given LPC to study its role in allergic disease manifestation, with or without CE sensitization. The involvement of NKT cells in LPC induced response was studied by anti-CD1d antibody before CE/LPC exposure.

Results: CE challenge increased AHR, TLC, DLC, lung inflammation, Th2 type cytokines, sPLA2 activity and LPC level significantly as compared to control mice (p<0.05). sPLA2 inhibitor blocked its activity, LPC release and decreased AHR, and inflammatory parameters significantly (p<0.05). LPC exposure with or without CE sensitization increased the AHR, TLC, DLC, lung inflammation, and Th2 type cytokines significantly (p<0.05) demonstrating the role of LPC in allergic disease manifestation. CE challenge or LPC exposure increased LY49C+TCRβ+ NKT cells in BALF and spleen significantly (p<0.05), which was blocked by anti-CD1d antibody. It also decreased AHR and allergic inflammation parameters significantly (p<0.05). 

Conclusions: Allergen challenge increases sPLA2 activity and LPC release resulting in allergic airway disease manifestation via CD1d-restricted LY49C+TCRβ+ NKT cells.