Immunotherapy: Open Access
Open Access

Ly6C+ inflammatory monocytes regulate neutrophils inflammation response induced by lung injury

International Conference on Tumor & Cancer Immunology and Immunotherapy

July 28-30, 2016 Melbourne, Australia

Li Liu

Sichuan University, China

Posters & Accepted Abstracts: Immunother Open Acc

Abstract :

Cationic liposomes administration induces severe pulmonary inflammatory response and lung injury, but little is known about the regulation of the immune response. Cationic liposomes trigger inflammation by inducing necrosis of lung cells and releasing mitochondrial DNA (mtDNA). And the activation of inflammation depends on the TLR9 and STING pathways. We show the characteristic of dynamic that Ly6C+ inflammatory monocytes are recruited in Lung after the inflammatory neutrophils infiltrated in lung tissue after cationic liposomes dosing and these monocytes are required to prevent pulmonary inflammation and lung injury. We show that Ly6C+ inflammatory monocytes regulate neutrophils inflammation via the production of prostaglandin E2 (PGE2), the pulmonary inflammation trigged by cationic liposomes can be controlled by PGE2 analog treatment. IL-10-/- inflammatory monocytes demonstrate a previously unappreciated inflammation inhibiting function through producing PGE2 and the effect is eliminated by indomethacin, a COX-1 and COX-2 inhibitor. Our results suggest that mtDNA and necrotic lung cells reprogramming Ly6C+ inflammatory monocytes into dual phenotypes, acquiring both inflammatory and regulatory features. The findings highlight the importance of Ly6C+ inflammatory monocytes in pulmonary inflammation regulation during lung injury induced by cationic liposomes.

Biography :

Email: lilyscu1990@163.com