Interferon gamma induces inflammatory responses through the interaction of CEACAM1 and PI3K in airway epithelial cells.

ABSTRACT:

Background

Interferon gamma (IFNγ) plays an important role in the development of chronic lung diseases via the production of inflammatory mediators, although the exact mechanism remains unclear. The present study aimed at investigating the potential mechanisms by which IFNγ induced over-production of interleukins through the interaction between carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway.

Methods

IFN-γ induced over-production of interleukin (IL) 6 and IL8, and RNA expression of CEACAM1 and its subtypes or PI3K and its subtypes in human bronchial epithelial cells (HBE). The production of IL6 and IL8 or cell proliferation and movement were also evaluated in cell^CEACAM1- or cell

SUBMITTER: Zhu Y 

PROVIDER: S-EPMC6507156 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature