ASCB mini symposium 4

소개

학회 세미나 자료입니다.

목차

Abstract

Introduction

Materials & Methods

Conclusion

Reference

본문내용

Lungs are delicate and exposed to the environment, almost like an open wound. Consequently, the body has developed an elaborate immuno-defense system to combat inhaled pathogens and bacteria.
Recently Pseudomonas fluorescens has been considered as an opportunistic indoor pathogen, meaning that it exploits some breaks in the host defenses to initiate an infection. Pseudomonas infection initiates effective innate immune responses after contact with lung epithelial cells. MAPKs link a variety of extracellular signals to a diverse range of cellular responses such as proliferation, differentiation, and apoptosis.
Infection of epithelial cells has been shown to activate ERK1/2 as well as phospho inositide 3-kinase (PI3K), although the underlying mechanisms for their activation are not well defined. Both ERK1/2 and PI3K are generally elicited through the activation of cell surface receptors, such as epidermal growth factor (EGF) receptor (EGFR).
Epidermal growth factor receptor (EGFR) has been shown to play important roles in regulating diverse biological processes, including cell growth, differentiation, apoptosis, adhesion, and migration. Its role in regulating human Toll-like receptors (TLRs), key host defense receptors that recognize invading bacterial pathogens, however, remains unknown.
In this study, we investigated whether infection-induced EGFR activation and its subsequent activation of the ERK and PI3K pathways protect human Alveolar epithelial cells from apoptosis. We demonstrated that P. fluorescens infection activates EGFR in A549 and that subsequent activation of both MAPK and PI3K pathways plays an antiapoptotic role in P. fluorescens–infected A549.

참고자료

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