Abstract

Airway epithelial cells (AECs) are part of the frontline defense against infection of pathogens by providing both a physical barrier and immunological function. The role of AECs in the innate and adaptive immune responses, through the production of antimicrobial molecules and proinflammatory factors against a variety of pathogens, has been well established. Tuberculosis (TB), a contagious disease primarily affecting the lungs, is caused by the infection of various strains of mycobacteria. In response to mycobacteria infection, epithelial expression of Toll-like receptors and surfactant proteins plays the most prominent roles in the recognition and binding of the pathogen, as well as the initiation of the immune response. Moreover, the antimicrobial substances, proinflammatory factors secreted by AECs, composed a major part of the innate immune response and mediation of adaptive immunity against the pathogen. Thus, a better understanding of the role and mechanism of AECs in response to mycobacteria will provide insight into the relationship of epithelial cells and lung immunocytes against TB, which may facilitate our understanding of the pathogenesis and immunological mechanism of pulmonary tuberculosis disease.

Highlights

  • The lung is an organ lined by numerous distinct types of epithelial cells in different anatomical regions

  • This increasing of matrix metalloproteases (MMPs)-1 was mediated via phosphorylation of p38 mitogen-activated protein kinases (MAPKs) that was induced by synergism of conditioned medium from Mtb-infected monocytes (CoMTb)-driving TNF-β and G protein-coupled receptor activation, and the decreasing of tissue inhibitor of metalloproteinase 1 (TIMP-1) secretion

  • A growing body of evidence supports the essential involvement of Airway epithelial cells (AECs) in both the innate and adaptive immune responses against mycobacterial infection

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Summary

Introduction

The lung is an organ lined by numerous distinct types of epithelial cells in different anatomical regions. Increasing evidence has demonstrated that epithelial cells play critical functions in initiating and expanding airway host defense mechanisms in the lung and providing the initial defense against inhaled microorganisms These epithelial cells are capable of regulating innate immunity and producing functional molecules that physically interacted with immunocytes to activate adaptive immunity [1, 2]. In response to invasion of pathogens, airway epithelial cells (AECs) secrete various microorganism killing effectors, such as mucins antimicrobial peptides (AMPs) and reactive oxygen species (ROS), into the airway lumen to control the composition of airway surface liquid (ASL) These cells produce proinflammatory cytokines, growth factors, and chemokines that recruit and activate phagocytes to the site of infection eliminating pathogens by phagocytosis. An emphasis was placed on the recently recognized functions of epithelial cells in innate and adaptive immunity against mycobacteria, the pathogen recognition and host defense of AECs to Mtb

Airway Epithelial Cells and Pathogen Recognition of Mycobacteria
Airway Epithelial Cells and Their Host Defenses
Airway Epithelial Cells
Concluding Remarks
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