Control of lung defence by mucins and macrophages: ancient defence mechanisms with modern functions

被引:59
作者
Janssen, William J. [1 ,2 ]
Stefanski, Adrianne L. [2 ]
Bochner, Bruce S. [3 ]
Evans, Christopher M. [2 ]
机构
[1] Natl Jewish Hlth, Dept Med, Denver, CO USA
[2] Univ Colorado, Dept Med, Sch Med, Aurora, CO USA
[3] Northwestern Univ, Dept Med, Div Allergy Immunol, Feinberg Sch Med, Chicago, IL 60611 USA
关键词
OBSTRUCTIVE PULMONARY-DISEASE; COMMON VARIABLE IMMUNODEFICIENCY; HUMAN RESPIRATORY-TRACT; HELICOBACTER-PYLORI INFECTION; BRONCHOALVEOLAR LAVAGE FLUIDS; HUMAN ALVEOLAR MACROPHAGES; APOPROTEIN-A CONCENTRATION; HUMAN AIRWAY EPITHELIUM; BLOOD GROUP ANTIGENS; TOLL-LIKE RECEPTORS;
D O I
10.1183/13993003.00120-2015
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Owing to the need to balance the requirement for efficient respiration in the face of tremendous levels of exposure to endogenous and environmental challenges, it is crucial for the lungs to maintain a sustainable defence that minimises damage caused by this exposure and the detrimental effects of inflammation to delicate gas exchange surfaces. Accordingly, epithelial and macrophage defences constitute essential first and second lines of protection that prevent the accumulation of potentially harmful agents in the lungs, and under homeostatic conditions do so effectively without inducing inflammation. Though epithelial and macrophage-mediated defences are seemingly distinct, recent data show that they are linked through their shared reliance on airway mucins, in particular the polymeric mucin MUC5B. This review highlights our understanding of novel mechanisms that link mucus and macrophage defences. We discuss the roles of phagocytosis and the effects of factors contained within mucus on phagocytosis, as well as newly identified roles for mucin glycoproteins in the direct regulation of leukocyte functions. The emergence of this nascent field of glycoimmunobiology sets forth a new paradigm for considering how homeostasis is maintained under healthy conditions and how it is restored in disease.
引用
收藏
页码:1201 / 1214
页数:14
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