Airway smooth muscle as an immunomodulatory cell

被引：72

作者：

Damera, Gautam ^{[1
]}

Tliba, Omar ^{[1
,2
]}

Panettieri, Reynold A., Jr. ^{[1
]}

机构：

[1] Univ Penn, Airways Biol Initiat, Pulm Allergy & Crit Care Div, 125 S 31st St, Philadelphia, PA 19104 USA

[2] Thomas Jefferson Univ, Sch Pharm, Dept Pharmaceut Sci, Philadelphia, PA 19107 USA

来源：

PULMONARY PHARMACOLOGY & THERAPEUTICS | 2009年 / 22卷 / 05期

关键词：

Synthetic function; Airway remodeling; Mesenchymal cells; Airway hyperresponsiveness; Hyperplasia; Hypertrophy; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; IFN-GAMMA; MAST-CELL; TNF-ALPHA; INTERFERON-GAMMA; MESSENGER-RNA; UP-REGULATION; INCREASED EXPRESSION; VCAM-1; EXPRESSION;

D O I：

10.1016/j.pupt.2008.12.006

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Although pivotal in regulating bronchomotor tone in asthma, airway smooth muscle (ASM) also modulates airway inflammation in asthma. ASM myocytes secrete or express a wide array of immunomodulatory mediators in response to extracellular stimuli, and in chronic severe asthma, increases in ASM mass may also render the airway irreversibly obstructed. Although the mechanisms by which ASM secretes cytokines and chemokines are shared with those regulating immune cells, there exist unique ASM signaling pathways that may provide novel therapeutic targets. This review provides an overview of our current understanding of the proliferative as well as synthetic properties of ASM. (C) 2008 Elsevier Ltd. All rights reserved.

引用

页码：353 / 359

页数：7

共 86 条

[81] Endogenous and exogenous IL-6 inhibit aeroallergen-induced Th2 inflammation [J].