TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airwaysReport as inadecuate




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Respiratory Research

, 12:125

First Online: 01 December 2011Received: 17 July 2011Accepted: 24 September 2011

Abstract

Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors TLRs are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin.

Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells SCs of the airways such as epithelial cells ECs, endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.

KeywordsAirway diseases dendritic cells epithelial cell pulmonary stromal cells TLR4 List of abbreviationsAPCantigen presenting cells

BMbone marrow

DAMPdamage associated molecular pattern molecule

DCdendritic cells

dnIκB-αdominant negative inhibitor of NF-κB translocation

ECepithelial cell

ERK1-2extracellular signal-regulated kinase 1-2

GM-CSFgranulocyte macrophage-colony-stimulating factor

HDMhouse dust mite

HMGB1high mobility group box 1

HPChematopoietic cell

HSPheat shock protein

ICE miceIL-1R1 and caspase-1-deficient mice

IL-1interleukin-1

IRAKIL-1R-associated kinase

LPSlipopolysaccharide

MAPKsmitogen-activated protein kinases

MIP-3αmacrophage inflammatory protein 3α

MyD88myeloid differentiation factor 88

OVAovalbumin

SCstructural cell

TIRAPToll-IL-1R domain-containing adaptor protein

TLRToll-like receptor

TRAF6tumor necrosis factor receptor-associated factor 6

TRAMTRIF-related adaptor molecule

TRIF3TIR domain-containing adaptor inducing IFN-β.

Electronic supplementary materialThe online version of this article doi:10.1186-1465-9921-12-125 contains supplementary material, which is available to authorized users.

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Author: Frederic Perros - Bart N Lambrecht - Hamida Hammad

Source: https://link.springer.com/







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