The respiratory epithelium and airway smooth muscle homeostasis: its relevance to asthma

Knight, Darryl A.; Stewart, Geoffrey A.; Thompson, Philip J.

doi:10.1111/j.1365-2222.1994.tb00980.x

Cited by 21 publications

(9 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides its barrier/fence function, it plays a key role in regulating the underlying tissue response to external stimuli (55). The harmful effects of cigarette smoke start with epithelial damage followed by an inflammatory response that propagates into the subepithelial tissue (56).…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

Forteza

Casalino‐Matsuda

Falcon

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Cigarette smoke (CigS) induces hyaluronan fragmentation and increases epithelial permeability. Results: CigS and HA fragments decrease E-cadherin expression that is prevented by knocking down layilin. Conclusion: HA fragments bind to layilin and signal through RhoA/ROCK to inhibit E-cadherin. Significance: Airway epithelium is our first line of defense against inhaled insults. HA fragments released by CigS disrupt this barrier.

show abstract

Section: Discussionmentioning

confidence: 99%

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

Forteza

Casalino‐Matsuda

Falcon

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…The airway epithelium is not simply a mechanical barrier, but is in the key position to regulate the underlying tissue response to external stimuli, through the synthesis and release of a multitude of pro-and anti-inflammatory molecules. 7 As the submucosal region, including the lamina propria, are the major sites of the remodelling seen in asthma and are in close proximity to the epithelial cell layer, it is likely that altered production of these molecules influences the composition of this tissue region. 2 Indeed, the inflamed epithelium is an important source of chemokines, cyclo-and lipoxygenase-derived mediators, reactive oxygen species, cytokines and peptides (for a review see Holgate et al 8 ).…”

Section: Mediator Production By the Epitheliummentioning

confidence: 99%

Epithelium–fibroblast interactions in response to airway inflammation

Knight

2001

Immunol Cell Biol

104

View full text Add to dashboard Cite

Dramatic changes to the architecture of the airway walls have been commonly described in the airways of patients with asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Much research has focused on how airway inflammation drives these structural changes, particularly in terms of the mechanisms/mediators that are involved, and a number of parallels are observed between the disease phenotypes. For example, the increased deposition of extracellular matrix (ECM) at focal sites in the airway wall is seen in asthma and all interstitial lung diseases that involve fibrosis. In addition, increased expression of a number of well characterized cytokines and growth factors, such as TGF-beta and epidermal growth factor (EGF) have been demonstrated in these diseases. However, the role of the lesser-known cytokines, including the leukaemia inhibitory factor (LIF) and other members of the IL-6 family of cytokines in the pathogenesis of airway remodelling and fibrosis is largely unknown. However, the use of genetic manipulation in vivo and more specific inhibitors/antibodies in vitro has now provided increasing evidence to support the hypothesis that a complex interaction exists between these cytokines, ECM and integrins in regulating the function of both epithelial cells and fibroblasts.

show abstract

“…The human respiratory epithelium is a critical component of the innate immune system, acting as both a physical barrier to the environment and as a modulator of local airway inflammation because of its capacity to synthesize a variety of mediators including cytokines, leukotrienes, nitric oxide, antioxidants and prostanoid. [3][4][5] Several studies have indicated that HDMs induce the release of mediators such as interleukin (IL)-8, IL-6, tumor necrosis factor-α (TNF-α), granulocyte macrophage-colony stimulating factor (GM-CSF), and regulated on activation, normal T cell expressed and secreted (RANTES) from airway epithelial cells. [6][7][8][9] These mediators trigger the accumulation of inflammatory cells such as eosinophils and neutrophils to perpetuate chronic allergic airway inflammation.…”

mentioning

confidence: 99%

Effect of <i>1.8-Cineole</i> in <i>Dermatophagoides pteronyssinus</i>-Stimulated Bronchial Epithelial Cells and Mouse Model of Asthma

Lee

Song

Park

et al. 2016

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

1.8-Cineole (eucalyptol) is a phytoncide, a volatile organic compound derived from plants. Phytoncides are known to have an anti-inflammatory effect. However, the effects of 1.8-cineole in house dust mite (HDM)-stimulated bronchial epithelial cells are poorly understood. The objective of this study was to assess the effect of 1.8-cineole in HDM-stimulated bronchial epithelial cells and in the HDM-induced murine asthma model. The purpose of the present study is to evaluate the anti-inflammatory effects and mechanism of 1.8-cineole action in HDM-induced airway inflammation. Human bronchial epithelial cells (HBECs) were cultured with Dermatophagoides pteronyssinus (Der p) and 1.8-cineole. Cytokine protein levels, phosphorylation of protein kinases, and intracellular Toll-like receptor 4 (TLR4) expressions were measured. In the murine model, BALB/C mice were sensitized with Der p and were exposed to Der p via intranasal route during the challenge period. 1.8-Cineole was given by inhalation 6 h before the each challenge. Treatment with 1.8-cineole inhibited the Der p-induced cytokine protein expression, phosphorylation of p38 mitogen-activated protein kinase (MAPK) and Akt and intracellular TLR4 expression in HBECs. In the Der p-induced mouse model, airway hyper-responsiveness (AHR) and the number of eosinophils in bronchoalveolar lavage fluid (BALF) was also significantly reduced by 1.8-cineole treatment. The treatment of 1.8-cineole inhibited the increased production of interleukin (IL)-4, IL-13 and IL-17A in BALF after Der p challenge. These results suggest that 1.8-cineole suppresses Der p-induced IL-8, IL-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) production in HBECs. Finally, we confirmed that 1.8-cineole decreases AHR and eosinophilic airway inflammation in Der p-induced asthma mice.

show abstract

The respiratory epithelium and airway smooth muscle homeostasis: its relevance to asthma

Cited by 21 publications

References 83 publications

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

Epithelium–fibroblast interactions in response to airway inflammation

Effect of <i>1.8-Cineole</i> in <i>Dermatophagoides pteronyssinus</i>-Stimulated Bronchial Epithelial Cells and Mouse Model of Asthma

Contact Info

Product

Resources

About