airway epithelium

Similarly, the expression of Slit3 is upregulated when aligning airway epithelium with endothelium.

In 2007, an excitatory GABAergic system was described in the airway epithelium.

Human rhinovirus infection of airway epithelium induces ICAM-1.

In addition to these cell-mediated mechanisms of elimination, antimicrobial peptides secreted by the airway epithelium contribute to host defense.

Its mechanism of action is by interruption of the Th2 lymphocyte immune response that underlies the inflammatory hyperresponsiveness in the airway epithelium of asthmatics.

In contrast, iNOS and nNOS were limited primarily to the airway epithelium, and their levels did not increase following exposure to hypoxia.

Studies of STAT6 transgenic mice suggest the interesting possibility that IL-13 signaling occurring only through the airway epithelium is required for most of these effects.

ET-1 mRNA was expressed mainly in hyperplastic type II pneumocytes and airway epithelium (fig 2, panel F).

Prominent staining was seen in the lungs of patients with CFA, which was localised predominantly to the airway epithelium and type II pneumocytes.

The airway epithelium together with alveolar macrophages and dendritic cells play a major role in the initial recognition of bacterial products getting into the lower airways with the air.

Activation of NPSR in the airway epithelium has a number of effects including upregulation of matrix metalloproteinases which are involved in the pathogenesis of asthma.

The result is a viscoelastic product of interwoven molecules which, combined with other secretions (e.g., from the airway epithelium and the submucosal glands in the respiratory system), is called mucus.

ET-1-IR in both airway epithelium and type II pneumocytes correlated significantly with young granulation tissue and type II cell proliferation (table II).

Lastly, the intercellular adhesion molecule, ICAM-1, a cluster B gene, was previously found to be increased on inflamed airway epithelium in a primate model of pulmonary inflammation [ 34].

For example, these basal cells respond to injury of the airway epithelium, migrating to cover a site denuded of differentiated epithelial cells, and subsequently differentiating to restore a healthy epithelial cell layer.

Furthermore, previous studies of smoker individuals with COPD and normal lung function showed the presence of CD8 + /CXCR3 + T cells in the airway epithelium and submucosa [44].

Immunostains for ET-1 and big ET-1 and expression of ET-1 mRNA were most prominent in airway epithelium and type II pneumocytes, particularly those lining areas of young granulation tissue.

To analyse the correlations further, we summed the histology grades (young granulation tissue and type II pneumocyte proliferation) and correlated this with the summed airway epithelium and type II pneumocyte staining.

The airway epithelium, type II pneumocytes, and vascular endothelium of ET-1-stained sections were also graded semiquantitatively from 0 to 4, with grade 0 representing no staining, grade 1 focal staining, and grades 2, 3, and 4 diffuse weak, moderate, and strong staining, respectively.

Exposure to cigarette smoke activates an inflammatory cascade in the airway epithelium resulting in the production of a number of potent cytokines and chemokines, with accompanying damage to the lung epithelium, increased permeability, and recruitment of macrophages and neutrophils to the airway [ 3 ] .