488 research outputs found
Cell adhesion molecules and the bronchial epithelium
We thank Professor David Garrod, Dr.Tom Fleming, Dr. Dorian
Haskard, and Professor Tak Lee for supplying some of the antibodies used
in our studies.The bronchial epithelium is the major barrier between the host and the provoking antigens in bronchial
asthma. Recent studies have indicated that the epithelium is a truly stratified structure, with the superficial
columnar cells depending on the underlying basal cells for anchorage. Only columnar cells are shed into
bronchial lavage fluid. The epithelium is more fragile in asthma and more cells are lost in clusters. Desmosomes
appear to be the major structural adhesion mechanism at the plane of cleavage between the columnar
cells and the basal cells. The as- and 134-integrins, which contribute to hemidesmosomes and anchor
cells to the underlying basement membrane, are expressed solely by basal cells. The apical aspects of
the columnar cells are sealed by tight and intermediate junctions. There is constitutive expression of ICAM-1
and E-selectin in the vasculature of the bronchial mucosa, and ICAM is also present within the epithelium.
These findings indicate that the bronchial epithelium is a complex structure that, as a mucosal surface,
has constitutive expression of inflammatory cell adhesion molecules to serve normal leukocyte traffic.peer-reviewe
The site of disruption of the bronchial epithelium in asthmatic and non-asthmatic subjects
Attention has recently
been focused on the basal cells of the
tracheobronchial epithelium as the
mechanism of anchorage of the tall
columnar cells, which themselves do not
appear to form hemidesmosomes with
the basement membrane of the epithelium.
Residual basal cells have been described
as remaining attached to the
basement membrane after epithelial
denudation. This led this group to formulate
the hypothesis that there may be
a potential plane of cleavage between the
basal cells and the overlying columnar
cell layer within the bronchial epithelium,
which becomes disrupted in
asthma.peer-reviewe
University Band Symphonic Band
Braden Auditorium Wednesday Evening April 22, 1998 8:00p.m
University Band Symphonic Band Symphonic Winds
Braden Auditorium Thursday Evening November 19, 1998 7:30p.m
Symphonic Band University Band
Braden Auditorium Thursday Evening November 20, 1997 8:00 p.m
University Band Symphonic Band
Braden Auditorium Thursday Evening April 29, 1999 8:00p.m
Transforming growth factor-beta promotes rhinovirus replication in bronchial epithelial cells by suppressing the innate immune response
Rhinovirus (RV) infection is a major cause of asthma exacerbations which may be due to a deficient innate immune response in the bronchial epithelium. We hypothesized that the pleiotropic cytokine, TGF-?, influences interferon (IFN) production by primary bronchial epithelial cells (PBECs) following RV infection. Exogenous TGF-?(2) increased RV replication and decreased IFN protein secretion in response to RV or double-stranded RNA (dsRNA). Conversely, neutralizing TGF-? antibodies decreased RV replication and increased IFN expression in response to RV or dsRNA. Endogenous TGF-?(2) levels were higher in conditioned media of PBECs from asthmatic donors and the suppressive effect of anti-TGF-? on RV replication was significantly greater in these cells. Basal SMAD-2 activation was reduced when asthmatic PBECs were treated with anti-TGF-? and this was accompanied by suppression of SOCS-1 and SOCS-3 expression. Our results suggest that endogenous TGF-? contributes to a suppressed IFN response to RV infection possibly via SOCS-1 and SOCS-3
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