Biology Reference
In-Depth Information
What is Known of Receptor Expression and HRV
Infection of the Airway Epithelium?
The upper airway epithelium (nasal cavities and nasopharynx) is the
major site of HRV replication,
126
but occasionally the lower airways
(tracheobronchial tree) also become infected.
127-130
In any case, no
marked cytopathic effect is observed.
The respiratory epithelium is built from different cell types,
131
pre-
dominantly from ciliated columnar (epithelial) cells (the most abun-
dant) and mucous goblet cells. Both are polarized with an apical and
a basolateral plasma membrane separated by tight junctions. The basal
(short) cells are small and rounded and are in contact with the basal
lamina; they can differentiate into the other cell types.
In bronchial tissue infected
ex vivo
with the major group HRV16,
only a small subset of the epithelial cells shows virus replication.
128
Whether this is related to receptor expression is not clear. The few
data that are available on the expression of ICAM-1 in normal nasal
epithelium
in situ
are contradictory. Whereas in earlier studies ICAM-1
was not found, more recent work demonstrated the presence of the
receptor in both ciliated and basal cells in inferior turbinates.
132
In
nasal polyps and nasopharyngeal lymph nodes, receptor expression is
predominantly restricted to the basal cells and only traces are found
at the ciliated surface of columnar cells. Thus, with increasing differ-
entiation of the basal cells to columnar ciliated cells, expression of
ICAM-1 decreases.
133,134
Using primary cultures of polarized tracheal
epithelial cells, ICAM-1 was found on both the apical and basolateral
plasma membrane, although total expression was low as compared to
HeLa cells.
128,135
Furthermore, when such cells are cultured under
conditions that permit full differentiation into ciliated cells, ICAM-1
expression decreases.
136
However, major group HRVs preferentially
replicate in less differentiated tracheal epithelial cells. These studies
suggest that susceptibility to infection by major group HRVs corre-
lates with the level of ICAM-1 expression. Nevertheless, expression of
ICAM-1 in the nasal epithelium has not been quantified
in situ
and
the polarity of expression is unknown.