Article
reference:
H.J. Bootsma, M. Egmont-Petersen, P.W.M. Hermans. "Transcriptional response to pneumococcal adherence," Infection and Immunity, Vol. 75, No. 11, pp. 5489-5499, 2007.
Abstract:
Infection of the human host by Streptococcus pneumoniae begins with
colonization of the nasopharynx, which is mediated by adherence of
bacteria to respiratory epithelium. Several studies have indicated
an important role for the pneumococcal capsule in this process.
Here, we used microarrays to characterize the in vitro transcriptional
response of human nasopharyngeal epithelial Detroit 562 cells to
adherence of serotype 2-encapsulated strain D39, serotype
19F-encapsulated strain G54, serotype 4-encapsulated strain TIGR4,
and their nonencapsulated derivatives (delta-cps). In total, 322 genes
were found to be upregulated in response to adherent pneumococci.
Twenty-two genes were commonly induced, including those encoding
several cytokines (e.g., IL-1Beta, IL-6), chemokines (e.g., IL-8,
CXCL1/2), and transcriptional regulators (e.g., FOS), consistent
with an innate immune response mediated by Toll-like receptor
signaling. Interestingly, 85% of genes were induced specifically
by one or more encapsulated strains, suggestive of a capsule-dependent
response, although purified type 2 polysaccharides alone had no effect.
Over a third of these loci encoded products predicted to be involved
in transcriptional regulation and signal transduction, in particular
the MAPK signaling pathways. Real-time PCR of a subset of ten genes
confirmed microarray data and showed a time-dependent upregulation
of especially innate immunity genes. Downregulation of epithelial
genes was most pronounced upon adherent D39Deltacps, as 68% of the 161
genes identified was only repressed using this nonencapsulated
strain. In conclusion, we identified a subset of host genes
specifically induced by encapsulated strains during in vitro
adherence, underlining the complexity of interactions occurring
during the initial stages of pneumococcal infection.
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