Abstract
Among the major enteric pathogens, Campylobacter jejuni is
considered an important source of diarrheal illness in humans.
In contrast to the acute gastroenteritis in humans, C. jejuni
exhibits prolonged cecal colonization at a high level with little
or no pathology in chickens. Although several known virulence
determinants of C. jejuni have been found to be associated
with a higher degree of pathogenesis in humans, to date, little
is known about their functions in the persistent colonization
of chickens. The present study was undertaken to assess the
role of C. jejuni in imparting differential host immune responses
in human and chicken cells. Based on the abundance
of major genes encoding virulence factors (GEVFs), we used
a particular isolate that harbors the cadF, flaA, peb1, racR,
ciaB, cdtB, and hcp genes. This study showed that hypervirulent
C. jejuni isolate that encodes a functional type VI secretion
system (T6SS) has a greater ability to invade and create
characteristic “attaching and effacing” lesions in human
INT407 compared to primary chicken embryo intestinal cells
(CEICs). Furthermore, we demonstrated that the higher bacterial
invasion in human INT407 triggered higher levels of
expression of major proinflammatory cytokines, such as IL-
1β and IL-6, and significant downregulation of IL-17A gene
expression (P ≤ 0.05). The findings of the present study suggest
that the enhanced ability of C. jejuni to invade human
cells is tightly regulated by proinflammatory cytokines in the
gut and possibly holds the keys to the observed differences
in pathogenesis between human and chicken cells.
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