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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Thirty-nine human isolates of Campylobacter jejuni obtained
from a national university hospital during 2007–2010 and
38 chicken isolates of C. jejuni were collected from poultry
farms during 2009–2010 in South Korea were used in this
study. Campylobacter genomic species and virulence-associated
genes were identified by PCR. Pulsed-field gel electrophoresis
(PFGE) and multilocus sequence typing (MLST)
were performed to compare their genetic relationships. All
isolates were highly resistant to ciprofloxacin, nalidixic acid,
and tetracycline. Of all isolates tested, over 94% contained
seven virulence associated genes (flaA, cadF, racR, dnaJ, cdtA,
cdtB, and cdtC). All isolates were classified into 39 types by
PFGE clustering with 90% similarity. Some chicken isolates
were incorporated into some PFGE types of human isolates.
MLST analysis for the 39 human isolates and 38 chicken isolates result ed in 14 and 23 sequence types (STs), respectively,
of which 10 STs were new. STs overlapped in both chicken
and human isolates included ST-21, ST-48, ST-50, ST-51,
and ST-354, of which ST-21 was the predominant ST in both
human and chicken isolates. Through combined analysis of
PFGE types and STs, three chicken isolates were clonally related
to the three human isolates associated with food poisoning
(VII-ST-48, XXII-ST-354, and XXVIII-ST-51). They
were derived from geographically same or distinct districts.
Remarkably, clonal spread of food poisoning pathogens between
animals and humans was confirmed by population
genetic analysis. Consequently, contamination of campylobacters
with quinolone resistance and potential virulence genes in poultry production and consumption may increase
the risk of infections in humans.
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