High-Level Ciprofloxacin-Resistant Campylobacter jejuni Isolates Circulating in Humans and Animals in Incheon, Republic of Korea.

Campylobacter jejuni is one of the major causative pathogens of outbreaks or sporadic cases of diarrhoeal diseases worldwide. In this study, we compared the phenotypic and genetic characteristics of C. jejuni isolates of human and food-producing animal origins in Korea and examined the genetic relatedness between these two groups of isolates. Regardless of isolation source, all C. jejuni isolates harboured four virulence genes, cadF, cdtB, ciaB and racR, whereas the wlaN and virB11 genes were more frequently observed in human isolates. Antimicrobial susceptibility testing showed that the majority of C. jejuni isolates displayed high-level resistance to fluoroquinolone (95.2%) or tetracycline (76.2%) antibiotics, and 12.4% of isolates exhibited multidrug resistance (more than three classes of antibiotics tested). Pulsed-field gel electrophoresis (PFGE) of all Campylobacter isolates revealed 51 different SmaI-PFGE patterns and six major clusters containing both human and animal isolates. These results indicate that genetically diverse strains of C. jejuni with antimicrobial drug-resistance and virulence properties have prevailed in Incheon. Nevertheless, some particular populations continue to circulate within the community, providing the evidence for an epidemiological link of C. jejuni infections between humans and food-producing animals. Therefore, the continued monitoring and surveillance of C. jejuni isolates of human and food-producing animal origins are required for public health and food safety.

TCDD-up-regulation of IGFBP-6 and IL-5R alpha subunit genes in vivo and in vitro.

Although the potent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been well known for its immunosuppressive activity, the mechanisms of its action have been difficult to elucidate. This is partly due to its inability to exert its effects in vitro. To further elucidate the underlying mechanisms of TCDD effects, we screened for genes that are regulated by the in vivo TCDD treatment of mice that are challenged with allogeneic tumor cells. RNA, collected from lymphoid organs including the thymus, draining lymph nodes, and bone marrow, was reverse-transcribed to cDNA and hybridized to DNA arrays that consisted of 588 genes (ClonTech, USA). The expression of the NF-kappaB p65, c-jun, and p27(Kip1) genes was increased by the TCDD treatment, as previously reported. In addition, we found that the expression of several genes, which were not reported as regulated by TCDD, were modulated by TCDD. Some genes, including insulin-like growth factor-binding protein-6 (IGFBP-6) and IL-5R alpha, were upregulated; while other genes, including CD14, were down-regulated. The expression of the IGFBP-6 and IL-5R alpha subunit genes by TCDD in the thymus was confirmed by RT-PCR and Western blot analyses. Furthermore, TCDD effects on the expression of the IGFBP-6 gene was also observed with EL4 mouse thymoma cells. This suggests that IGFBP-6 may be involved in thymic atrophy, and EL4 cells may be used as an in vitro model for studying molecular mechanisms of thymic atrophy.