Effects of interaction between Escherichia coli verotoxin and lipopolysaccharide on cytokine induction and lethality in mice.
In Escherichia coli 0157 infections, verotoxins (VT) play a critical role in causing the disease, although other factors such as lipopolysaccharide (LPS) and inflammatory cytokines may affect the progression and course of the disease. The present study examined the roles of VT and LPS in induction of serum cytokines and lethality in mice. LD50 of VT2 (13 ng) was c. 10(4)-fold smaller than that of LPS (400 microg). Although the lethal toxicity of these toxins was examined in several experimental conditions, such as VT2 (5, 10, 20, 40 ng/mouse) alone or in combination with LPS (100 microg/mouse) at various times (-2 days to +2 days), no evidence of synergy was observed. VT2 did not augment LPS-induced tumour necrosis factor-alpha (TNF-alpha) or interleukin-6 production, and conversely suppressed TNF-alpha production when it was injected 2 days before LPS challenge. The data failed to indicate either synergic or additive effects of VT and LPS on cytokine production or lethality in mice. In contrast, antagonistic interactions were clearly observed in cytokine production in certain conditions. The results suggested that these toxins may be co-operatively involvedin the pathology of VT-related diseases, but not through synergic interactions.
Suzuki
Kuri
K
Tateda
Kazuhiro
K
First Department of Urology and Departments of *Microbiology and ‡Pathology, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540 and †Denkaseiken Co. Ltd. Gosenshi, Minami-motomachi 1-2-2, Niigata 959-16, Japan.
Matsumoto
Tetsuya
T
First Department of Urology and Departments of *Microbiology and ‡Pathology, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540 and †Denkaseiken Co. Ltd. Gosenshi, Minami-motomachi 1-2-2, Niigata 959-16, Japan.
Gondaira
Fumio
F
First Department of Urology and Departments of *Microbiology and ‡Pathology, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540 and †Denkaseiken Co. Ltd. Gosenshi, Minami-motomachi 1-2-2, Niigata 959-16, Japan.
Tsujimoto
Shirou
S
First Department of Urology and Departments of *Microbiology and ‡Pathology, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540 and †Denkaseiken Co. Ltd. Gosenshi, Minami-motomachi 1-2-2, Niigata 959-16, Japan.
Yamaguchi
Keizo
K
First Department of Urology and Departments of *Microbiology and ‡Pathology, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540 and †Denkaseiken Co. Ltd. Gosenshi, Minami-motomachi 1-2-2, Niigata 959-16, Japan.
D000818:Animals; D001427:Bacterial Toxins / Q000276:immunology*; D003106:Colon / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D004927:Escherichia coli Infections / Q000097:blood / Q000276:immunology*; D019453:Escherichia coli O157 / Q000472:pathogenicity*; D005786:Gene Expression Regulation; D006651:Histocytochemistry; D007375:Interleukin-1 / Q000096:biosynthesis / Q000097:blood; D015850:Interleukin-6 / Q000096:biosynthesis / Q000097:blood; D007668:Kidney / Q000473:pathology; D007928:Lethal Dose 50; D008070:Lipopolysaccharides / Q000276:immunology*; D008099:Liver / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D022641:Shiga Toxin 2; D013047:Specific Pathogen-Free Organisms; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis
D001427:Bacterial Toxins; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D022641:Shiga Toxin 2; D014409:Tumor Necrosis Factor-alpha