Yersinia pseudotuberculosis infection in children, resembling Izumi fever and Kawasaki syndrome

Sato, Koichiro; Ouchi, Kazunobu; Taki, Masashi

doi:10.1097/00006454-198303000-00011

Cited by 98 publications

(55 citation statements)

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“…There is still controversy regarding the exact cause of KD (bacterial superantigens, conventional bacterial antigens or other antigens) [23][24][25][26]46], and we do not conclude that bacterial superantigens are the cause of KD. However, the results of the present study suggest that while antigen-and cytokineneutralizing antibodies in PHIG may be partly responsible for the effect of PHIG on KD, the inhibitory effect of PHIG on IL-12 production and other proinflammatory cytokine production can be one of the important mechanisms of the therapeutic effect of PHIG.…”

Section: Discussionmentioning

confidence: 82%

“…Although the aetiology is still unknown, the possibility that bacteria, their components and bacterial superantigens of staphylococcus or streptococcus, are involved in this disease has been considered [23][24][25]. Bacterial superantigeninduced toxic shock syndrome mimics KD in some aspects and some patients with infective enteritis due to Yersinia pseudotuberculosis meet the diagnostic criteria of KD [26]. No specific virus has been identified in KD patients; instead, marked granulocytosis, which is not usually seen in viral infections, is observed in KD.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of IL-12 synthesis of peripheral blood mononuclear cells (PBMC) stimulated with a bacterial superantigen by pooled human immunoglobulin: implications for its effect on Kawasaki disease (KD)

Takata

Seki²,

Dobashi

et al. 1998

Clinical and Experimental Immunology

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SUMMARYThe aim of this study was to further assess the role of pooled human immunoglobulin (PHIG) on cytokine production from PBMC stimulated with a bacterial superantigen. Human PBMC were cultured with Streptococcus pyrogenic exotoxin A (SPE-A) with or without PHIG and several proinflammatory cytokine levels of culture supernatants were measured. Serum cytokine levels of KD patients before and after PHIG therapy were also examined. PHIG greatly reduced the production of IL-12, interferongamma (IFN-g) and other cytokines from SPE-A-stimulated PBMC, while exogenous IL-12, but neither IL-1 nor tumour necrosis factor-alpha (TNF-a), restored IFN-g production inhibited by PHIG. Although PHIG partially adsorbed SPE-A, its inhibitory effect on cytokine production was not played by anti-SPE-A antibody. Although purified CD4þ T cells cultured with human HLA-DR-transfected mouse L cells and SPE-A could not effectively produce IFN-g, they produced large amounts of IFN-g if exogenous IL-12 was introduced. KD patients in the acute phase had higher levels of serum IFN-g than did controls and patients with bacterial infection. Although IL-12 levels of children with or without KD were not significantly different, IL-12 levels of children were much higher than those of adults. However, serum levels of IL-12 of KD patients were transiently but significantly decreased by PHIG therapy and IFN-g amounts subsequently reverted to basal levels thereafter. These findings indicate that PHIG inhibits IL-12 production of SPE-A-activated monocytes and thereby decreases IFN-g synthesis by T cells and suggest that inhibition of IL-12 and IFN-g production is an important part of the mechanisms underlying PHIG therapy on KD.

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Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Inhibition of IL-12 synthesis of peripheral blood mononuclear cells (PBMC) stimulated with a bacterial superantigen by pooled human immunoglobulin: implications for its effect on Kawasaki disease (KD)

Takata

Seki²,

Dobashi

et al. 1998

Clinical and Experimental Immunology

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“…7 There is a strong resemblance between Yersinia infection and KD symptoms, and some patients with Yersinia infection met the criteria for KD and even demonstrate coronary aneurysms. 10,11 However, there is still controversy as to whether Yersinia is the cause of KD. In our study, we found 3 patients with Izumi fever who met the KD criteria.…”

Section: Discussionmentioning

confidence: 99%

Kawasaki Disease Before Kawasaki at Tokyo University Hospital

Shibuya

Kato

et al. 2002

Pediatrics

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“…KD resembles acute streptococcosis (16) in its clinical symptoms and also brings about cardiovascular lesions in 20 to 40% of all patients.…”

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confidence: 99%

Serologic Evidence That Streptococcal Superantigens Are Not Involved in the Pathogenesis of Kawasaki Disease

Morita

Imada

Igarashi

et al. 1997

Microbiology and Immunology

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Kawasaki disease (KD) is an acute multisystem vasculitis of unknown etiology and is associated with marked activation of T cells and monocyte macrophages, leading to the assumption that superantigens are involved in its pathogenesis. To determine if an association exists between streptococcal superantigens and KD, we examined serum antibody responses to superantigens in sera from 50 paired acute and convalescent KD patients using purified recombinant streptococcal superantigens, such as SPEA, SPEC, SSA and MF. We found a very low frequency of detection of anti-superantigen antibodies by ELISA and no marked IgG seroconversion to each superantigen, indicating the absence of a serological relationship between toxin-producing streptococcal infection and the onset of KD.

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Yersinia pseudotuberculosis infection in children, resembling Izumi fever and Kawasaki syndrome

Cited by 98 publications

References 0 publications

Inhibition of IL-12 synthesis of peripheral blood mononuclear cells (PBMC) stimulated with a bacterial superantigen by pooled human immunoglobulin: implications for its effect on Kawasaki disease (KD)

Inhibition of IL-12 synthesis of peripheral blood mononuclear cells (PBMC) stimulated with a bacterial superantigen by pooled human immunoglobulin: implications for its effect on Kawasaki disease (KD)

Kawasaki Disease Before Kawasaki at Tokyo University Hospital

Serologic Evidence That Streptococcal Superantigens Are Not Involved in the Pathogenesis of Kawasaki Disease

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