Lethal and severe coronary arteritis in DBA/2 mice induced by fungal pathogen, CAWS, Candida albicans water-soluble fraction

Nagi-Miura, Noriko; Harada, Toshie; Shinohara, Hiroyasu; Kurihara, Ken; Adachi, Yoshiyuki; Ishida-Okawara, Akiko; Oharaseki, Toshiaki; Takahashi, Kei; Naoe, Shiro; Suzuki, Kazuo; Ohno, Naohito

doi:10.1016/j.atherosclerosis.2005.08.014

Cited by 49 publications

(52 citation statements)

References 56 publications

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“…The presence of Candida sequences is intriguing in light of murine models of coronary arteritis based on exposure to Candida glucans comprising mannose, β-1,3-glucan and β-1,6-glucan. Vulnerability to disease varies by mouse strain and is associated with elevated levels of IL-6, TNF-α, and IFN-γ (21,22). Similar to KD, vasculitis can be abrogated by use of i.v.…”

Section: Resultsmentioning

confidence: 99%

Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan

Rodó

Curcoll

Robinson

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

183

155

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Evidence indicates that the densely cultivated region of northeastern China acts as a source for the wind-borne agent of Kawasaki disease (KD). KD is an acute, coronary artery vasculitis of young children, and still a medical mystery after more than 40 y. We used residence times from simulations with the flexible particle dispersion model to pinpoint the source region for KD. Simulations were generated from locations spanning Japan from days with either high or low KD incidence. The postepidemic interval and the extreme epidemics (1979, 1982, and 1986) pointed to the same source region. Results suggest a very short incubation period (<24 h) from exposure, thus making an infectious agent unlikely. Sampling campaigns over Japan during the KD season detected major differences in the microbiota of the tropospheric aerosols compared with ground aerosols, with the unexpected finding of the Candida species as the dominant fungus from aloft samples (54% of all fungal strains). These results, consistent with the Candida animal model for KD, provide support for the concept and feasibility of a windborne pathogen. A fungal toxin could be pursued as a possible etiologic agent of KD, consistent with an agricultural source, a short incubation time and synchronized outbreaks. Our study suggests that the causative agent of KD is a preformed toxin or environmental agent rather than an organism requiring replication. We propose a new paradigm whereby an idiosyncratic immune response, influenced by host genetics triggered by an environmental exposure carried on winds, results in the clinical syndrome known as acute KD.northeastern China source | agriculture | heart disease | FLEXPART | cereal croplands

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Section: Resultsmentioning

confidence: 99%

Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan

Rodó

Curcoll

Robinson

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

183

155

View full text Add to dashboard Cite

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“…1 and 2). Analysis of serial sections of the aorta stained with H&E suggested that the vasculitis in CBA/N mice was mild compared with that in DBA/2 mice, because aortic stenosis was mild and no reduction in survival rate was observe after CAWS administration (10,14). Previous studies have shown that elastic fiber injury occurs in the aorta close to the beginning of the coronary artery in mice that develop CAWS-vasculitis (10).…”

Section: Discussionmentioning

confidence: 95%

IL-10 Is a Negative Regulatory Factor of CAWS-Vasculitis in CBA/J Mice as Assessed by Comparison with Bruton’s Tyrosine Kinase-Deficient CBA/N Mice

Miura

Komai²,

Adachi³

et al. 2009

The Journal of Immunology

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Candida albicans water-soluble fraction (CAWS), a mannoprotein-β-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, exhibits vasculitis-inducing activity (CAWS-vasculitis) in mice. The sensitivity to CAWS-vasculitis varies greatly among mouse strains. This study examined the factors contributing to or inhibiting CAWS-vasculitis using CAWS-vasculitis-resistant CBA/J mice and Bruton’s tyrosine kinase-deficient CBA/N mice, which is a CAWS-vasculitis-sensitive strain that has the same origin as CBA/J mice. After stimulation with various kinds of pathogen-associated molecular patterns, the production of inflammatory cytokines IL-6 and IFN-γ was induced in CBA/N mice, whereas that of immunosuppressive IL-10 was induced in CAWS-vasculitis-resistant CBA/J mice. Furthermore, the production of tissue inhibitor of metalloproteinase 1, an endogenous matrix metalloproteinase inhibitor, was observed in CBA/J mice. The results strongly suggest that the difference in the production of these cytokines is closely linked to the development of CAWS-vasculitis.

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“…[7][8][9][10][11][12] An acute lethal reaction occurred within 1 h after the i.v. administration of CAWS to mice, in the form of anaphylactic shock.…”

Section: Discussionmentioning

confidence: 99%

“…CAWS was found to be composed of a mannoprotein-b-glucan complex, to be able to activate limulus G factor, 6) to demonstrate an activating effect on vascular endothelial cells, platelets, and lymphocytes, and to demonstrate vasculitis-inducing activity when administered to mice. [7][8][9][10][11] Moreover, CAWS caused an acute lethal reaction when administered intravenously to mice. The vasculitis was strongly related to the structure of the mannan moiety, and the activity was significantly reduced in the presence of a beta-1,2-linked mannosyl segment which was synthesized under specific conditions.…”

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confidence: 99%

Involvement of Platelet Activating Factor, Histamine and Serotonin in Acute Lethal Shock Induced by Candida albicans Water-Soluble Extracellular Polysaccharide Fraction (CAWS) in Mice

Nagi-Miura

Shingo

Kurihara

et al. 2007

Biological & Pharmaceutical Bulletin

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Patients are becoming increasingly susceptible to infectious diseases. Deep mycoses are grave infections that occur in compromised hosts including patients with hematopoietic malignant diseases such as leukemia and malignant tumors, or AIDS, and continue to be a serious problem despite the availability of advanced medical technology. 1)The fungal cell wall typically contains b-glucans as its main constituent, and b-glucans are detected in the blood of patients with deep mycoses. Measurements of blood b-glucan levels are universally employed for the early diagnosis of deep mycoses. [2][3][4][5] We obtained a water-soluble extracellular polysaccharide fraction (Candida albicans water-soluble fraction: CAWS) in the culture supernatant obtained by culturing Candida spp. in a completely synthetic medium. CAWS was found to be composed of a mannoprotein-b-glucan complex, to be able to activate limulus G factor, 6) to demonstrate an activating effect on vascular endothelial cells, platelets, and lymphocytes, and to demonstrate vasculitis-inducing activity when administered to mice.7-11) Moreover, CAWS caused an acute lethal reaction when administered intravenously to mice. The vasculitis was strongly related to the structure of the mannan moiety, and the activity was significantly reduced in the presence of a beta-1,2-linked mannosyl segment which was synthesized under specific conditions.12) We found that water-soluble fractions derived from other strains of C. albicans and other species including C. parapsilosis and Saccharomyces cerevisiae were also lethal when administered intravenously (i.v.) to mice, suggesting that the toxicity is universal among yeast-like fungi. However, the water-soluble fraction derived from C. albicans strain NBRC 1385 (CAWS) was the most lethal CAWS of these species and strains. In addition, the toxicity varied depending on the strain of mouse.13) These differences among strains are a good example of the genetic background of the host having a remarkable effect on the expression of pathogen-associated molecular patterns (PAMPs). Detailed analyses of the toxicity of CAWS at the molecular level will be useful for the development of therapies against pathogenic fungi.We describe herein the results of our study of the mechanism underlying the acute lethal reaction to CAWS, using various inhibitors. MATERIALS AND METHODS Experimental AnimalsMale C3H/HeN and ICR mice were acquired from Japan SLC. The animals were raised in a specific pathogen-free (SPF) environment. Mice were purchased at 5 weeks of age and used at 6 to 8 weeks of age.Fungi Candida albicans strain NBRC 1385 was acquired from NITE Biological Resource Center on Sabouraud agar medium (Difco, U.S.A.) at 25°C, and sub-cultured once every 3 months.Preparation of the C. albicans Water-Soluble Extracellular Polysaccharide Fraction (CAWS) CAWS was prepared from C. albicans strain NBRC 1385 in accordance with conventional methods.3) The culture was performed in 5 l of C-limiting medium (Sucrose; 10 g, (NH 4 ) 2 SO 4 ; 2 g, KH 2 PO 4 ; 2 g,...

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Lethal and severe coronary arteritis in DBA/2 mice induced by fungal pathogen, CAWS, Candida albicans water-soluble fraction

Cited by 49 publications

References 56 publications

Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan

Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan

IL-10 Is a Negative Regulatory Factor of CAWS-Vasculitis in CBA/J Mice as Assessed by Comparison with Bruton’s Tyrosine Kinase-Deficient CBA/N Mice

Involvement of Platelet Activating Factor, Histamine and Serotonin in Acute Lethal Shock Induced by Candida albicans Water-Soluble Extracellular Polysaccharide Fraction (CAWS) in Mice

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