Efficacy of oral amphotericin B for refractory atopic dermatitis with specific IgE to Candida albicans and food allergens in sera

Kitamura, Kazuko; Suga, Chizuka; Onuma, Sumi; Kawaguchi, Toshiko; Yamazaki, Fusae; Suguro, Hiroshi; Ikezawa, Zenrō

doi:10.2332/allergolint.46.125

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…9 Moreover, several recent examples have shown that oral administration of antifungal agents to AD patients has displayed therapeutic efficacy with improvement of dermatitis. 4,10,11 To study the pathogenetic roles of C. albicans in these allergic diseases, it is important to analyze the induction process of anti-Candida IgE and/or IgG antibodies in Candida-colonized individuals. However, it is not yet known how specific Candida IgE antibodies are produced in modern human life.…”

Section: Introductionmentioning

confidence: 99%

Production of anti‐Candida antibodies in mice with gut colonization of Candida albicans

Tansho

Abe

Ishibashi

et al. 2004

Mediators of Inflammation

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BACKGROUND: Production of antibodies that are specific for allergens is an important pathological process in inflammatory allergic diseases. These contain the antibodies against antigens of Candida albicans, one of the normal microbial flora in an intestinal tract. We studied the effects of the prednisolone administration on the production of anti-Candida antibodies in the gastrointestinally C. albicans-colonized mice. METHODS AND MATERIALS: BALB/c mice, treated with antibacterial antibiotics to decontaminate indigenous intestinal bacterial flora, were inoculated intragastrically with C. albicans. The mice, in which C. albicans grows intestinally, were administered prednisolone to induce temporary immunosuppression. The Candida growth in their intestinal tract and their antibody response to Candida were examined. RESULTS: Antibiotic treatment allowed establishment of C. albicans gastrointestinal colonization, but did not cause subsequent systemic dissemination of C. albicans in all the animals. When these animals received an additional treatment with prednisolone, they showed a significantly higher population of C. albicans in their feces than those of animals treated with antibiotics alone, and the organisms were recovered even from their kidney. This systemic dissemination by C. albicans appeared to be temporal, because all the mice survived without any symptoms for more than 2 months. Examination of the serum titers of total immunoglobulin (Ig)E antibodies and specific IgE and IgG antibodies against Candida antigens demonstrated that titers of total IgE increased, partially by day 14 and clearly at day 27, in prednisolone-treated Candida-colonized mice. Without prednisolone treatment, an increment of the serum titer was scarcely observed. By day 27, corresponding to the increase of total IgE, the anti-Candida IgE and IgG titer increased in mice of the prednisolone-treated group. CONCLUSION: Administration of prednisolone to Candida-colonized mice can induce production of the IgG, IgE antibodies against Candida antigens, perhaps through temporal systemic dissemination of Candida from the intestinal tract.

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Section: Introductionmentioning

confidence: 99%

Production of anti‐Candida antibodies in mice with gut colonization of Candida albicans

Tansho

Abe

Ishibashi

et al. 2004

Mediators of Inflammation

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“…In AD patients, Th1-type immunity has been shown to shift to Th2-type ( Fig. 1) since the patients immediately react to skin testing using Candida-antigen (Tanaka et al, 1994;Kitamura et al, 1997), and Candida-specific IgE increases with the severity of the symptoms of AD (Tanaka et al, 1994). Specifically, AD patients displayed a significantly lower incidence of positive patch test reactions to C. albicans allergen than the healthy control subjects, and the patients with negative C. albicans patch tests tended to have www.intechopen.com…”

Section: Antigen-specific Inflammation Caused Via Activation Of Antigmentioning

confidence: 99%

“…and Malassezia spp. has been implicated as an exacerbating or intractable factor in the symptoms of AD (Savolainen et al, 1993;Tanaka et al, 1994;Kitamura et al, 1997;Morita et al, 1999;Linder et al, 2000;Faergemann 2002;Kanda et al, 2002;Svejgaard et al, 2004). Candida spp.…”

Section: Antigen-specific Inflammation Caused Via Activation Of Antigmentioning

confidence: 99%

Fungus as an Exacerbating Factor of Atopic Dermatitis, and Control of Fungi for the Remission of the Disease

Nakashima¹,

Niwano²

2012

Atopic Dermatitis - Disease Etiology and Clinical Management

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An Assessment of the Role of Candida albicans Antigen in Atopic Dermatitis

Morita¹,

Hide²,

Yoneya

et al. 1999

The Journal of Dermatology

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An immediate hypersensitivity reaction to Candida albicans (C. albicans) antigen has been observed in patients with atopic dermatitis. Recent data from a comparative study of the immune response to C. albicans antigen in patients with atopic dermatitis and non-atopics suggest a shift form type 1 helper T cells to type 2 helper T cells in the immune response to C. albicans antigen in atopic dermatitis. To delineate the role of C. albicans in the pathogenesis in atopic dermatitis, we evaluated skin reaction of C. albicans antigen, as well as the serum IgE antibody level against C. albicans in patients with atopic dermatitis, patients with nasal allergy, and non-atopics. In addition, the clinical effect of antifungal drugs was evaluated in the patients with atopic dermatitis. As a result, we found that immediate hypersensitivity to C. albicans antigen is strongly correlated with the patients with atopic dermatitis. On the other hand, the delayed-type hypersensitivity to this antigen, which is highly prevalent in atopics without dermatitis as well as non-atopics, was reduced in most of these patients. Antifungal drugs markedly improved the skin manifestations in patients with atopic dermatitis that have IgE antibodies against C. albicans, and the serum IgE levels also decreased. These results suggest that C. albicans antigen is a potent intrinsic factor in inducing skin lesions in atopic dermatitis because of IgE-mediated hypersensitivity of C. albicans antigen.

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Efficacy of oral amphotericin B for refractory atopic dermatitis with specific IgE to Candida albicans and food allergens in sera

Cited by 3 publications

References 9 publications

Production of anti‐Candida antibodies in mice with gut colonization of Candida albicans

Production of anti‐Candida antibodies in mice with gut colonization of Candida albicans

Fungus as an Exacerbating Factor of Atopic Dermatitis, and Control of Fungi for the Remission of the Disease

An Assessment of the Role of Candida albicans Antigen in Atopic Dermatitis

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