Inhibitory effect of Lactobacillus plantarum K-1 on passive cutaneous anaphylaxis reaction and scratching behavior in mice

Lactobacillus plantarum K-1 (LP) inhibiting AP-1 (c-Jun) and NF-κB activations was isolated from kimchi, and its inhibitory activity against scratching behavior and passive cutaneous anaphylaxis reaction in mice was investigated. Heat-inactivated LP (heated at 60°C for 30 min) potently inhibited the...

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Veröffentlicht in:Archives of pharmacal research 2011, 34(12), , pp.2117-2123
Hauptverfasser: Jang, Se-Eun, Trinh, Hien-Trung, Chung, Yong-Hyun, Han, Myung Joo, Kim, Dong-Hyun
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Sprache:eng
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Zusammenfassung:Lactobacillus plantarum K-1 (LP) inhibiting AP-1 (c-Jun) and NF-κB activations was isolated from kimchi, and its inhibitory activity against scratching behavior and passive cutaneous anaphylaxis reaction in mice was investigated. Heat-inactivated LP (heated at 60°C for 30 min) potently inhibited the expression of TNF-α and IL-4 as well as the activation of their transcription factors, NF-κB and c-jun, in phorbol 12′-myristate 13′-acetate-stimulated RBL-2H3 cells. LP (1 ×10 10 CFU per mouse) showed a potent inhibition against passive cutaneous anaphylaxis reaction induced by the IgE-antigen complex in mice, inhibiting it by 87.5%. LP (1 × 10 10 CFU/mouse) inhibited histamine-induced scratching behavior by 58.9% compared to the control group. LP significantly inhibited vascular permeability induced by histamine. The inhibitory activity of LP against vascular permeability was in proportion to its inhibition against scratching behavior. LP potently inhibited histamine-induced cytokine production: it (1 × 10 10 CFU per mouse) inhibited IL-4, IL-1β, and TNF-α expression by 88.9%, 88.6%, and 98.9%, respectively. LP also inhibited IgE level increased by histamine by 85.3%. It inhibited histamine-induced the activations of their transcription factors, NF-κB and c-Jun. Based on these findings, LP may improve allergic diseases, such as anaphylaxis, atopic dermatitis, rhinitis, and pruritus by inhibiting the expression of IgE-switching cytokine IL-4 and proinflammatory cytokines IL-1β and TNF-α via NF-κB and AP-1 signaling pathways.
ISSN:0253-6269
1976-3786
DOI:10.1007/s12272-011-1215-8