Bee Venom Ameliorates Ovalbumin Induced Allergic Asthma ViaModulating CD4(+)CD25(+) Regulatory T Cells in MiceCytokine, 2012 Oct 30. pii: S1043-4666(12)00722-3Asthma is a potentially life-threatening inflammatorydisease of the lung characterized by the presence of large numbers of CD4(+) Tcells. These cells produce the Th2 and Th17 cytokines that are thought toorchestrate the inflammation associated with asthma. Bee venom (BV) has traditionally been used to relieve painand to treat chronic inflammatory diseases. Recent reports have suggested thatBV might be an effective treatment for allergic diseases. However, there arestill unanswered questions related to the efficacy of BV therapy in treatingasthma and its therapeutic mechanism. In this study, we evaluated whether BV could inhibit asthmaand whether BV inhibition of asthma could be correlated with regulatory T cells(Treg) activity. We found that BV treatment increased Treg populations andsuppressed the production of Th1, Th2 and Th17-related cytokines in an in vitroculture system, including IL2, IL4, and IL17. Interestingly, production ofIL10, an anti-inflammatory cytokine secreted by Tregs, was significantlyaugmented by BV treatment. We next evaluated the effects of BV treatment onallergic asthma in an ovalbumin (OVA)-induced mouse model of allergic asthma.Cellular profiling of the bronchoalveolar lavage (BAL) and histopathologicanalysis demonstrated that peribronchial and perivascular inflammatory cellinfiltrates were significantly lowered following BV treatment. BV alsoameliorated airway hyperresponsiveness, a hallmark symptom of asthma. Inaddition, IL4 and IL13 levels in the BAL fluid were decreased in the BV treatedgroup. Surprisingly, the beneficial effects of BV treatment onasthma were eradicated following Treg depletion by anti-CD25 antibodyinjection, suggesting that the major therapeutic targets of BV were Tregs. These results indicate that BV efficiently diminishesbronchial inflammation in an OVA-induced allergic asthma murine model, and thatthis effect might correlate with Tregs, which play an important role inmaintaining immune homeostasis and suppressing the function of other T cells tolimit the immune response. These results also suggest that BV has potentialtherapeutic value for controlling allergic asthma responses.
19 Kasım 2012 Pazartesi
Bee Venom May Help Control Allergic Asthma
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Bee Venom Ameliorates Ovalbumin Induced Allergic Asthma ViaModulating CD4(+)CD25(+) Regulatory T Cells in MiceCytokine, 2012 Oct 30. pii: S1043-4666(12)00722-3Asthma is a potentially life-threatening inflammatorydisease of the lung characterized by the presence of large numbers of CD4(+) Tcells. These cells produce the Th2 and Th17 cytokines that are thought toorchestrate the inflammation associated with asthma. Bee venom (BV) has traditionally been used to relieve painand to treat chronic inflammatory diseases. Recent reports have suggested thatBV might be an effective treatment for allergic diseases. However, there arestill unanswered questions related to the efficacy of BV therapy in treatingasthma and its therapeutic mechanism. In this study, we evaluated whether BV could inhibit asthmaand whether BV inhibition of asthma could be correlated with regulatory T cells(Treg) activity. We found that BV treatment increased Treg populations andsuppressed the production of Th1, Th2 and Th17-related cytokines in an in vitroculture system, including IL2, IL4, and IL17. Interestingly, production ofIL10, an anti-inflammatory cytokine secreted by Tregs, was significantlyaugmented by BV treatment. We next evaluated the effects of BV treatment onallergic asthma in an ovalbumin (OVA)-induced mouse model of allergic asthma.Cellular profiling of the bronchoalveolar lavage (BAL) and histopathologicanalysis demonstrated that peribronchial and perivascular inflammatory cellinfiltrates were significantly lowered following BV treatment. BV alsoameliorated airway hyperresponsiveness, a hallmark symptom of asthma. Inaddition, IL4 and IL13 levels in the BAL fluid were decreased in the BV treatedgroup. Surprisingly, the beneficial effects of BV treatment onasthma were eradicated following Treg depletion by anti-CD25 antibodyinjection, suggesting that the major therapeutic targets of BV were Tregs. These results indicate that BV efficiently diminishesbronchial inflammation in an OVA-induced allergic asthma murine model, and thatthis effect might correlate with Tregs, which play an important role inmaintaining immune homeostasis and suppressing the function of other T cells tolimit the immune response. These results also suggest that BV has potentialtherapeutic value for controlling allergic asthma responses.
Bee Venom Ameliorates Ovalbumin Induced Allergic Asthma ViaModulating CD4(+)CD25(+) Regulatory T Cells in MiceCytokine, 2012 Oct 30. pii: S1043-4666(12)00722-3Asthma is a potentially life-threatening inflammatorydisease of the lung characterized by the presence of large numbers of CD4(+) Tcells. These cells produce the Th2 and Th17 cytokines that are thought toorchestrate the inflammation associated with asthma. Bee venom (BV) has traditionally been used to relieve painand to treat chronic inflammatory diseases. Recent reports have suggested thatBV might be an effective treatment for allergic diseases. However, there arestill unanswered questions related to the efficacy of BV therapy in treatingasthma and its therapeutic mechanism. In this study, we evaluated whether BV could inhibit asthmaand whether BV inhibition of asthma could be correlated with regulatory T cells(Treg) activity. We found that BV treatment increased Treg populations andsuppressed the production of Th1, Th2 and Th17-related cytokines in an in vitroculture system, including IL2, IL4, and IL17. Interestingly, production ofIL10, an anti-inflammatory cytokine secreted by Tregs, was significantlyaugmented by BV treatment. We next evaluated the effects of BV treatment onallergic asthma in an ovalbumin (OVA)-induced mouse model of allergic asthma.Cellular profiling of the bronchoalveolar lavage (BAL) and histopathologicanalysis demonstrated that peribronchial and perivascular inflammatory cellinfiltrates were significantly lowered following BV treatment. BV alsoameliorated airway hyperresponsiveness, a hallmark symptom of asthma. Inaddition, IL4 and IL13 levels in the BAL fluid were decreased in the BV treatedgroup. Surprisingly, the beneficial effects of BV treatment onasthma were eradicated following Treg depletion by anti-CD25 antibodyinjection, suggesting that the major therapeutic targets of BV were Tregs. These results indicate that BV efficiently diminishesbronchial inflammation in an OVA-induced allergic asthma murine model, and thatthis effect might correlate with Tregs, which play an important role inmaintaining immune homeostasis and suppressing the function of other T cells tolimit the immune response. These results also suggest that BV has potentialtherapeutic value for controlling allergic asthma responses.
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