OM-85 is an immunomodulator of interferon-β production and inflammasome activity.

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6 mars 2017

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info:eu-repo/semantics/altIdentifier/doi/10.1038/srep43844

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info:eu-repo/semantics/altIdentifier/pmid/28262817

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info:eu-repo/semantics/altIdentifier/eissn/2045-2322

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_8B66392D35BF9

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A.T. Dang et al., « OM-85 is an immunomodulator of interferon-β production and inflammasome activity. », Serveur académique Lausannois, ID : 10.1038/srep43844


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The inflammasome-IL-1 axis and type I interferons (IFNs) have been shown to exert protective effects upon respiratory tract infections. Conversely, IL-1 has also been implicated in inflammatory airway pathologies such as asthma and chronic obstructive pulmonary disease (COPD). OM-85 is a bacterial extract with proved efficacy against COPD and recurrent respiratory tract infections, a cause of co-morbidity in asthmatic patients. We therefore asked whether OM-85 affects the above-mentioned innate immune pathways. Here we show that OM-85 induced interferon-β through the Toll-like receptor adaptors Trif and MyD88 in bone marrow-derived dendritic cells. Moreover, it exerted a dual role on IL-1 production; on the one hand, it upregulated proIL-1β and proIL-1α levels in a MyD88-dependent manner without activating the inflammasome. On the other hand, it repressed IL-1β secretion induced by alum, a well-known NLRP3 activator. In vivo, OM-85 diminished the recruitment of inflammatory cells in response to peritoneal alum challenge. Our findings therefore suggest that OM-85 favors a protective primed state, while dampening inflammasome activation in specific conditions. Taken together, these data bring new insights into the mechanisms of OM-85 action on innate immune pathways and suggest potential explanations for its efficacy in the treatment of virus-induced airway diseases.

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