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Broncho‐Vaxom® (OM‐85 BV) soluble components stimulate sinonasal innate immunity
Author(s) -
Triantafillou Vasiliki,
Workman Alan D.,
Patel Neil N.,
Maina Ivy W.,
Tong Charles C. L.,
Kuan Edward C.,
Kennedy David W.,
Palmer James N.,
Adappa Nithin D.,
WaizelHaiat Salomon,
Cohen Noam A.
Publication year - 2019
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.22276
Subject(s) - medicine , innate immune system , respiratory system , receptor , immunostimulant , stimulation , nitric oxide , immunology , respiratory tract , immunity , pharmacology , microbiology and biotechnology , immune system , biology
Background Broncho‐Vaxom® (OM‐85 BV) is an extract of infectious respiratory bacteria that is used as an immunostimulant outside of the United States for the prevention and treatment of bronchitis and rhinosinusitis. Prior studies have shown that use of OM‐85 BV is associated with reduction in frequency of respiratory infection and decreased duration of antibiotic usage. However, the effects of OM‐85 BV on respiratory mucosal innate immunity are unknown. Methods Human sinonasal epithelial cells were grown at an air‐liquid interface (ALI). Ciliary beat frequency (CBF) and nitric oxide (NO) production in response to stimulation with OM‐85 BV was measured in vitro. Pharmacologic inhibitors of bitter taste receptor (T2R) signaling were used to determine if this pathway was taste‐receptor–mediated. Results Apical application of OM‐85 BV resulted in an NO‐mediated increase in CBF ( p  < 0.05) and increased NO production ( p  < 0.0001) when compared to saline‐stimulated control cultures. ALI pretreatment with taste receptor pathway inhibitors blocked OM‐85 BV–induced increases in NO. Conclusion OM‐85 BV has ciliostimulatory and immunogenic properties that may be partially responsible for its observed efficacy as a respiratory therapeutic. These responses were NO‐dependent and consistent with T2R activation. Further work is necessary to elucidate specific component‐receptor signaling relationships.

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