Background:

Azithromycin hydrate is a macrolide antibiotic useful for the treatment of a number of bacterial infections.

Azithromycin (2 μM) augments rhinovirus-induced IFNβ expression in primary bronchial epithelial cells from asthmatics, which is associated with over-expression of RIG-I like receptors and repression of viral replication. Knockdown of MDA5, but not knockdown of RIG-I, diminishes azithromycin (2 μM)-enhanced viral-induced IFNβ expression in asthmatic primary bronchial epithelial cells[1]. Azithromycin specifically reduces MMP-9 mRNA and protein levels without affecting NF-κB in endotoxin-challenged monocytic THP-1 cells[2].

Azithromycin (50 mg/kg) has no effect on bronchoalveolar lavage inflammatory parameters and LDH levels in a mouse model of asthma exacerbation. Azithromycin induces neither general inflammatory parameters nor LDH release in a mouse model of asthma exacerbation, and augments expression of interferon-stimulated genes and the pattern recognition receptor MDA5 but not RIG-I in exacerbating mice[1].

参考文献:
[1]. Menzel M, et al. Azithromycin augments rhinovirus-induced IFNβ via cytosolic MDA5 in experimental models of asthma exacerbation. Oncotarget. 2017 Mar 18.
[2]. Vandooren J, et al. Differential inhibition of activity, activation and gene expression of MMP-9 in THP-1 cells by azithromycin and minocycline versus bortezomib: A comparative study. PLoS One. 2017 Apr 3;12(4):e0174853.