Lactobacillus rhamnosus dampens cytokine and chemokine secretion from primary human nasal epithelial cells infected with rhinovirus

To investigate the effect of Lactobacillus rhamnosus on viral replication and cellular response to human rhinovirus (HRV) infection including the secretion of antiviral and inflammatory mediators from well-differentiated nasal epithelial cells (WD-NECs). The WD-NECs from healthy adult donors (N = 6) were cultured in vitro, exposed to different strains of L. rhamnosus (D3189, D3160 or LB21), and infected with HRV (RV-A16) after 24 hours. Survival and adherence capacity of L. rhamnosus in a NEC environment was confirmed using CFSE-labelled isolates, immunofluorescent staining and confocal microscopy. Shed virus and viral replication were quantified using TCID50 assays and RT-qPCR, respectively. Cytotoxicity was measured by lactate dehydrogenase (LDH) activity. Pro-inflammatory mediators were measured by multiplex immunoassay, and interferon (IFN)-λ1/3 was measured using a standard ELISA kit. L. rhamnosus was able to adhere to and colonise WD-NECs prior to RV-A16 infection. L. rhamnosus did not affect shed RV-A16, viral replication or RV-A16-induced IFN-λ1/3 production, or LDH release. Pre-exposure to L. rhamnosus, particularly D3189, reduced the secretion of RV-A16-induced pro-inflammatory mediators by WD-NECs. These findings demonstrate that L. rhamnosus differentially modulate RV-A16 induced innate inflammatory immune responses in primary NECs from healthy adults.