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

J Appl Microbiol. 2024 Feb 1;135(2):lxae018. doi: 10.1093/jambio/lxae018.

Abstract

Aims: 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).

Methods and results: 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 h. Survival and adherence capacity of L. rhamnosus in a NEC environment were 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. Lactobacillus rhamnosus was able to adhere to and colonize WD-NECs prior to the RV-A16 infection. Lactobacillus rhamnosus did not affect shed RV-A16, viral replication, 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.

Conclusions: These findings demonstrate that L. rhamnosus differentially modulates RV-A16-induced innate inflammatory immune responses in primary NECs from healthy adults.

Keywords: human rhinovirus; immunomodulation; inflammation; innate immunity; lactobacilli; nasal epithelium.

MeSH terms

  • Adult
  • Cells, Cultured
  • Chemokines / pharmacology
  • Cytokines
  • Enterovirus Infections*
  • Epithelial Cells
  • Humans
  • Inflammation
  • Inflammation Mediators / pharmacology
  • Lacticaseibacillus rhamnosus*
  • Rhinovirus / physiology

Substances

  • Cytokines
  • Chemokines
  • Inflammation Mediators