| Summary: | <i>Salmonella</i> Typhimurium (<i>S.</i> Typhimurium) is an aggressive zoonotic pathogen that causes enteritis and diarrhea. Antibiotic therapy is still the primary method at present. However, the increasing emergence of multi-drug resistant bacteria weakens the therapeutic efficacy of antibiotics. Probiotics have been widely studied as an alternative antibiotic therapy. In this study, we established an IPEC-J2 cell model of <i>S.</i> Typhimurium infection, aiming to determine the protective effect of <i>Lactobacillus johnsonii</i> L531 (<i>L. johnsonii</i> L531) on <i>S.</i> Typhimurium infection. As our data showed, <i>S.</i> Typhimurium infection resulted in a robust inflammatory response demonstrated by promoted protein levels of the inflammatory-related pathway (TLR4, MyD88, p-IκBα, and p-p65), increased cytokine levels of IL-6, IL-1β, IL-18, and TNF-α, and activated the NLRP3 inflammasome via promoting its assembly. However, <i>L. johnsonii</i> L531 pre-incubation inhibited the activation of the above inflammatory signaling pathways and reduced the expression levels of pro-inflammatory cytokines. In addition, <i>L. johnsonii</i> L531 alleviated the damage of <i>S.</i> Typhimurium to tight junctions ZO-1, Occludin, and Claudin-1. In summary, our findings suggested that <i>L. johnsonii</i> L531 alleviated <i>S.</i> Typhimurium-induced tight junction injury by inhibiting the TLR4/NF-κB/NLRP3 inflammasome signaling pathway.
|
|---|