Effects of probiotics on the enhancement of the innate mucosal immune response against pathogenic bacteria
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Updated: Nov 17, 2025

Investigating the Effects of Probiotics on Pneumococcal Colonization Using an In Vitro Adherence Assay
Published on: April 28, 2014
Andy Darma1, Alpha Fardah Athiyyah1, Reza Gunadi Ranuh1
1Department of Child Health, Dr. Soetomo Hospital, School of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Background And Objectives:
Probiotics have been widely used for host immune system enhancement but with limited knowledge regarding the immunomodulation mechanisms by which they assist the mucosal innate immune response. We investigated the effects of probiotics on the modulation of the innate mucosal immune response particularly in association with Toll-like receptor (TLR)-2, TLR-4 and nuclear factor-kappa B (NF-κB) p65 and p105.
Materials And Methods:
We randomized 24 male BALB/c mice into four groups. Two groups were administered probiotics for 21 consecutive days; one of these groups was challenged with Lipopolysaccharide (LPS) on day 15. The third group was challenged with only LPS. The fourth group remained untreated. All mice were sacrificed after 21 days. An immunohistochemistry procedure on the ileum was performed and monoclonal antibodies specific for TLR-2, TLR-4 and NF-κB p65 and p105 were used for the analysis of innate lymphoid cells.
Results:
In the LPS-only treated group, there was a significant decrease in p105, indicating an alternative transcription pathway for the process of pro-inflammatory cytokine production. In the probiotics-only treated group there was significant enhancement of TLR-2 and TLR-4 and NF-κB p65 and p105. When mice treated with probiotics were exposed to LPS, there was a significant decrease in NF-κB p65 and p105, indicating employment of the classical pathway for pro-inflammatory cytokine production.
Conclusion:
Probiotics can enhance the innate mucosal immune response in healthy mice and can maintain the homeostasis of the gut mucosal immune response against LPS through the activation of the classical NF-κB pathway.
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