Early administration of probiotic Lactobacillus acidophilus and/or prebiotic inulin attenuates pathogen-mediated intestinal inflammation and Smad 7 cell signaling
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Updated: May 23, 2026

Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation
Published on: July 27, 2022
Ondulla T Foye1, I-Fei Huang, Christine C Chiou
1Mucosal Immunology Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Insights
Probiotics and prebiotics reduce gut inflammation in infant mice infected with Citrobacter rodentium. These interventions enhance host immunity by modulating NF-κB and Smad 7 signaling pathways.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Gut-associated immunity immaturity is a key factor in pediatric mortality from enteric infections.
- Enteric pathogens like Citrobacter rodentium pose significant risks to infant health.
- Understanding host-pathogen interactions is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the impact of Lactobacillus acidophilus (probiotic), inulin (prebiotic), and synbiotics on pathogen-induced inflammation in a pediatric enteric disease model.
- To determine the effects of these interventions on NF-κB and Smad 7 signaling pathways.
- To assess the modulation of host immune responses against Citrobacter rodentium infection.
Main Methods:
- A murine model of infantile enteric disease was utilized.
- Newborn mice were administered Lactobacillus acidophilus, inulin, or synbiotics bi-weekly for four weeks.
- Mice were subsequently challenged with Citrobacter rodentium, and intestinal inflammation, bacterial colonization, and signaling pathways (NF-κB, Smad 7, IL-10, TGF-β) were analyzed.
Main Results:
- Probiotic, prebiotic, and synbiotic treatments significantly reduced intestinal inflammation and bacterial colonization post-Citrobacter rodentium challenge.
- Synbiotic treatment enhanced colonic IL-10 and transforming growth factor-β expression and inhibited NF-κB signaling.
- All interventions (synbiotic, probiotic, prebiotic) attenuated Citrobacter rodentium-induced Smad 7 expression.
Conclusions:
- Lactobacillus acidophilus, inulin, and synbiotics show potential in promoting host-protective immunity against enteric infections in infants.
- These interventions may attenuate Citrobacter rodentium-induced intestinal inflammation by modulating NF-κB and Smad 7 signaling.
- The findings support the use of probiotics and prebiotics for managing pediatric enteric diseases.
Abstract:
Immaturity of gut-associated immunity may contribute to pediatric mortality associated with enteric infections. A murine model to parallel infantile enteric disease was used to determine the effects of probiotic, Lactobacillus acidophilus (La), prebiotic, inulin, or both (synbiotic, syn) on pathogen-induced inflammatory responses, NF-κB, and Smad 7 signaling. Newborn mice were inoculated bi-weekly for 4 weeks with La, inulin, or syn and challenged with Citrobacter rodentium (Cr) at 5 weeks. Mouse intestinal epithelial cells (CMT93) were exposed to Cr to determine temporal alterations in NF-Kappa B and Smad 7 levels. Mice with pretreatment of La, inulin, and syn show reduced intestinal inflammation following Cr infection compared with controls, which is associated with significantly reduced bacterial colonization in La, inulin, and syn animals. Our results further show that host defense against Cr infection correlated with enhanced colonic IL-10 and transforming growth factor-β expression and inhibition of NF-κB in syn-treated mice, whereas mice pretreated with syn, La, or inulin had attenuation of Cr-induced Smad 7 expression. There was a temporal Smad 7 and NF-κB intracellular accumulation post-Cr infection and post-tumor necrosis factor stimulation in CMT93 cells. These results, therefore, suggest that probiotic, La, prebiotic inulin, or synbiotic may promote host-protective immunity and attenuate Cr-induced intestinal inflammation through mechanisms affecting NF-κB and Smad 7 signaling.
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