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A Bacterial Oral Feeding Assay with Antibiotic-Treated Mosquitoes
Published on: September 12, 2020
Probiotic supplementation restores normal microbiota composition and function in antibiotic-treated and in
Katri Korpela1,2, Anne Salonen3, Outi Vepsäläinen4
1Immunobiology Research Programme, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland. katri.korpela@helsinki.fi.
Insights
Probiotic supplementation can help restore infant gut microbiota disrupted by antibiotics or C-section birth. This intervention, especially with breastfeeding, corrects microbial imbalances and supports infant health.
Area of Science:
- Microbiome research
- Infant health
- Probiotics and immunology
Background:
- Caesarean birth and antibiotic use in infancy disrupt gut microbiota.
- Microbiota disruption is linked to increased risk of metabolic, inflammatory, and immunological diseases.
- Early life gut microbiota development is critical for long-term health.
Purpose of the Study:
- To investigate if probiotic supplementation can counteract negative effects of antibiotic use or caesarean birth on infant gut microbiota.
- To assess the impact of a specific multispecies probiotic on infant microbiota composition and function.
Main Methods:
- Double-blind, placebo-controlled randomized clinical trial.
- Mothers received probiotics or placebo during pregnancy; infants received the same supplement.
- Infant fecal samples analyzed at 3 months using taxonomic, metagenomic, and metaproteomic methods.
Main Results:
- Probiotic supplementation significantly impacted microbiota composition, with effects varying by infant diet.
- Breastfed infants receiving probiotics showed increased Bifidobacteria and reduced Proteobacteria/Clostridia.
- In the probiotic group, negative effects of antibiotics and birth mode on microbiota were reduced or eliminated.
Conclusions:
- Probiotic mixtures can correct adverse microbiota changes induced by antibiotics or caesarean birth.
- Combined probiotic supplementation and breastfeeding are effective in restoring infant gut microbiota.
- This approach supports healthy microbial development and may mitigate associated disease risks.
Background:
Infants born by caesarean section or receiving antibiotics are at increased risk of developing metabolic, inflammatory and immunological diseases, potentially due to disruption of normal gut microbiota at a critical developmental time window. We investigated whether probiotic supplementation could ameliorate the effects of antibiotic use or caesarean birth on infant microbiota in a double blind, placebo-controlled randomized clinical trial. Mothers were given a multispecies probiotic, consisting of Bifidobacterium breve Bb99 (Bp99 2 × 108 cfu) Propionibacterium freundenreichii subsp. shermanii JS (2 × 109cfu), Lactobacillus rhamnosus Lc705 (5 × 109 cfu) and Lactobacillus rhamnosus GG (5 × 109 cfu) (N = 168 breastfed and 31 formula-fed), or placebo supplement (N = 201 breastfed and 22 formula-fed) during pregnancy, and the infants were given the same supplement. Faecal samples of the infants were collected at 3 months and analyzed using taxonomic, metagenomic and metaproteomic approaches.
Results:
The probiotic supplement had a strong overall impact on the microbiota composition, but the effect depended on the infant's diet. Only breastfed infants showed the expected increase in bifidobacteria and reduction in Proteobacteria and Clostridia. In the placebo group, both birth mode and antibiotic use were significantly associated with altered microbiota composition and function, particularly reduced Bifidobacterium abundance. In the probiotic group, the effects of antibiotics and birth mode were either completely eliminated or reduced.
Conclusions:
The results indicate that it is possible to correct undesired changes in microbiota composition and function caused by antibiotic treatments or caesarean birth by supplementing infants with a probiotic mixture together with at least partial breastfeeding.
Trial Registration:
clinicaltrials.gov NCT00298337 . Registered March 2, 2006.
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