IngredientsBifidobacterium infantis was first formally described by Reuter in 1963 as a distinct species. Subsequently, Bifidobacterium infantis Reuter 1963 (Approved Lists 1980) was reclassified as a later heterotypic synonym of Bifidobacterium longum Reuter 1963 (Approved Lists 1980). A formal proposal was later made to reclassify the three biotypes of Bifidobacterium longum as three subspecies: Bifidobacterium longum subsp. longum subsp. nov., and Bifidobacterium longum subsp. infantis. The organism is therefore most accurately referred to in current scientific literature as Bifidobacterium longum subsp. infantis, though the shorthand B. infantis remains widely used in clinical and research contexts. The type strain is deposited under accession numbers including ATCC 15697, DSM 20088, JCM 1222, and NCTC 11817, among others.
The genus Bifidobacterium comprises Gram-positive, anaerobic, and nonmotile bacteria. Bifidobacteria are Gram-positive, heterofermentative, anaerobic bacteria with a distinctive bifid (i.e., "Y") shape. The mole percentage of G+C bases of the DNA of the genus Bifidobacterium is 58 for human-type strains, and the rest of the species have a mole percentage of G+C ranging between 55 and 66.
B. longum subsp. infantis (BI) and B. longum subsp. longum (BL) are dominant early colonizers of the infant gut and play important roles in carbohydrate metabolism and immunostimulation, making them key candidates for infant probiotics, particularly in at-risk settings. Yet BI remains classified as a BL subspecies in most taxonomies, and widely used metagenomic databases and pipelines aggregate BI and BL into a single "B. infantis-longum complex" (BIL), obscuring species-level patterns in clinical and population studies.
B. infantis is one of a few microorganisms capable of metabolizing human breast milk and is a pioneer colonizer in the guts of breastfed infants. Bifidobacterium longum subsp. infantis is a subspecies of Bifidobacterium that is predominantly found in the stools of breast-fed infants and is characterized by a bacillar form. Bifidobacteria were first identified in the feces of breastfed infants by Henry Tissier at the Pasteur Institute in 1900.
The extensive metabolic adaptation of B. infantis to non-industrialized diets is consistent with its near-exclusive distribution in low- and middle-income countries. Geo-specific lineages carry distinct metabolic signatures for local dietary substrates, including plant glycans, lipids, and micronutrients characteristic of traditional diets in sub-Saharan Africa and South Asia, supporting the view that B. infantis has historically been a dominant early-life Bifidobacterium. However, B. infantis is now rarely observed in highly industrialized high-income countries, particularly in the first months of life, despite broadly similar breastfeeding rates.
Two strains have received by far the greatest clinical and commercial attention: EVC001 (formerly known as Evolve BioSystems strain, ATCC SD-7035) and 35624 (marketed under various trade names for adults). B. infantis is frequently used as a targeted probiotic supplement for both infants and adults, with specific well-studied strains such as B. longum subsp. infantis EVC001 and 35624 commercially available. The supplement is administered in various forms, including powdered sachets or oil-based drops, which can be mixed with human milk or formula, and for infants it is typically given early in life to establish the proper microbial community structure.
B. infantis EVC001 has been delivered in clinical trials as 156 mg of live bacteria (1.8 × 1010 CFU) diluted in 469 mg of lactose as an excipient; mothers were instructed to mix the powder with 5 mL of expressed breast milk and feed the mixture to their infant using a feeding syringe, with the probiotic stored at −20 °C during the study.
Since originally isolated in 1899, the genus Bifidobacterium has been demonstrated to predominate in the gut microbiota of breastfed infants and to benefit the host by accelerating maturation of the immune response, balancing the immune system to suppress inflammation, improving intestinal barrier function, and increasing acetate production. The bifidogenic impact of human milk was first observed by the eminent Dr. Paul György, whose pioneering work on human milk led to his discovery of a "bifidus factor" in human milk — that is, human milk oligosaccharides (HMOs) and HMOs bound to glycoprotein.
Historically, bifidobacteria were the dominant intestinal bacteria in breastfed infants, and while still abundant in infants in developing nations, levels of intestinal bifidobacteria are low among infants in developed nations. The recognition that the composition of early-life gut microbiota was deeply influenced by breastfeeding and environment guided subsequent decades of probiotic research.
The pattern of near-absence in highly industrialized countries suggests that lifestyle changes associated with industrialization — including earlier weaning, formula use, and antibiotic exposure — have eroded ecological niches that once favored metabolically diverse B. infantis. A study of US children found that only 15 of 203 (7.4%) children under 2 years old harbored B. infantis. This decline has become a subject of significant concern in neonatal and developmental microbiome research.
The most functionally distinctive feature of B. infantis is its uniquely comprehensive capacity to metabolize human milk oligosaccharides (HMOs). HMOs are abundant in breast milk and are thought to act as prebiotics selecting for specific bacterial populations in the infant gut. They are characterized by a lactose molecule at the reducing end to which subunits of lacto-N-biose (LNB; type 1 chain) or N-acetyl-lactosamine (type 2 chain) are attached in tandem, with fucose and sialic acid residues at terminal positions. Over 200 different HMO structures have been determined.
B. longum subsp. infantis is unique among gut microbes in its capacity to transport into its cytoplasm and consume the full range of human milk oligosaccharides. Mechanistically, B. longum subsp. infantis and B. breve import HMOs using ATP-binding cassette (ABC) transporters and then degrade the oligosaccharides taken up to monosaccharides intracellularly. This differs from B. bifidum, which employs membrane-attached glycoside hydrolases to break HMOs down extracellularly prior to import.
The enzyme 1,3-β-Galactosyl-N-acetylhexosamine phosphorylase (GLNBP), which catalyzes the reversible phosphorolysis of galacto-N-biose (GNB) and lacto-N-biose I (LNB), is a key enzyme explaining the metabolism of HMOs. Infant-type bifidobacteria possess the intracellular pathway to specifically metabolize GNB and LNB, known as the GNB/LNB pathway.
B. infantis is uniquely identified by the presence of five HMO-metabolizing gene clusters. The global transcriptional regulation of these pathways has been further characterized: a bioinformatic regulon reconstruction approach has implicated NagR, a transcription factor from the ROK family, as a negative global regulator of gene clusters encoding lacto-N-biose/galacto-N-biose (LNB/GNB), lacto-N-tetraose (LNT), and lacto-N-neotetraose (LNnT) utilization pathways in B. longum subsp. infantis.
B. infantis produces short-chain fatty acids (SCFAs), particularly acetate, which provides an important role in nutrition and intestinal and immune development, facilitates direct binding to intestinal cells, and stimulates anti-inflammatory and inhibits pro-inflammatory cytokine release by intestinal cells. Acetate produced by bacteria acts in vivo to promote the defense functions of host epithelial cells, and acetate produced by B. infantis becomes a carbon source that stimulates the growth and function of butyrate-producing microbes. B. infantis becomes dominant in the gut and reduces pH by its unique ability to metabolize all HMOs into acidic end products, lactate, and acetate.
Characterization of the fecal metabolome of breastfed Bangladeshi infant cohorts revealed higher amounts of the tryptophan metabolite indole-3-lactic acid (ILA) in feces with high levels of B. infantis. ILA is enriched when B. infantis is grown on HMOs, and it acts by inhibiting the release of inflammatory cytokines in intestinal epithelial cells in vitro through the activation of the aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2–related factor 2 (Nrf2)-targeted genes. Through this production of the tryptophan metabolite indole-3-lactic acid, B. infantis improves intestinal barrier integrity. Bifidobacterium-dominant gut enterotypes are associated with reduced levels of inflammatory cytokines and calprotectin, as well as increased production of beneficial tryptophan metabolites, such as ILA.
Natural B. infantis strains show extreme biogeographic stratification and predicted adaptations to local plant-glycan-rich diets and breast-milk-derived substrates, including urea and B vitamins. This metabolic diversity has important implications for the design of infant probiotics, particularly in low- and middle-income country settings. Existing genomic knowledge of the BIL complex is heavily biased, as most reference genomes and probiotic strains derive from a small number of historical isolates from high-income countries, with limited representation of naturally circulating strains in low- and middle-income countries.
B. longum subspecies infantis is well adapted to the infant gut and has co-evolved with the mother-infant dyad and gut microbiome, in part due to its ability to consume complex carbohydrates found in human milk. B. infantis and its human host have a symbiotic relationship that protects the preterm or term neonate and nourishes a healthy gut microbiota prior to weaning.
A key Phase I clinical trial (the IMPRINT Study) evaluated the safety and colonization capacity of B. infantis EVC001 in breastfed term infants. The IMPRINT Study was initiated to determine the safety and tolerability of supplementing breastfed infants with B. infantis EVC001; eighty mother-infant dyads were enrolled in either lactation support plus B. infantis supplementation (BiLS) or lactation support alone (LS), with BiLS infants fed 1.8–2.8 × 1010 CFU B. infantis EVC001 daily starting on postnatal day 7. The mean log10 change in fecal Bifidobacterium from Day 6 to Day 28 was significantly higher for BiLS infants compared to LS infants (p = 0.0002).
A follow-up persistence study found strikingly durable colonization. Breastfed infants could be stably colonized at high levels by provision of B. infantis EVC001, with significant changes to the overall microbiome composition persisting more than a month later, whether the infants were born vaginally or by caesarean section. This observation is consistent with previous studies demonstrating the capacity of this subspecies to utilize human milk glycans as a nutrient and underscores the importance of pairing a probiotic organism with a specific substrate. Furthermore, fecal B. infantis was 2.5–3.5 log units higher at 6–12 months in the EVC001-supplemented group compared with the unsupplemented group (P < 0.01), a relationship that strengthened with the exclusion of infants who consumed infant formula and antibiotics.
A clinical study investigated the impact of B. infantis EVC001 colonization on enteric inflammation in exclusively breastfed term infants. Stool samples were collected from infants randomly selected to receive either 1.8 × 1010 CFU B. infantis EVC001 daily for 21 days or breast milk alone (controls), starting at postnatal day 7. Fecal calprotectin concentration negatively correlated with Bifidobacterium abundance (P < 0.0001; ρ = −0.72), and proinflammatory cytokines were significantly lower in EVC001-fed infants on days 40 and 60 postnatally compared with baseline and control infants. These findings indicate that gut dysbiosis (absence of B. infantis) is associated with increased intestinal inflammation, and that early addition of EVC001 to the diet represents a novel strategy to prevent enteric inflammation during a critical developmental phase.
A separate randomized study of B. infantis M-63 confirmed these findings in a different infant cohort. Fecal samples were collected from 111 healthy infants randomly administered 1.0 × 109 CFU of B. infantis M-63 or placebo daily from 7 days to 3 months of age. Administering B. infantis M-63 significantly increased gut Bifidobacterium, while Enterobacteriaceae abundance and proinflammatory cytokine levels decreased. Bifidobacterium-dominant enterotypes were associated with reduced levels of inflammatory cytokines and calprotectin, and increased production of indole-3-lactic acid (ILA). This study provides evidence that supplementation with B. infantis M-63 in infants may significantly reduce inflammation during the critical early postnatal period.
Necrotizing enterocolitis (NEC) is a disease mainly of preterm infants with a 30–50% mortality rate and long-term morbidities for survivors, and treatment strategies have not improved in decades, prompting research into prevention strategies, particularly with probiotics.
A systematic review with meta-analysis was conducted selecting RCTs evaluating probiotics compared to placebo or no treatment in preterm and/or low birth weight infants, analyzing probiotic effects on NEC, late-onset sepsis (LOS), and mortality separately for trials in which the probiotic contained B. infantis and those that did not. 67 RCTs were included (n = 14,606), of which 16 used probiotics containing B. infantis. Meta-analysis of all RCTs indicated that probiotics reduced the risk of NEC, LOS, and mortality.
A nonconcurrent retrospective analysis at a single level IV NICU examined the impact of B. infantis EVC001 specifically. The nonconcurrent retrospective analysis of two cohorts of very low birth weight (VLBW) infants not exposed and exposed to B. infantis EVC001 probiotic at Oregon Health & Science University from 2014 to 2020 reported evidence supporting probiotic use as an effective means of NEC reduction, while emphasizing the challenge of determining optimal strain, formulation, dosing, duration, and target population.
The mechanistic basis has been partly explored in animal models. Administration of B. infantis significantly reduced the incidence of NEC in a rat model, decreased expression of pro-inflammatory cytokines including IL-6, Cxcl1, TNFα, IL-23, and iNOS, and decreased expression of the antimicrobial peptides Reg3b and Reg3g. At the cellular level, using secretions from Bifidobacterium longum subsp. infantis, research showed that fetal enterocyte reduction of IL-6 activation after IL-1β stimulation is mediated through Toll-like receptor-4 (TLR-4) and specifically affects IL-1 receptor-associated kinase 2 (IRAK-2) mRNA and c-Jun and c-Fos phosphorylation of the activator-protein 1 (AP-1) transcription factor.
Evidence strength: Meta-analyses of RCTs in preterm infants demonstrate significant reduction in NEC with probiotic supplementation broadly. The evidence specific to B. infantis-containing preparations is promising but the subgroup analysis within broader meta-analyses limits direct attribution; large, adequately powered RCTs using B. infantis alone in extremely preterm populations are still needed. Mechanistic data largely derives from animal models and in vitro systems.
In IBS, patients typically present with significantly lower levels of Bifidobacteria in fecal and duodenal mucosa samples, yet other major bacterial groups remain preserved. This observation stimulated interest in supplementation with B. infantis 35624 for IBS management.
A major multicenter, randomized, double-blind, placebo-controlled trial examined the dose-response of encapsulated B. infantis 35624 in women with IBS. Subjects were randomly allocated to receive either a daily capsule of B. infantis at a dosage of 1 × 106, 1 × 108, or 1 × 1010 CFU, or placebo, for 4 weeks. The authors reported a beneficial treatment effect for B. infantis at a dosage of 1 × 108 CFU, which persisted throughout the subsequent two-week washout period, while dosages of 1 × 106 or 1 × 1010 CFU did not yield significant reductions in abdominal pain. The improvement in global symptom assessment exceeded placebo by more than 20% (p < 0.02).
Evidence suggests that Bifidobacteria supplementation, which serves to restore a balanced microbial composition, modulates immune function, gut microbiota, and intestinal mucosal adhesion in IBS patients, with studies demonstrating positive effects on epithelial cell adherence, reinforcement of tight junctions, stimulation of IgA production, and cell-mediated immunity, which are impaired in IBS patients.
An earlier trial delivered B. infantis through a daily malted milk beverage over 8 weeks. O'Mahony and colleagues investigated the impact of Bifidobacteria infantis on abdominal pain delivered through this vehicle over 8 weeks, with significant time-course improvements observed following treatment, with improvements in abdominal pain evident at week 1, peaking at week 2, with sustained suppression of symptoms up to trial cessation.
Evidence strength: The evidence base for B. infantis 35624 in IBS is among the more robust available in probiotic research, resting on multiple randomized, double-blind, placebo-controlled trials. However, three clinical trials and a simple review have demonstrated improvement in symptoms, although further studies are needed; a guideline and systematic review did not demonstrate superiority in symptomatic relief when compared to other species of probiotics, a meta-analysis did not show the efficacy of the isolated use of Bifidobacterium, and the evidence of an association between supplementation with Bifidobacterium and symptomatic control in patients with IBS is not clear, with some studies seeming to demonstrate benefits in improving symptoms (SORT C).
B. infantis 35624 exerts beneficial immunoregulatory effects by mimicking commensal-immune interactions. In one study, the impact of oral administration of B. infantis 35624 for 6–8 weeks on inflammatory biomarker and plasma cytokine levels was assessed in patients with ulcerative colitis (UC) (n = 22), chronic fatigue syndrome (CFS) (n = 48), and psoriasis (n = 26) in three separate randomized, double-blind, placebo-controlled interventions, with the effect on immunological biomarkers in healthy subjects (n = 22) also assessed. At baseline, both gastrointestinal (UC) and non-gastrointestinal (CFS and psoriasis) patients had significantly increased plasma levels of C-reactive protein (CRP) and the pro-inflammatory cytokines TNF-α and IL-6. The study found reductions in these inflammatory markers following supplementation, representing evidence that B. infantis may modulate systemic inflammatory processes beyond the gastrointestinal tract. This evidence is, however, preliminary — drawn from single, relatively small randomized controlled trials in each condition.
Administration of B. infantis EVC001 is also associated with an increase in intestinal IFNβ, a known inducer of regulatory T cells (Tregs), and supplementation contributes to reducing the amount of virulence factors in the infant gut, restricting the establishment of pathogenic bacterial communities.
Epidemiological associations between early-life B. infantis deficiency and atopic disease have been reported. The most consistent findings from cohort studies include decreased abundance of Bifidobacterium, a commensal bacterium generally present at higher levels in infancy and associated with human milk consumption, in infants with cow's milk allergy and multisensitized atopy, and a decrease in Bifidobacterium abundance between infancy and school age in children who developed peanut allergy. Results from clinical studies suggest potential beneficial effects in populations of children with colic, including improved tolerance and a protective effect against the development of atopic dermatitis.
Evidence strength: The evidence linking B. infantis supplementation to reduced atopic disease risk in humans is largely observational and associational. Clinical intervention data is limited, and most available interventional data involves multi-strain probiotic preparations or other Bifidobacterium species. This remains an active research area warranting appropriately powered prospective trials.
A study supplementing mice with B. infantis 15697 significantly enhanced the synthesis of bile acids, especially tauroursodeoxycholic acid and taurocholic acid, while promoting the growth of probiotics and inhibiting the colonization of antibiotic-resistant bacteria and the spread of antibiotic resistance genes (ARGs). This finding reveals the important role of B. infantis in regulating the gut microbiota and inhibiting the spread of ARGs, and provides a theoretical basis for developing new probiotic intervention strategies. This evidence is currently preclinical (animal model data only).
Dosages vary substantially by indication, strain, and population. The following are derived only from published clinical studies:
In 2007, the European Food Safety Authority (EFSA) assigned qualified presumption of safety (QPS) status to the bacterial species B. longum, which includes subspecies infantis, indicating that this taxonomic group does not raise any safety concerns. The QPS status, which applies to all strains of B. infantis reviewed, indicates that none of those strains have been associated with human clinical disease.
In the IMPRINT Phase I clinical trial, B. infantis EVC001 was found to be well-tolerated and safely consumed by healthy term infants for 21 consecutive days. All adverse events reported by mothers enrolled in the study were typical of infants of that age, and their incidences were not increased by the B. infantis feedings.
Based on available knowledge, B. infantis has not been associated with any reports on antibiotic resistance. This is a relevant safety consideration for any probiotic organism, particularly one used in vulnerable neonatal populations.
The EFSA QPS status indicates that the taxonomic group does not raise any safety concerns, and no strains of B. infantis have been associated with human clinical disease.
The most extensive safety data exists for healthy term and preterm infants, and for adult IBS patients. In the context of extremely premature infants, current recommendations for probiotic supplementation in Sweden and Denmark do not include extremely preterm infants due to lack of evidence in this population, although this young subgroup is notably the most at risk for experiencing adverse outcomes. Ongoing trials such as the PEPS trial aim to address this evidence gap. Immunocompromised individuals have not been specifically studied in the available published trial data for B. infantis, and the general probiotic literature advises caution in such populations, as bacteremia has been rarely reported with probiotic organisms in immunocompromised hosts.
Antibiotic exposure has been shown to reduce Bifidobacterium colonization while enriching mobile antibiotic resistance genes, thereby elevating risks of severe infections in this population. The clinical implication is that concomitant antibiotic administration would be expected to reduce colonization and efficacy of supplemented B. infantis. Consistent with this, the relationship between EVC001 supplementation and persistent colonization strengthened with the exclusion of infants who consumed infant formula and antibiotics.
A notable finding from the colonization literature is that efficacy is dependent on substrate availability. Breastfed infants could be stably colonized at high levels by provision of B. infantis EVC001, and this observation is consistent with studies demonstrating the capacity of this subspecies to utilize human milk glycans as a nutrient, underscoring the importance of pairing a probiotic organism with a specific substrate. In the absence of human milk-derived HMOs, colonization and persistence of B. infantis are substantially reduced.
Health conditions that Bifidobacterium infantis may help support.
Bifidobacterium infantis 35624 has demonstrated efficacy in alleviating IBS symptoms including abdominal discomfort in RCTs, associated with normalization of anti-inflammatory to pro-inflammatory cytokine ratios. Clinical reports confirm patients receiving B. infantis had less abdominal discomfort versus placebo.
Bifidobacterium infantis NLS super strain was evaluated in a randomized double-blind placebo-controlled trial in active celiac disease patients (Smecuol et al., J Clin Gastroenterol 2013). It has also been studied in a registered ClinicalTrials.gov RCT (NCT03271138) specifically for persistent GI symptoms in CeD patients on GFD. In vitro data support its capacity to reduce gliadin-induced intestinal permeability and inflammatory markers.
Bifidobacterium infantis M-63 was part of a tested Bifidobacterium mixture (BB536, M-63, M-16V) in children with seasonal allergic rhinitis and intermittent asthma, showing improved quality of life. It is one of the dominant bifidobacteria in the infant gut, supporting early immune development, and is linked in clinical and mechanistic literature to allergy risk reduction when present in sufficient abundance in early life.
Bifidobacterium infantis is the preeminent early-life gut colonizer in breastfed infants and is uniquely adapted to metabolize human milk oligosaccharides (HMOs). Clinical evidence supports its use in improving infant gut microbiota, reducing intestinal inflammation markers, and supporting gut barrier development. It is considered a foundational probiotic for infant digestive health.
Bifidobacterium infantis is a dominant bifidobacterium in breastfed infant gut microbiome and is incorporated in pediatric probiotic formulations for immune support. Clinical studies of combinations including B. infantis show reduced rates of respiratory infections in infants and young children. It is part of the ProbioKid® formulation with clinical evidence for URTI prevention in children supplemented for 3–9 months.
Bifidobacterium infantis (B. longum subsp. infantis) has been studied for infantile colic due to its key role in establishing healthy gut microbiota in breastfed infants. Infants with colic show reduced Bifidobacteria, and B. infantis supplementation is studied as a corrective probiotic intervention. Multi-strain probiotic preparations containing B. infantis have demonstrated reductions in colic crying duration.
Bifidobacterium infantis (syn. B. longum subsp. infantis) is a probiotic with documented effects on IBS-C including constipation symptoms. A pivotal multicenter RCT (n=362 IBS patients) of B. infantis 35624 demonstrated significant improvement in bowel movement difficulty and constipation vs. placebo. It is among the Bifidobacterium species included in constipation probiotic systematic reviews.
Bifidobacterium infantis is recognized for its role in gut microbiota modulation in infants and has been studied in the context of reducing diarrhea and gastrointestinal disturbances. It is among the Bifidobacterium species included in broader probiotic reviews demonstrating benefit for diarrhea in children.
Bifidobacterium infantis is a component of the VSL#3 multi-strain probiotic studied in diverticular disease remission trials. As part of multi-strain formulations, B. infantis-containing probiotics have demonstrated maintained remission in diverticular disease over 12-month RCTs.
Bifidobacterium infantis is a predominant strain in healthy breastfed infant gut microbiota and has been studied for its role in preventing food allergy and allergic sensitization. Observational studies link reduced B. infantis abundance to increased food allergy risk. It is included in probiotic interventions evaluated for prevention of atopic disease linked to food sensitivity.
Bifidobacterium infantis (B. longum subsp. infantis) is the dominant probiotic species in breastfed infants, with unparalleled HMO-utilization capacity. It is the subject of extensive clinical research demonstrating its role in establishing a healthy infant gut microbiome and reducing gut dysbiosis linked to inflammatory conditions.
Bifidobacterium infantis has been specifically shown to increase plasma tryptophan levels and influence central serotonin transmission, directly linking it to the gut-brain axis. It is classified as a key psychobiotic strain and has shown anti-inflammatory and mood-modulating effects in IBS and stress research.
Bifidobacterium infantis 35624 suppresses histamine-related allergic symptoms and demonstrates strong anti-inflammatory effects. In combination with B. longum BB536 (Lac-B), it significantly decreased histamine levels and suppressed histidine decarboxylase and H1 receptor gene expression. It belongs to Bifidobacteriaceae, which is more abundant in healthy subjects than HIT patients.
Bifidobacterium infantis 35624 (reclassified as B. longum 35624) is the most studied individual probiotic strain specifically for IBS. A 2025 strain-specific meta-analysis (32 articles) confirmed its efficacy for key IBS symptoms. An 8-week RCT with 75 participants demonstrated significant reductions in pain, discomfort, bloating, and constipation. A landmark RCT confirmed it normalizes the gut IL-10/IL-12 cytokine ratio—a unique mechanistic marker for IBS immune dysregulation.
Bifidobacterium infantis 35624 has been studied specifically in IBD and IBS, demonstrating significant immunomodulatory effects including normalization of the IL-10/IL-12 ratio and reduction of systemic and mucosal inflammatory markers in UC patients in controlled trials.
Bifidobacterium infantis is documented in the female urinary microbiome literature as part of the Bifidobacterium genus relevant to urinary tract health. Its use in urogenital probiotic preparations traditionally derives from its role as a beneficial infant intestinal bacterium with systemic protective properties that extend to urinary flora maintenance via gut-urinary axis modulation.
Body systems that Bifidobacterium infantis may help support.
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