Probiotics for IBD: Evidence-Based Strains, Mechanisms, and How They Support Intestinal Inflammation
A science-backed look at how specific probiotic strains influence gut inflammation, barrier function, and the microbiome in inflammatory bowel disease
Inflammatory bowel disease (IBD) isn't a single condition — it's an umbrella term covering two chronic, relapsing disorders of the gastrointestinal tract: ulcerative colitis (UC) and Crohn's disease (CD). What they share, beyond the fatigue, pain, and unpredictability patients know all too well, is a common biological thread: a disturbed gut microbiome, a compromised intestinal barrier, and a dysregulated immune response that drives ongoing inflammation.
That shared mechanism is precisely why probiotics have attracted so much attention from gastroenterologists and microbiome researchers over the past two decades. If dysbiosis — an imbalance in the gut's microbial community — plays a causative role in IBD, then targeted restoration of beneficial bacteria should be a logical part of the therapeutic conversation. The research supports this logic, though with important nuances worth understanding.
This guide examines what the peer-reviewed evidence actually shows about probiotics and IBD: which strains have the strongest mechanistic and clinical support, how they influence intestinal inflammation at the molecular level, and what to look for when choosing a supplement that reflects the science. For deeper dives into condition-specific evidence, see our detailed guides on probiotics for ulcerative colitis and probiotics for Crohn's disease.
Key Takeaways
- IBD is characterized by microbial dysbiosis. Patients consistently show reduced microbial diversity, depletion of protective bacteria like Faecalibacterium prausnitzii and Bifidobacteria, and expansion of pro-inflammatory species — creating a biological rationale for microbiome-targeted therapy.[1]
- Probiotic evidence is stronger for ulcerative colitis than Crohn's disease. Meta-analyses of randomized controlled trials show consistent benefits for UC in induction and maintenance of remission, while evidence for CD is more mixed and strain-specific.[2]
- Multi-strain formulations combining Lactobacillus and Bifidobacterium species show the most reproducible clinical benefits — modulating gut microbiota, reducing pro-inflammatory cytokines, and improving quality of life scores in IBD patients.[3]
- Short-chain fatty acids (SCFAs) — especially butyrate — are the central metabolic currency linking probiotics, prebiotics, and reduced intestinal inflammation. SCFAs strengthen tight junctions, fuel colonocytes, and regulate immune responses through GPCR signaling.[4]
- Inulin-type fructans produced a 77% clinical response rate in mild-to-moderate UC patients at 15 g/day, driven primarily by increased butyrate production rather than compositional microbiome changes.[5]
- Spore-forming Bacillus strains — including B. coagulans and B. subtilis — have demonstrated reduced intestinal permeability, dampened pro-inflammatory cytokine release, and improved gut microbiome composition in dysbiosis and IBD-like models.[6]
Understanding IBD and the Microbiome Connection
Inflammatory bowel disease affects an estimated 2.4 million Americans, with age- and sex-standardized prevalence of roughly 721 cases per 100,000 population — 378 for ulcerative colitis and 305 for Crohn's disease.[7] The incidence peaks in early adulthood and plateaus through middle age, though pediatric and older-onset cases are increasingly recognized.
Why the Microbiome Matters in IBD
While the precise cause of IBD remains unclear, decades of research converge on a three-part model: genetic susceptibility interacts with environmental triggers and microbial dysbiosis to produce a dysregulated mucosal immune response against the gut's own bacterial residents.[8] In both UC and CD, the gut microbiome shows distinctive patterns that differ measurably from healthy controls.
Patients with IBD tend to show a consistent microbial signature: reduced overall diversity, expansion of Proteobacteria (including adherent-invasive E. coli), decreased Firmicutes, and — critically — depletion of key anti-inflammatory, butyrate-producing species.[8] A meta-analysis of 11 studies involving 1,180 subjects found that Faecalibacterium prausnitzii, one of the most abundant commensals in healthy guts, is significantly reduced in IBD patients compared to healthy controls.[1] This matters because F. prausnitzii produces butyrate and secretes metabolites that block NF-κB activation — one of the master switches of inflammatory gene expression.[9]
Dysbiosis in IBD: What Changes
IBD-associated dysbiosis involves both what's missing and what's overrepresented. Protective species like F. prausnitzii, Roseburia hominis, and certain Bifidobacteria are depleted, while pro-inflammatory taxa — particularly in the Enterobacteriaceae family — expand. The result is less butyrate, more lipopolysaccharide (LPS), a weakened mucus layer, and an immune system that's chronically primed for inflammation. This cycle, known as gut dysbiosis, is both a driver and a consequence of IBD inflammation.
The Barrier Breakdown
Alongside microbial shifts, IBD features a structurally compromised intestinal barrier. Tight junction proteins — claudin-1, occludin, and zonula occludens-1 (ZO-1) — are dysregulated in inflamed tissue, permitting excessive translocation of bacterial products into the lamina propria and bloodstream.[10] This "leaky gut" physiology amplifies immune activation and sustains the inflammatory loop. Understanding this mechanism clarifies why barrier support is a core therapeutic target — one probiotics can directly address, as discussed in our guide to probiotics for leaky gut and barrier repair.
How Probiotics Work in IBD: The Mechanisms
Probiotics don't "treat" IBD in the pharmacological sense — they work by influencing the same biological systems that drive the disease. The mechanisms are multi-layered, interdependent, and backed by both in vitro and clinical research.
1. Microbiota Modulation
Probiotic strains compete with pathogenic bacteria for adhesion sites and nutrients, lowering intestinal pH through lactic acid production and creating a less hospitable environment for pro-inflammatory species.
2. Barrier Enhancement
Specific strains upregulate tight junction proteins (ZO-1, occludin, claudin-1) and stimulate goblet cell MUC2 production, repairing and reinforcing the mucosal barrier.
3. Immune Modulation
Probiotics shift dendritic cell and T-cell populations toward tolerance — promoting regulatory T cells (Tregs), increasing IL-10, and dampening Th17-driven inflammatory cytokines like TNF-α and IL-6.
4. SCFA Production
Probiotic fermentation of dietary fibers yields short-chain fatty acids — butyrate, acetate, and propionate — that fuel colonocytes, tighten junctions, and regulate gene expression.
The SCFA Connection
Short-chain fatty acids sit at the center of this mechanism web. Butyrate, produced when beneficial bacteria ferment prebiotic fibers, is the primary energy source for colonocytes and has been shown in multiple studies to promote tight junction assembly, maintain transepithelial electrical resistance (a measure of barrier integrity), and activate GPR41, GPR43, and GPR109A receptors that modulate immune cell behavior.[4] Fecal SCFA levels are reduced in active IBD, and restoring butyrate production is one of the most validated strategies for calming mucosal inflammation.[11]
For a deeper look at the SCFA pathway and practical ways to increase butyrate production, see our complete guide to increasing butyrate and SCFAs.
Immune Rebalancing
An in vitro study using dendritic cells isolated from IBD patients examined four probiotic strains — Lactobacillus salivarius, Bifidobacterium bifidum, Bacillus coagulans, and Bacillus subtilis natto — and found that all four strains could generate tolerogenic dendritic cells capable of producing anti-inflammatory cytokines.[12] This kind of immune rebalancing is exactly what the dysregulated IBD gut needs: a signal that shifts the immune set-point from "attack" to "tolerate."
Multi-Pathway Support from a Single Formula
Because IBD involves multiple overlapping mechanisms — dysbiosis, barrier damage, immune dysregulation, and reduced SCFA production — strain diversity matters. MicroBiome Restore combines 26 clinically studied strains across the Lactobacillus, Bifidobacterium, and Bacillus genera to address each of these pathways in parallel, rather than relying on any single strain to do all the work.
Evidence-Backed Probiotic Strains for IBD
The clinical literature on probiotics in IBD spans decades and dozens of strains. Below are the species with the strongest published evidence for either UC, CD, or both — and the mechanisms that explain their effects. Each of these strains is included in MicroBiome Restore's 26-strain formula.
Lactobacillus rhamnosus (LGG)
Among probiotic strains, Lactobacillus rhamnosus GG has one of the longest and most detailed research dossiers in gastroenterology. Preclinical work has demonstrated that LGG adheres to colonic mucosa of UC patients both in vitro and in vivo, and reduces the expression of pro-inflammatory cytokines including TNF-α and IL-17.[13] A randomized double-blind clinical trial (LGGinUC) evaluated LGG monotherapy at two doses over one month in UC patients with mild-to-moderate activity on stable mesalamine, assessing clinical, endoscopic, histological, and molecular outcomes.[13]
LGG has also shown adjunctive benefit when combined with IBD oral therapies like mesalamine, and remains one of the most extensively characterized probiotic strains for intestinal mucosal health.[8] Read more about the broader research on L. rhamnosus benefits.
Lactobacillus plantarum
L. plantarum has emerged as one of the most mechanistically interesting probiotics in IBD research. Preclinical studies show that it can restore damaged mucosal barrier function, regulate microbiota imbalance, and reduce symptom scores in colitis models.[14] Mechanistically, L. plantarum preserves intestinal tight junction proteins (claudin-3, occludin, ZO-1), reduces pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), and increases MUC-2 expression — the core structural protein of the protective mucus layer.[15]
Additional research shows L. plantarum downregulates the TLR4/MyD88/NF-κB signaling pathway, one of the primary drivers of colonic inflammation.[16] For a deeper look at its broader clinical profile, see our guide to Lactobacillus plantarum health benefits.
Bifidobacterium infantis
B. infantis has a particularly well-documented role in UC. Levels of this species are strikingly reduced in intestinal tissue from UC patients, and it has demonstrated anti-inflammatory effects through multiple mechanisms — maintaining gut flora balance, modulating immune responses, and producing metabolites that support mucosal repair.[17] A human study tracking B. infantis colonization in UC patients found that the strain survives gastrointestinal transit, colonizes the colon, and can be recovered from biopsies in transverse and descending colon segments — supporting its direct mucosal activity.[18]
Research has also shown that B. infantis may help maintain host genome stability in UC by regulating DNA repair pathways — a particularly relevant mechanism given the elevated colorectal cancer risk in long-standing UC.[17] You can find more clinical context in our article on Bifidobacterium infantis clinical evidence.
Bifidobacterium bifidum and Lactobacillus acidophilus
These two species appear together in several of the most cited IBD probiotic studies. A combination product containing L. acidophilus, B. bifidum, and Streptococcus, administered for two months to UC patients, reduced IL-1β expression while increasing IL-10 and secretory IgA in colonic tissue.[19] In preclinical DSS-colitis models, the combination reduced myeloperoxidase activity (a neutrophil infiltration marker) and suppressed TNF-α, IL-6, and IFN-γ.[20]
Mechanistically, B. bifidum increases epithelial resistance in Caco-2 cell monolayers, reduces LPS-induced colonic damage, enhances regulatory T cell populations, and activates the aryl hydrocarbon receptor — a transcription factor increasingly recognized as central to intestinal immune homeostasis.[21] For more on individual strain benefits, see our guides to Lactobacillus acidophilus and Bifidobacterium lactis.
Bifidobacterium longum and Bifidobacterium breve
A randomized controlled pilot trial of active UC tested a synbiotic containing B. longum with an inulin/FOS prebiotic blend. After the short intervention, sigmoidoscopy scores trended toward improvement, and — more compellingly — mRNA levels of β-defensins 2, 3, and 4 (strongly upregulated in active UC) were significantly reduced, as were TNF-α and IL-1α.[22] Biopsies in the treatment group showed reduced inflammation and regeneration of epithelial tissue.
B. longum's primary metabolites are SCFAs and conjugated linoleic acid (CLA), which contribute to antioxidant activity and regulate reactive oxygen species — both highly relevant in the oxidative-stress-heavy environment of the inflamed colon.[23]
Lactobacillus salivarius
L. salivarius UCC118 has been evaluated in long-term IBD remission maintenance trials, including a 12-month randomized, double-blind, placebo-controlled study in patients with Crohn's disease and ulcerative colitis.[24] Preliminary murine work showed the strain, particularly when combined with B. infantis, reduced disease progression in models of chronic intestinal inflammation. In dendritic-cell studies from IBD patients, L. salivarius was among the strains able to generate tolerogenic immune responses.[12]
Bacillus coagulans, Bacillus subtilis, and Bacillus clausii
Spore-forming Bacillus probiotics offer a distinct advantage: their spores survive stomach acid, bile salts, and heat, germinating in the intestine where they exert their effects.[25] A randomized, double-blind, placebo-controlled trial of B. coagulans Unique IS-2 in adults with IBD receiving standard medical treatment evaluated the strain's effects on gut microbiota composition, serum cytokines, neurotransmitters, and IBD symptoms — representing one of the few direct Bacillus RCTs in IBD patients.[26]
A separate RCT of Bacillus clausii UBBC-07 in UC and CD patients over four weeks showed increased Firmicutes, Lactobacillus, Bifidobacterium, and Faecalibacterium abundance, with a significant rise in anti-inflammatory cytokines and reduction of pro-inflammatory cytokines.[3] And an in vitro gut model study of B. coagulans + B. subtilis showed improved transepithelial resistance (a barrier integrity marker) and reduced NF-κB activity in an IBD-like Caco-2/THP1 co-culture system.[6]
For more on individual Bacillus strain evidence, explore our guides to Bacillus coagulans benefits and Bacillus subtilis clinical research.
| Strain | Primary IBD-Relevant Mechanism | Key Evidence |
|---|---|---|
| L. rhamnosus | Mucosal adhesion; reduces TNF-α, IL-17 | LGGinUC trial; extensive mucosal studies[13] |
| L. plantarum | Tight junction preservation; NF-κB inhibition | Preclinical DSS colitis; MUC-2 upregulation[15] |
| L. acidophilus + B. bifidum | Cytokine rebalancing; IgA support | Reduced IL-1β, increased IL-10 in UC[19] |
| B. infantis | Colonic colonization; genome stability | Mucosal survival in UC; reduced DSBs[17][18] |
| B. longum (+ prebiotic) | Reduces β-defensins, TNF-α, IL-1α | RCT pilot in active UC[22] |
| L. salivarius | Tolerogenic dendritic cell induction | 12-month remission maintenance trial[24] |
| B. coagulans | Barrier integrity; cytokine modulation | RCT in IBD; preclinical synbiotic models[26] |
| B. subtilis | TEER improvement; NF-κB reduction | In vitro IBD-like co-culture model[6] |
| B. clausii | Restores Firmicutes, Lactobacillus, Faecalibacterium | RCT in UC and CD patients[3] |
26 Clinically Studied Strains in One Filler-Free Formula
MicroBiome Restore brings every strain above — plus additional evidence-backed Lactobacillus, Bifidobacterium, and Bacillus species — into a single daily serving at 15 billion CFU. No titanium dioxide, no microcrystalline cellulose, no magnesium stearate.
UC vs. CD: Why Evidence Differs
Meta-analyses have consistently shown that probiotic evidence is more robust for ulcerative colitis than for Crohn's disease. A meta-analysis pooling 18 randomized trials in UC found significant benefits across varied conditions (p = 0.007), while nine CD trials showed a non-significant trend (p = 0.07).[2] The likely explanation is biological: UC inflammation is confined to the colonic mucosa where probiotic strains naturally reside and exert their effects, whereas CD can involve transmural inflammation anywhere from mouth to anus, which is a more challenging target for luminal interventions.
This doesn't mean probiotics are useless in CD — synbiotic combinations (probiotics plus prebiotics) have shown efficacy trends in CD, and individual patients may respond differently based on their specific dysbiosis profile. But it underscores why both conditions deserve their own deeper treatment, which you'll find in our ulcerative colitis and Crohn's disease guides.
The Role of Prebiotics in IBD Support
Probiotics get most of the attention, but in IBD the fermentable fibers that feed those bacteria — prebiotics — arguably matter just as much. The mechanism is direct: prebiotics drive SCFA production, and SCFAs — butyrate in particular — are what actually perform many of the barrier-strengthening and anti-inflammatory functions we've discussed.
The Inulin Evidence
A pilot clinical trial enrolled 25 patients with mild-to-moderately active UC and gave them either 7.5 g or 15 g daily of oligofructose-enriched inulin (an inulin-type fructan) for 9 weeks. The results were striking: 77% of patients in the high-dose group showed a clinical response, compared to 33% in the low-dose group (P = 0.04).[5]
Just as important was what drove the response. The high-dose group showed significantly increased fecal butyrate, and butyrate levels correlated negatively with Mayo clinical score (r = −0.50, P = 0.036) — meaning more butyrate, less disease activity. Interestingly, shifts in microbiota composition did not correlate with improvement. The study concluded that the prebiotic's benefit in UC stemmed from metabolic changes in the existing microbiome rather than from dramatic compositional remodeling.[5]
A broader review of prebiotics in UC reinforces these findings, noting that inulin-type fructans consistently improve clinical activity indices, reduce fecal calprotectin, and increase SCFA production in mild-to-moderate UC patients.[27] Learn more about how Jerusalem artichoke delivers natural inulin-type fructans that support butyrate-producing bacteria.
Why Prebiotic Selection Matters for Sensitive Guts
Not all prebiotic fibers are created equal, especially for people with inflamed or hypersensitive digestive tracts. Highly fermentable FODMAPs can trigger bloating and gas in already-irritated colons. Gentler prebiotics with strong fermentation profiles — like acacia fiber — may be better tolerated during active inflammation while still delivering SCFA-producing benefits. Read more about acacia fiber for sensitive guts.
A Synbiotic Approach by Design
MicroBiome Restore pairs its 26 probiotic strains with 9 organic prebiotics — Jerusalem artichoke (a rich inulin source), acacia fiber, maitake mushroom, fig fruit, and marine botanicals including bladderwrack, Norwegian kelp, and oarweed. This synbiotic design means the beneficial bacteria you're introducing have the metabolic substrate they need to produce SCFAs and colonize effectively — rather than arriving in a gut that can't sustain them.
What to Look for in a Probiotic for IBD
Walking into a supplement aisle, probiotic options run from single-strain capsules at a few billion CFU to proprietary "50-strain" blends without clear labeling. For anyone navigating IBD, the selection criteria matter more than most people realize.
Multi-Strain Diversity Across Genera
The evidence base strongly favors multi-strain formulations combining Lactobacillus and Bifidobacterium species — ideally with the addition of spore-forming Bacillus strains that survive gastric transit reliably. A 2025 review of recent IBD clinical trials concluded that the most favorable results came from multi-strain formulations combining these genera, which demonstrated gut microbiota modulation, reduced pro-inflammatory cytokines, and clinical improvements.[3]
A single strain — no matter how well-studied — addresses only part of the problem. IBD involves barrier dysfunction, immune dysregulation, dysbiosis, and reduced SCFA production in parallel, and these require different mechanisms and different strains working together. See our guide to multi-strain probiotics without MCC for more on this design principle.
Clean Formulation: Why Fillers Matter in IBD
This is where IBD patients need to pay particular attention. Many commercial probiotics are loaded with inactive ingredients — microcrystalline cellulose, magnesium stearate, titanium dioxide, silicon dioxide — that can aggravate already-inflamed intestines. These aren't active ingredients; they're manufacturing aids, included to make tablets press more smoothly or to extend shelf life.
For a compromised gut, adding these can undermine the very bacteria you're trying to introduce. Learning to read probiotic labels to spot hidden fillers is a skill every IBD patient should develop. Look for products using clean capsule materials — pullulan capsules, for instance, are fermented, prebiotic, and offer delayed release without synthetic coatings.
Adequate CFU Count
Colony-forming units represent viable bacterial organisms per dose. IBD clinical trials demonstrating meaningful outcomes typically used doses in the range of 1 billion to 10 billion CFU per individual strain. A comprehensive multi-strain formula delivering 15 billion CFU total provides therapeutic-range dosing across multiple bacterial species. More isn't always better — strain selection and formulation quality matter as much as raw CFU count.
Pair with Compatible Prebiotics
Given how central SCFA production is to the probiotic-IBD mechanism, formulas that include prebiotic fibers alongside the bacterial strains provide a metabolic advantage. For sensitive guts, gentler prebiotics like acacia fiber often work better than aggressive FODMAP fibers.
Checklist: Choosing a Probiotic When You Have IBD
Look for: Multi-strain formula covering Lactobacillus, Bifidobacterium, and Bacillus genera; 10–15+ billion CFU; included prebiotics; filler-free formulation; delayed-release capsule technology (like pullulan); transparent strain-level labeling.
Avoid: Single-strain products with limited IBD-relevant evidence; formulas containing microcrystalline cellulose, titanium dioxide, magnesium stearate, or other synthetic flow agents; proprietary blends that obscure individual strain quantities; probiotics without third-party verification of CFU viability.
A Note on Medical Care
Probiotics are not a replacement for IBD medications or medical supervision. If you have IBD — particularly if you're in active flare, on biologic therapy, or immunocompromised — talk to your gastroenterologist before starting any new supplement. Probiotics are best viewed as adjunctive support alongside (not instead of) evidence-based medical treatment. This article is educational and does not constitute medical advice.
Frequently Asked Questions
Should people with IBD take probiotics?
The evidence generally supports probiotic use as adjunctive therapy in IBD, with stronger support in ulcerative colitis than Crohn's disease. Meta-analyses of randomized trials show probiotics can help induce and maintain remission in UC, particularly multi-strain formulations combining Lactobacillus and Bifidobacterium.[2][3] That said, probiotics are not a substitute for standard IBD medications, and anyone with IBD should discuss supplementation with their gastroenterologist — especially if they're immunocompromised or in active flare.
What's the best probiotic for IBD?
There's no single "best" strain; the evidence supports multi-strain combinations. The strains with the strongest IBD-relevant evidence include Lactobacillus rhamnosus, L. plantarum, L. acidophilus, L. salivarius, Bifidobacterium infantis, B. bifidum, B. longum, B. breve, B. lactis, and spore-forming Bacillus species like B. coagulans, B. subtilis, and B. clausii. A formula covering multiple genera at adequate CFU counts, paired with supporting prebiotic fibers, reflects current research best.
How do probiotics reduce intestinal inflammation?
Probiotics work through four interconnected mechanisms: (1) rebalancing the gut microbiota by competing with pathogens, (2) strengthening the intestinal barrier through tight junction upregulation and MUC-2 production, (3) modulating immune responses — shifting toward regulatory T cells and reducing TNF-α, IL-6, and IL-1β, and (4) producing short-chain fatty acids (especially butyrate) that fuel colonocytes and signal through anti-inflammatory GPCR pathways.[4][11]
How long does it take for probiotics to work in IBD?
Most clinical trials showing meaningful benefits for IBD outcomes ran for 4 to 12 weeks, with some remission maintenance studies extending to 12 months. Subjective improvements in bloating, stool frequency, or energy may appear within 2–4 weeks; measurable shifts in inflammatory markers like calprotectin typically require longer consistent use. The inulin-UC trial, for example, measured outcomes at 9 weeks.[5]
Can probiotics replace my IBD medication?
No. Current evidence positions probiotics as adjunctive support — complementary to, not a substitute for, established IBD therapies like mesalamine, corticosteroids, immunomodulators, or biologics. Several trials showing probiotic benefit specifically tested them alongside standard treatment. Stopping prescribed medications without medical guidance can trigger serious flares.
Are probiotics safe during an IBD flare?
For most IBD patients, well-formulated probiotics are considered safe, and some strains have been studied specifically during active disease. However, severe flares, immunocompromised status, central venous access, or recent abdominal surgery can change the risk profile. Always discuss new supplements with your gastroenterologist during active disease, and discontinue if you notice worsening symptoms after starting a new formula.
Putting the Science Into Practice
The probiotic-IBD story isn't one of miracle cures — it's a story of biological alignment. The same systems that go wrong in IBD (dysbiosis, barrier dysfunction, immune dysregulation, reduced SCFA production) are precisely the systems that well-chosen probiotic strains can help re-regulate. The evidence is strongest for ulcerative colitis, promising but more variable for Crohn's disease, and consistently stronger for multi-strain formulations that pair probiotics with supportive prebiotic fibers.
What matters for anyone navigating IBD is choosing a supplement that reflects this evidence: meaningful strain diversity across Lactobacillus, Bifidobacterium, and Bacillus genera; adequate CFU counts; complementary prebiotics; and — critically — a formulation free of the fillers and flow agents that can work against the gut you're trying to support. For a full breakdown of how MicroBiome Restore was engineered around these principles, see our complete product guide.
For more condition-specific clinical evidence, explore our deeper guides on probiotics for ulcerative colitis, probiotics for Crohn's disease, and related inflammatory conditions like probiotics for diverticulitis.
Science-Backed Support for Your Gut
MicroBiome Restore delivers 26 clinically studied probiotic strains, 9 organic prebiotics, and 80+ trace minerals in a filler-free pullulan capsule. Engineered around the mechanisms that matter for intestinal health — barrier integrity, SCFA production, and microbiome diversity.
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