What Is Lactobacillus reuteri DSM 17938?

Lactobacillus reuteri DSM 17938 is a specific strain of probiotic bacterium, originally isolated from a human host, that has become one of the most extensively studied probiotics in pediatric medicine. It was deliberately engineered from an earlier strain by stripping away unwanted antibiotic-resistance genes, and it has since accumulated a sizable body of clinical trial evidence across infant colic, childhood diarrhea, functional abdominal pain, and neonatal care. The strain’s formal taxonomy has been updated to Limosilactobacillus reuteri, though most product labels and clinical literature still use the older Lactobacillus name.

Where the Strain Came From

The story starts with a strain called L. reuteri ATCC 55730, isolated from a human source around 1990 and used in early probiotic research. When researchers examined ATCC 55730 more closely, they discovered it carried two small rings of DNA called plasmids. One harbored a tetracycline-resistance gene, the other a lincosamide-resistance gene. Because regulators and scientists increasingly worry about probiotic bacteria passing antibiotic resistance to harmful bugs in the gut, these plasmids were a liability. Researchers removed both plasmids and confirmed the resulting daughter strain had lost the associated resistances. That cleaned-up strain was deposited in a culture collection as DSM 17938 and became the version used in virtually all subsequent clinical work.¹

L. reuteri belongs to a broad genus of gram-positive, oxygen-tolerant bacteria that ferment sugars to produce lactic acid. The species can colonize several human body sites, though it is found most commonly in the gastrointestinal tract. What sets DSM 17938 apart from other members of the species is less about dramatic genetic differences and more about the paper trail: this particular strain has been put through dozens of randomized controlled trials and is the one behind most commercially available L. reuteri supplements marketed for infants and children.

How It Works in the Gut

No single mechanism explains everything DSM 17938 does, and researchers are still filling in the details. But three broad pathways stand out in the literature: antimicrobial compound production, gut-barrier reinforcement, and immune modulation.

The antimicrobial angle centers on a substance called reuterin. When glycerol is available in the gut, L. reuteri converts it into reuterin, a broad-spectrum antimicrobial compound active against gram-positive and gram-negative bacteria, as well as yeasts, fungi, and some viruses.² Reuterin’s effects on harmful gut bacteria are well documented, though its impact on the normal commensal bacteria you want to keep around has been less clear.³

The barrier-reinforcement story comes from cell-culture experiments. When intestinal cells are challenged with a harmful strain of E. coli, pretreating them with DSM 17938 reduces the damage to tight junctions, the protein structures that hold gut lining cells together. The probiotic strain also dials down inflammatory signals like IL-6 and TNF-α that the infection would otherwise ramp up.⁴ These findings are encouraging, but they come from cell lines rather than living humans, so there is a gap between what happens in a dish and what happens in your intestines. An exploratory trial in adults with diarrhea-predominant irritable bowel syndrome found that six weeks of DSM 17938 did not significantly improve gut permeability markers compared with placebo, a reminder that lab-level effects do not always translate neatly into clinical outcomes.⁵

On the immune side, a trial in colicky infants found that 28 days of DSM 17938 increased expression of FoxP3, a marker for regulatory T cells, which are the immune system’s peacemakers. The same study saw increases in toll-like receptor expression, though that shift seemed to be age-related rather than probiotic-specific.⁶ Animal work on necrotizing enterocolitis, a dangerous bowel condition in premature newborns, has shown that DSM 17938 reduces intestinal inflammation and increases regulatory T cells through a pathway involving a receptor called TLR2.⁷

Infant Colic

If there is a flagship use for DSM 17938, it is infant colic. This is also the area with some of the most striking numbers. In a randomized trial, infants given the strain for 30 days cried about 75 minutes per day on average, compared with roughly 148 minutes per day in the placebo group.⁸ A real-world clinic-based study reported even more dramatic results, with mean crying time dropping from about 248 minutes per day at baseline to roughly 46 minutes at the end of treatment, and 85 percent of infants meeting a clinical response threshold of at least 50 percent reduction in crying.⁹

These results sound dramatic, and they have convinced several pediatric gastroenterology societies to include DSM 17938 in their colic guidelines. Still, the real-world study lacked a placebo group, so placebo response and natural resolution of colic over time could account for some of the improvement. The randomized data is stronger, but colic trials are inherently tricky because crying is subjective, the condition resolves on its own eventually, and parental expectations can shape reporting. The weight of evidence is positive, but it’s fair to say the effect size probably lands somewhere between the tightly controlled trials and the more optimistic open-label numbers.

Childhood Diarrhea

Acute gastroenteritis in young children is one of the other well-studied targets. Individual trials have shown that DSM 17938 shortens diarrhea duration by around 14 to 15 hours on average. In one outpatient study, the percentage of children still experiencing diarrhea at 48 hours was about 45 percent in the probiotic group versus 87 percent in controls.¹⁰ A more recent Thai trial reported a similar pattern, with about 65 percent of children in the probiotic group recovering within 48 hours versus 36 percent of controls.¹¹

When these individual trials are pooled together in a meta-analysis, the average reduction in diarrhea duration comes out to roughly 0.9 days. A meta-analysis also found a modest reduction in how long children stayed in the hospital. The researchers who conducted that review made an important caveat, though: the effect sizes were small and of limited clinical relevance, and the individual trials had methodological limitations.¹² In practical terms, the evidence suggests DSM 17938 shaves some hours off an unpleasant illness rather than transforming the course of it. That modest benefit may still be worthwhile when you’re the parent of a sick toddler, but it is not a game-changer.

Functional Abdominal Pain in Children

Functional abdominal pain is a common and frustrating pediatric problem: recurring belly pain with no identifiable structural cause. Multiple randomized trials have tested DSM 17938 here, and the pattern has been consistent. In one trial, children taking the probiotic had pain episodes drop to about twice a week versus nearly four times a week in the placebo group, with pain intensity also significantly lower after four weeks.¹³ Another trial found children taking DSM 17938 logged significantly more pain-free days over the study period, with a median of roughly 90 pain-free days versus 51 in controls.¹⁴

Pooled data from two parts of a study involving about 100 children confirmed the pattern, showing children in the probiotic group gained an average of roughly 26 more pain-free days over the treatment period, with differences in pain intensity emerging from the second month onward and becoming more pronounced by the fourth.¹⁵ This is one of the more convincing areas for DSM 17938 because multiple independent groups have found similar results, and the outcome measures, while still subjective, are consistent across trials.

Preterm Infants

Premature babies face a set of gastrointestinal challenges that full-term infants do not, including slow feeding tolerance, a higher risk of a serious bowel condition called necrotizing enterocolitis (NEC), and susceptibility to bloodstream infections known as late-onset sepsis. DSM 17938 has been studied specifically in this population.

A meta-analysis of randomized controlled trials in preterm infants found that DSM 17938 reduced the time to reach full enteral feeding by an average of about 2.7 days, lowered the risk of NEC (stage II or greater) by roughly 43 percent, and reduced the risk of late-onset sepsis by about 28 percent. It did not significantly reduce mortality.¹⁶ An individual trial in preterm infants also reported fewer daily reflux episodes in the probiotic group and a shorter time to full feeding, consistent with the meta-analytic findings.¹⁷

These are meaningful outcomes in a vulnerable population. Reaching full feeding faster means less time on intravenous nutrition, which carries its own risks. And NEC can be devastating, so even modest risk reductions matter. That said, neonatal intensive care units vary widely in their probiotic practices, and not all hospitals have adopted routine probiotic supplementation for preterm infants, partly because of ongoing debates about which strains to use and at what doses.

Gastric Motility and Regurgitation

One of the more interesting findings with DSM 17938 is its effect on how quickly the stomach empties. In infants with functional regurgitation, a common condition in which babies spit up frequently without any underlying structural problem, DSM 17938 has been shown to speed up gastric emptying and reduce the number of daily spit-up episodes.¹⁸ A follow-up study using a formula supplemented with the strain and thickened with starch found a similar pattern: regurgitation episodes dropped from about 7.4 per day to 2.6 per day over four weeks in the test group, versus a smaller decline in controls.¹⁹

The mechanism behind this motility effect may involve the enteric nervous system, the vast network of neurons that controls gut movement independently of the brain. Research has shown that L. reuteri can increase the excitability of certain sensory neurons in the gut wall, altering ion channel activity in ways that could affect both how the gut moves and how it processes pain signals.²⁰ This connection between gut bacteria and the enteric nervous system is part of a larger story about the gut-brain axis, and it may partly explain why a single strain can seemingly affect such different conditions as colic, regurgitation, and abdominal pain.

Where the Evidence Falls Short

It would be misleading to suggest DSM 17938 works for everything it has been tested against. A pilot study examined whether the strain, combined with a related L. reuteri strain and a proton-pump inhibitor (without antibiotics), could eradicate Helicobacter pylori, the bacterium behind most stomach ulcers. The cure rate was only about 12.5 percent in the probiotic group versus roughly 4 percent with placebo, far too low to be clinically useful.²¹ The strain is not a substitute for standard antibiotic-based H. pylori treatment.

The IBS-D trial mentioned earlier is another example. Despite promising lab data on gut barrier protection, the strain did not move the needle on intestinal permeability or epithelial damage markers in adults with irritable bowel syndrome. This disconnect between cell-culture results and human trials is common in probiotic research and underscores why individual strain claims need to be evaluated against clinical data, not just mechanistic studies.

Safety Profile

Safety data on DSM 17938 is reassuring across age groups. In a randomized, masked trial in healthy adults, no serious adverse events were attributed to the probiotic, and the rate of common everyday symptoms did not differ between the probiotic and placebo groups.²² In a study of healthy children aged two to five conducted under an investigational new drug protocol, no severe adverse events were observed and adverse event rates did not differ between the probiotic and placebo groups. Some statistically significant differences in minor symptoms showed up in the home-diary data, but the researchers characterized them as not biologically meaningful.²³

The removal of antibiotic-resistance plasmids during the strain’s creation was specifically intended to address one of the main theoretical safety concerns with probiotic bacteria: the possibility that resistance genes could transfer to pathogenic organisms in the gut. This makes DSM 17938 somewhat unusual among commercial probiotic strains in having been proactively modified to reduce that risk.

Does It Actually Survive the Trip Through Your Gut?

A probiotic that dies in stomach acid before reaching the intestines is not much use. Human feeding studies have confirmed that DSM 17938 survives transit through the gastrointestinal tract. After three weeks of daily consumption, researchers detected a significant increase in viable probiotic bacteria in fecal samples compared to baseline, confirmed by both culturing and DNA-based methods. No such increase appeared in the placebo group.²⁴

Survival and permanent colonization are different things, though. Like most probiotics, DSM 17938 appears to pass through the gut rather than setting up a lasting colony. Once you stop taking it, the levels drop back toward baseline. This means its effects depend on continued, regular use rather than a one-time course that reshapes your microbiome permanently. Researchers have also explored microencapsulation techniques to further protect the bacteria during storage and passage through harsh gastric conditions, an ongoing area of food-science work aimed at improving shelf stability and delivery.²⁵

Oral Health Applications

Beyond the gut, L. reuteri has drawn some attention in dentistry. The same reuterin production that inhibits gut pathogens can also target bacteria involved in gum disease and dental caries. Research has suggested that L. reuteri shows potential in treating oral diseases through its antimicrobial properties, and some commercial oral-health lozenges and tablets already contain this species. The evidence here is thinner than in the pediatric GI space, with fewer large randomized trials, but the biological rationale is sound given what is known about reuterin’s broad antimicrobial activity. If you see L. reuteri in a dental probiotic product, DSM 17938 or its sister strain ATCC PTA 6475 is likely behind it.

Whether swallowing a gut-targeted supplement delivers meaningful amounts to the oral cavity is a separate question. Oral-health products typically use lozenges or chewable tablets designed to release the bacteria in the mouth rather than capsules meant to survive stomach acid intact. The delivery format matters, and a product designed for gut health is not automatically useful for your teeth.