Helicobacter pylori infection in humans is associated with a spectrum of gastroenterologic and hematologic diseases including chronic gastritis, peptic ulcers, gastric adenocarcinoma, gastric mucosa–associated lymphoid tissue lymphoma, sideropenic anemia, and primary immune thrombocytopenia. Successful eradication of the bacterium is a major component in the treatment of these conditions. However, despite the cost of therapy, the rates of eradication after triple therapies are decreasing, with standard amoxicillin plus clarithromycin-based triple therapy achieving eradication rates of only about 75% in many series, albeit with an apparent geographic variation, in agreement with differing patterns of antibiotic resistance throughout the world. 1–3 Quadruple second-line therapy has, likewise, resulted in unsatisfactory eradication rates. Although unsuccessful eradication can be due to increasing antimicrobial resistance, an additional important contributor is the high incidence of treatment-related side effects (including diarrhea, nausea, epigastric discomfort, and dysgeusia with a metallic taste), determining low compliance, and, consequently, incomplete therapy. Many of these gastrointestinal effects result from the modification of the ecologic equilibrium of intestinal microbiota due to the antibiotics. 4 The identification of alternative therapeutic strategies to overcome these limitations is a pressing issue. Although altering the duration of treatment or the choice of first-line antibiotics can target resistance patterns, lack of adherence to treatment because of adverse events has been addressed mostly through the addition of probiotics to eradication regimens, in an attempt to reestablish the gastrointestinal microbial equilibrium. Probiotics are live nonpathogenic microbial food products or supplements whose interaction with the host can benefit the health status of the latter, mostly through the modulation of the balance of its microflora, although direct antimicrobial effects have been described by some groups. 5 Probiotic bacteria are able to survive in the gastrointestinal tract despite the administration of antimicrobial eradication regimens, as shown by the recovery of probiotics from the feces of treated patients. 6 In addition, it has been demonstrated that the supplementation of eradication protocols with probiotics does impact the intestinal microflora. Whereas triple therapy results in significant increases in the facultative anerobe component of the microflora after the start of treatment, the addition of Lactobacillus acidophilus and Bifidobacterium bifidum midtreatment reverts this increase back to starting levels, and the addition from the start maintains a stable facultative anerobe population throughout treatment and follow-up. 7 Similarly, although the percentage of bifidobacteria in anerobes in the stool is significantly decreased by triple therapy, supplementation with an L. acidophilus-containing and B. lactiscontaining yogurt is able to restore the population of bifidobacteria to pretreatment levels. 8 Apart from the modification of gastrointestinal microflora, which can be harnessed to reduce treatment-associated side effects, probiotics have also been shown to exert direct inhibitory effects on H. pylori in both in vitro and in vivo animal models, with the potential to improve eradication rates. These effects have been demonstrated for several species of probiotics, including L. acidophilus, L. salivarius, L. rhamnosus, and B. bifidum, among others. 9–11 Proposed mechanisms underlying the beneficial interaction between probiotics and H. pylori, and the modulation of the colonization of the gastric mucosa by the latter, include the production of lactic acid with H. pylori inhibition because of decreasing gastric pH; the direct killing of H. pylori through secreted metabolites with antimicrobial properties, including bacteriocins, autolysins, and organic acids; the interference with H. pylori adhesion