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Life sciences · Journal article
Frontiers in Cellular and Infection Microbiology · August 12, 2026
Encouraging direction, but not yet definitive.
Cell-free supernatant from Lactiplantibacillus pentosus CROT01 demonstrates in vitro antibacterial and antibiofilm activity against H. pylori including clarithromycin-resistant strains, with genomic characterization showing bacteriocin-related genes and no virulence genes. This represents a proof-of-concept for a postbiotic strategy but requires in vivo efficacy studies before clinical translation.
In vitro mechanistic and genomic characterization study. H. pylori strains (including clarithromycin-resistant ATCC 700684); Lactiplantibacillus pentosus CROT01; RAW 264.7 macrophage cells; Caco-2 intestinal epithelial cells. Intervention: Cell-free supernatant from Lactiplantibacillus pentosus CROT01.
Inhibition zones against H. pylori ranged from 10.67 ± 0.58 to 17.33 ± 1.53 mm, including against clarithromycin-resistant strain ATCC 700684 MIC and MBC ranged from 12.5–50 mg/mL and 25–50 mg/mL respectively LCFS significantly inhibited biofilm formation and eradicated established H. pylori biofilms
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This work identifies a potential postbiotic therapeutic candidate for clarithromycin-resistant H. pylori, a clinically important problem. However, in vivo efficacy, safety, and mechanism validation in animal models or clinical trials are required before any therapeutic recommendation can be made.
In vitro study demonstrating real antibacterial and anti-biofilm activity of a probiotic cell-free supernatant against H. pylori including resistant strains, with supporting genomic characterization, but lacking clinical efficacy data and requiring in vivo confirmation.
As stated by the source record.
Quoted from the source exactly as published.
This work identifies a potential postbiotic therapeutic candidate for clarithromycin-resistant H. pylori, a clinically important problem. However, in vivo efficacy, safety, and mechanism validation in animal models or clinical trials are required before any therapeutic recommendation can be made.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Helicobacter pylori is a major gastric pathogen associated with chronic gastritis, peptic ulcers, and gastric cancer, while increasing antibiotic resistance has reduced the effectiveness of standard eradication therapies. This study investigated the antibacterial, antibiofilm, anti-inflammatory, probiotic-related, and genomic properties of cell-free supernatant (LCFS) derived from Lactiplantibacillus pentosus CROT01 against H. pylori. LCFS exhibited inhibitory activity against all tested H. pylori strains, including the clarithromycin-resistant strain ATCC 700684, with inhibition zones ranging from 10.67 ± 0.58 to 17.33 ± 1.53 mm. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) ranged from 12.5–50 mg/mL and 25–50 mg/mL, respectively. LCFS significantly inhibited biofilm formation and eradicated established H. pylori biofilms. Scanning electron microscopy revealed marked morphological alterations in treated cells, including membrane disruption, deformation, and cellular shrinkage. Anti-inflammatory activity was demonstrated through suppression of nitric oxide production in lipopolysaccharide-stimulated RAW 264.7 cells. In addition, L. pentosus CROT01 exhibited tolerance to acidic pH and pancreatin, high cell surface hydrophobicity, and moderate adhesion ability toward Caco-2 cells. Whole-genome sequencing identified several bacteriocin-associated genes, including plantaricin E, plantaricin F, pediocin, enterolysin A, and bovicin-related peptides, whereas no virulence-associated or acquired antimicrobial resistance genes were detected. Thus, these findings suggest that LCFS derived from L. pentosus CROT01 possesses promising anti- H. pylori activity and may represent a potential postbiotic-based strategy against antibiotic-resistant H. pylori infection.
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