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<p>Brucellosis, a chronic intracellular infection caused by <i>Brucella</i> spp., remains therapeutically challenging due to antimicrobial resistance and frequent relapse. Probiotic microorganisms produce antimicrobial proteins—including bacteriocins and thermostable peptides—that inhibit pathogen viability, modulate host immunity, and attenuate oxidative damage. In murine models, therapeutic administration of <i>Lactobacillus</i>-based probiotics reduced <i>Brucella</i> infection index by 58.75%, while prophylactic use yielded a 25% reduction. Co-treatment with rifampicin eliminated residual infection, outperforming antibiotics alone. Experimental and clinical data suggest probiotics enhance antioxidant markers—e.g., lower malondialdehyde and higher total glutathione—while modulating cytokine profiles toward Th1-skewed immunity, with increased IFN-γ and regulated IL-10. Pediatric trials report faster symptom resolution and improved oxidative balance under probiotic co-administration. Additionally, mucosal vaccines vectored by probiotic strains elicit strong IgA/IgG titers and T-cell responses, targeting <i>Brucella</i> antigens such as Omp16, Omp31, and SOD. Given the limitations of current antibiotic regimens and rising antimicrobial resistance, probiotic-based approaches could offer a promising adjunctive strategy. Despite preclinical promise, no phase III trials exist evaluating probiotic–antibiotic synergy in human brucellosis. Future directions include standardized strain selection, mechanistic optimization, and multicenter randomized trials to enable clinical translation of probiotic–protein therapeutics in brucellosis.</p>

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Complementary Use of Probiotics and Their Antimicrobial Proteins in Brucellosis: A Comprehensive Review of Mechanisms and Clinical Benefits

  • 期刊论文

  • 发表日期：

    2025年8月27日

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  • Narges Soozangar,
  • Elnaz Faghfuri,
  • Pourya Gholizadeh

摘要

Brucellosis, a chronic intracellular infection caused by Brucella spp., remains therapeutically challenging due to antimicrobial resistance and frequent relapse. Probiotic microorganisms produce antimicrobial proteins—including bacteriocins and thermostable peptides—that inhibit pathogen viability, modulate host immunity, and attenuate oxidative damage. In murine models, therapeutic administration of Lactobacillus-based probiotics reduced Brucella infection index by 58.75%, while prophylactic use yielded a 25% reduction. Co-treatment with rifampicin eliminated residual infection, outperforming antibiotics alone. Experimental and clinical data suggest probiotics enhance antioxidant markers—e.g., lower malondialdehyde and higher total glutathione—while modulating cytokine profiles toward Th1-skewed immunity, with increased IFN-γ and regulated IL-10. Pediatric trials report faster symptom resolution and improved oxidative balance under probiotic co-administration. Additionally, mucosal vaccines vectored by probiotic strains elicit strong IgA/IgG titers and T-cell responses, targeting Brucella antigens such as Omp16, Omp31, and SOD. Given the limitations of current antibiotic regimens and rising antimicrobial resistance, probiotic-based approaches could offer a promising adjunctive strategy. Despite preclinical promise, no phase III trials exist evaluating probiotic–antibiotic synergy in human brucellosis. Future directions include standardized strain selection, mechanistic optimization, and multicenter randomized trials to enable clinical translation of probiotic–protein therapeutics in brucellosis.