Pilus-mediated co-aggregation with Lactobacillus crispatus increases meningococcal susceptibility to antimicrobial agents by interfering with microcolony formation.
Lidberg. Kenny K; Pilheden. Sarah S; Nawarathne. Samuddi S; Rauscher. Katharina K; Jonsson. Ann-Beth AB
Key Findings
- Lactobacillus crispatus MV24 uniquely co‑aggregates with Neisseria meningitidis via bacterial pili
- Co‑aggregation disrupts meningococcal microcolony formation and reduces motility
- Disrupted bacteria become more susceptible to the antimicrobial peptide LL‑37, human beta‑defensin‑2, and the antibiotic cephalexin
Practical Outcomes
- The study hints that a probiotic containing L. crispatus could boost mucosal defenses against meningococcal infection, potentially enhancing the effectiveness of innate peptides and antibiotics. However, because the data are from in‑vitro experiments, there’s no established dosage or protocol for humans yet, so biohackers should treat this as a promising concept rather than a ready‑to‑use intervention.
Summary
Researchers found that a specific strain of Lactobacillus crispatus can stick to meningococcal bacteria in the nose, breaking up their clusters and making them easier for natural antimicrobial peptides like LL‑37 and antibiotics to kill. This suggests that certain probiotics might help the body fight off meningococcal colonization, but the work is still in the lab and not yet proven in people.
Abstract
Neisseria meningitidis asymptomatically colonizes the nasopharyngeal mucosa, but occasionally, the bacteria disseminate to cause sepsis and meningitis. In the epithelial cell layer, the pathogen co-colonizes with other resident inhabitants, such as Lactobacillus species that are part of the nasopharyngeal-oral microbiota. In this study, we investigated the interaction between lactobacilli and meningococci. We demonstrated that Lactobacillus crispatus strain MV24 can co-aggregate with meningococci, whereas all other Lactobacillus strains tested did not co-aggregate. The binding ability of L. crispatus was not strain- or serogroup-specific but was dependent on the ability of meningococci to form microcolonies. The finding that N. meningitidis lacking pili did not co-aggregate with L. crispatus, but that hyperpiliated N. meningitidis exhibited strong co-aggregation, led us to examine the interaction between purified meningococcal pili and lactobacilli. Our results showed that L. crispatus MV24 can bind to purified meningococcal Class I and II pili, explaining the aggregative clusters observed under the microscope. Co-aggregation with L. crispatus disrupted microcolony formation, and increased the killing of meningococci by LL-37, hBD2 and cephalexin. Further, co-aggregation had the added effect of impeding motility. N. meningitidis pili bind to L. crispatus, which interferes with the meningococcal microcolonies and increases sensitivity to antimicrobial agents. Taken together, our findings suggest that L. crispatus MV24 may have a beneficial effect on the host through co-aggregating with meningococci.
Study Information
pubmed
2025
2025-07-30T00:00:00.000Z
10.1186/s12866-025-04201-2
60