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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 3
2010 pubmed 179 citations

Exopolysaccharides of Lactobacillus rhamnosus GG form a protective shield against innate immune factors in the intestine.

Lebeer. Sarah S; Claes. Ingmar J J IJ; Verhoeven. Tine L A TL; Vanderleyden. Jos J; De Keersmaecker. Sigrid C J SC

Key Findings

  • LGG’s exopolysaccharide (EPS) layer acts as a shield against the host antimicrobial peptide LL‑37 and complement proteins
  • An EPS‑deficient LGG mutant persists poorly in the mouse gut, especially in the lower intestine
  • Sub‑inhibitory LL‑37 exposure triggers LGG to increase EPS production, enhancing its immune evasion

Practical Outcomes

  • Choose probiotic products that contain the full‑strength LGG strain with its natural EPS coating for better gut survival. The findings suggest that the EPS layer, not just adhesion, is key to probiotic effectiveness, so formulations that preserve or boost EPS may be more beneficial.

Summary

The study shows that the sugary coating (exopolysaccharides) on the probiotic Lactobacillus rhamnosus GG helps it survive the gut’s natural antimicrobial peptide LL‑37 and other immune factors. When the coating is missing, the bacteria disappear faster in the intestine, even though they stick to gut cells better in lab tests. Exposure to low levels of LL‑37 makes the bacteria produce more of this protective coating.

Abstract

Probiotic bacteria are administered as live microorganisms to provide a health benefit to the host. Insight into the adaptation factors that promote the survival and persistence of probiotics in the gastrointestinal tract (GIT) is important to understand their performance. In this study, the role of the long galactose-rich exopolysaccharides (EPS) of the prototypical probiotic strain Lactobacillus rhamnosus GG (LGG) was investigated. In a competition experiment with wild type, the isogenic EPS mutant CMPG5351 exhibited a reduced persistence in the murine GIT, especially in the lower parts of the intestine. This was surprising as our previous in vitro studies had shown an increased adhesion capacity for this EPS mutant. Follow-up assays indicated that this mutant is more sensitive towards host innate defence molecules, such as the LL-37 antimicrobial peptide and complement factors. This suggests that EPS forms a protective shield for LGG against these molecules in the GIT. Moreover, culturing LGG wild-type in subinhibitory concentrations of host defence factors such as LL-37 resulted in increased production of EPS, indicating that bacterial EPS production is modulated in the host to fine-tune the balance between adhesion and immune evasion. These observations are of interest in understanding the dynamics of adaptation of probiotics to the host environments.

Study Information

Provider

pubmed

Year

2010

Date

2010-08-17T00:00:00.000Z

DOI

10.1111/j.1751-7915.2010.00199.x

Citations

179

References

45