Effects of sequential Campylobacter jejuni 81-176 lipooligosaccharide core truncations on biofilm formation, stress survival, and pathogenesis.
Naito. Mizue M; Frirdich. Emilisa E; Fields. Joshua A JA; Pryjma. Mark M; Li. Jianjun J; Cameron. Andrew A; Gilbert. Michel M; Thompson. Stuart A SA; Gaynor. Erin C EC
Key Findings
- LL-37 is active against Campylobacter jejuni, killing the bacteria
- Loss of the LOS outer core increases biofilm formation and reduces resistance to complement killing
- Even small LOS truncations make the bacteria more sensitive to the antibiotic polymyxin B and cause modest changes in LL‑37 sensitivity
Practical Outcomes
- For biohackers, the result shows LL‑37 can act as an antibacterial agent against certain pathogens, but the study doesn’t provide dosage, safety, or application guidance for humans. It’s mainly a basic science insight rather than a ready‑to‑use protocol for longevity or health optimization.
Summary
The study looked at how changes in a bacterial surface sugar layer affect the bacteria’s ability to form biofilms, survive stress, and cause disease, and it also tested the natural antimicrobial peptide LL‑37 against the bacteria. They found LL‑37 can kill the pathogen, but the bacteria’s surface changes only slightly alter how sensitive they are to it. The main take‑away is that LL‑37 has antibacterial activity, but the findings are specific to a gut bug and not directly useful for human supplement or health protocols.
Abstract
Campylobacter jejuni is a highly prevalent human pathogen for which pathogenic and stress survival strategies remain relatively poorly understood. We previously found that a C. jejuni strain 81-176 mutant defective for key virulence and stress survival attributes was also hyper-biofilm and hyperreactive to the UV fluorescent dye calcofluor white (CFW). We hypothesized that screening for CFW hyperreactive mutants would identify additional genes required for C. jejuni pathogenesis properties. Surprisingly, two such mutants harbored lesions in lipooligosaccharide (LOS) genes (waaF and lgtF), indicating a complete loss of the LOS outer core region. We utilized this as an opportunity to explore the role of each LOS core-specific moiety in the pathogenesis and stress survival of this strain and thus also constructed DeltagalT and DeltacstII mutants with more minor LOS truncations. Interestingly, we found that mutants lacking the LOS outer core (DeltawaaF and DeltalgtF but not DeltagalT or DeltacstII mutants) exhibited enhanced biofilm formation. The presence of the complete outer core was also necessary for resistance to complement-mediated killing. In contrast, any LOS truncation, even that of the terminal sialic acid (DeltacstII), resulted in diminished resistance to polymyxin B. The cathelicidin LL-37 was found to be active against C. jejuni, with the LOS mutants exhibiting modest but tiled alterations in LL-37 sensitivity. The DeltawaaF mutant but not the other LOS mutant strains also exhibited a defect in intraepithelial cell survival, an aspect of C. jejuni pathogenesis that has only recently begun to be clarified. Finally, using a mouse competition model, we now provide the first direct evidence for the importance of the C. jejuni LOS in host colonization. Collectively, this study has uncovered novel roles for the C. jejuni LOS, highlights the dynamic nature of the C. jejuni cell envelope, and provides insight into the contribution of specific LOS core moieties to stress survival and pathogenesis.
Study Information
pubmed
2010
2010-02-05T00:00:00.000Z
10.1128/jb.01222-09