# Vibrio cholerae serotype impacts pathogenicity

**Authors:** Franz G. Zingl, Deborah R. Leitner, Bolutife Fakoya, Alexander A. Morano, Matthew K. Waldor

PMC · DOI: 10.1038/s41467-025-67908-w · 2026-01-19

## TL;DR

The study shows that the Ogawa serotype of Vibrio cholerae is more pathogenic due to a methylation modification that helps it survive in the gut.

## Contribution

The study reveals that O1 antigen methylation in Ogawa strains enhances pathogenicity by protecting against antimicrobial peptides.

## Key findings

- Ogawa strains show increased colonization and infectivity compared to Inaba strains.
- Methylation of the O1 antigen shields bacteria from antimicrobial peptides in the small intestine.

## Abstract

The O1 serogroup of Vibrio cholerae has caused all cholera pandemics and for over a century V. cholerae O1 outbreak strains have been characterized by their serotype. The two V. cholerae serotypes differ by the presence (Ogawa) or absence (Inaba) of methylation of the terminal sugar on the lipopolysaccharide O1-antigen. Serotype switching often occurs during epidemics and has historically been attributed to the pathogen adapting to immune pressures. Here we address the impact of serotype on V. cholerae pathogenicity using otherwise isogenic Ogawa and Inaba versions of several clinical V. cholerae O1 isolates. Our findings indicate that O1 antigen methylation in Ogawa strains promotes V. cholerae colonization, infectivity and resistance to antimicrobial peptides. We propose that methylation of the O1 antigen elevates colonization by shielding the bacterium from cationic antimicrobial peptides at the pH of the small intestine. These observations provide insights into the biological significance of the V. cholerae O1 serotypes.

Vibrio cholerae O1 outbreak strains are classified as Ogawa or Inaba serotypes, but the impact of serotype on pathogenicity is understudied. Here, the authors show that O1 antigen methylation in Ogawa strains promotes colonization and infectivity.

## Linked entities

- **Diseases:** cholera (MONDO:0015766)
- **Species:** Vibrio cholerae (taxon 666)

## Full-text entities

- **Genes:** Ttll5 (tubulin tyrosine ligase-like family, member 5) [NCBI Gene 320244] {aka 1700048H13Rik, 2310009M18Rik, 4930556H18Rik, D630041K24Rik, Stamp, mKIAA0998}, Sfmbt1 (Scm-like with four mbt domains 1) [NCBI Gene 54650] {aka 4930442N21Rik, 9330180L21Rik, Sfmbt, Smr}
- **Diseases:** ApS (MESH:D018420), cholera (MESH:D002771), infected (MESH:D007239), CDI (MESH:D020790), diarrhea (MESH:D003967), dislocation (MESH:D004204), weight loss (MESH:D015431), diarrheal (MESH:D004403)
- **Chemicals:** NH3 (MESH:D000641), Rhodamine B (MESH:C029773), chitin (MESH:D002686), AKI broth (-), 5-bromo-4-chloro-3-indolyl-beta-d-galactopyranoside (MESH:C044888), perosamine (MESH:C057033), isopropanol (MESH:D019840), ammonium (MESH:D064751), sugar (MESH:D000073893), glucose (MESH:D005947), O-antigen (MESH:D019081), fatty acid (MESH:D005227), TRIZOL (MESH:C411644), Km (MESH:D007612), GM1 (MESH:D005677), LPS (MESH:D008070), isoflurane (MESH:D007530), sodium chloride (MESH:D012965), MES (MESH:C004550), TMB (MESH:C021758), Cb (MESH:D002228), DAP (MESH:D003960), AMPs (MESH:C014308), PBS (MESH:D007854), agar (MESH:D000362), Suc (MESH:D013395), Rhodamine (MESH:D012235), glycerol (MESH:D005990), sodium bicarbonate (MESH:D017693), Sm (MESH:D013307), polystyrene (MESH:D011137), carbon (MESH:D002244), chloroform (MESH:D002725)
- **Species:** Vibrio cholerae (species) [taxon 666], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Ophiostoma sp. 1 (species) [taxon 2268574], Vibrio cholerae O1 (serogroup) [taxon 127906], Homo sapiens (human, species) [taxon 9606], Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Mus musculus (house mouse, species) [taxon 10090], Escherichia coli (E. coli, species) [taxon 562]
- **Mutations:** S158P

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12856009/full.md

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Source: https://tomesphere.com/paper/PMC12856009