Evidence map›Paper›PMID 31263955›Full record

ArticleMedical microbiology and immunology2019

Role of coaggregation in the pathogenicity and prolonged colonisation of Vibrio cholerae.

Yien Shin Toh, Soo Ling Yeoh, Ivan Kok Seng Yap, Cindy Shuan Ju Teh, Thin Thin Win, Kwai Lin Thong, Chun Wie Chong

Abstract read
PubMed Publisher
In one paragraph

Article in Medical microbiology and immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. The Regulatory Effect of Coaggregation BetweenFrontiers in cellular and infection microbiology · 2022
    Article
  4. Gene Analysis ofMicroorganisms · 2021
    Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Yien Shin TohSchool of Postgraduate Studies, International Medical University, Kuala Lumpur, Malaysia.
Soo Ling YeohInstitute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia.
Ivan Kok Seng YapSarawak Research and Development Council, Ministry of Education, Science, Technology and Research, Kuching, Sarawak, Malaysia.
Cindy Shuan Ju TehDepartment of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Thin Thin WinPathology Division, School of Medicine, International Medical University, Kuala Lumpur, Malaysia.
Kwai Lin ThongInstitute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia.
Chun Wie ChongDepartment of Life Sciences, School of Pharmacy, International Medical University, Kuala Lumpur, Malaysia. chongchunwie@gmail.com.ORCID http://orcid.org/0000-0002-6881-8883
IMU University · MYUniversity of Malaya · MYForest Department Sarawak · MYInstitute for Medical Research · MYUniversity Malaya Medical Centre · MY

Funding

Ministry of Higher Education, Malaysia FRGS/1/2014/SKK04/IMU/03/1
6 · The paper itself

Abstract

Cholera is an acute diarrheal illness caused by the Gram-negative bacterium Vibrio cholerae. The pathogen is known for its ability to form biofilm that confers protection against harsh environmental condition and as part of the colonisation process during infection. Coaggregation is a process that facilitates the formation of biofilm. In a preliminary in vitro study, high coaggregation index and biofilm production were found between V. cholerae with human commensals namely Escherichia coli and Enterobacter cloacae. Building upon these results, the effects of coaggregation were further evaluated using adult BALB/c mouse model. The animal study showed no significant differences in mortality and fluid accumulation ratio between treatment groups infected with V. cholerae alone and those infected with coaggregation partnership (V. cholerae with E. coli or V. cholerae with E. cloacae). However, mild inflammation was detected in both partnering pairs. Higher density of V. cholerae was recovered from faecal samples of mice co-infected with E. coli and V. cholerae in comparison with other groups at 24 h post-infection. This partnership also elicited slightly higher levels of interleukin-5 (IL-5) and interleukin-10 (IL-10). Nonetheless, the involvement of autoinducer-2 (AI-2) as the signalling molecules in quorum sensing system is not evident in this study. Since E. coli is one of the common commensals, our result may suggest the involvement of commensals in cholera development.

Indexed as

Bacterial AdhesionAnimalsBiofilmsCholeraDisease Models, AnimalEnterobacter cloacaeEscherichia coliFecesFemaleMice, Inbred BALB CMicrobial InteractionsVibrio choleraeVirulenceAdult mouse modelCoaggregationHuman commensalVibrio cholerae

Identifiers

PMID31263955
OpenAlexW2953539226

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.