Evidence map›Paper›PMID 26745982›Full record

ArticleWorld journal of microbiology & biotechnology2016

Salmonella typhimurium-induced M1 macrophage polarization is dependent on the bacterial O antigen.

Fengling Luo, Xiaoming Sun, Zhen Qu, Xiaolian Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in World journal of microbiology & biotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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  5. M1/M2 macrophages and their overlaps - myth or reality?Clinical science (London, England : 1979) · 2023
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  6. Review
  7. Article
  8. Pseudomonas aeruginosa biofilm is a potent inducer of phagocyte hyperinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  9. 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

4 authors at 1 institution in 1 country.

Fengling LuoState Key Laboratory of Virology, Medical Research Institute of Wuhan University and Department of Immunology and Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Road 185#, Wuhan, 430071, Hubei Province, China.
Xiaoming SunState Key Laboratory of Virology, Medical Research Institute of Wuhan University and Department of Immunology and Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Road 185#, Wuhan, 430071, Hubei Province, China.
Zhen QuState Key Laboratory of Virology, Medical Research Institute of Wuhan University and Department of Immunology and Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Road 185#, Wuhan, 430071, Hubei Province, China.
Xiaolian ZhangState Key Laboratory of Virology, Medical Research Institute of Wuhan University and Department of Immunology and Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Road 185#, Wuhan, 430071, Hubei Province, China. zhangxiaolian@whu.edu.cn.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, macrophages were shown to be capable of differentiating toward two phenotypes after antigen stimulation: a classically activated (M1) or an alternatively activated phenotype (M2). To investigate the effect of Salmonella enteric serovar typhimurium (S. typhimurium) on macrophage differentiation, we compared macrophage phenotypes after infection of murine bone marrow-derived macrophages with wild-type S. typhimurium and its isogenic rfc mutant. S. typhimurium C5 induced M1 macrophage polarization and enhanced inducible nitric oxide synthase expression by macrophages; this induction was dependent on Toll-like receptor 4. In contrast, the Δrfc mutant (S. typhimurium C5 rfc::Km(r)) lost this function and induced an M2 response in the macrophages. Here, we propose that S. typhimurium C5 is capable of polarizing macrophages towards the M1 phenotype and that this polarization is dependent on the O antigen encoded by rfc. Our finding indicates that M1 macrophage polarization induced by S. typhimurium may be related to the ability of this intracellular bacterium to survive and replicate within macrophages, which is essential for systemic disease.

Indexed as

AnimalsCell DifferentiationCytokinesGene DeletionHexosyltransferasesHost-Pathogen InteractionsMacrophagesMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicMutationNitric Oxide Synthase Type IIO AntigensPhenotypeSalmonella typhimuriumCytokinesHexosyltransferasesNitric Oxide Synthase Type IIO-antigen polymeraseO AntigensTlr4 protein, mouseToll-Like Receptor 4Macrophage polarizationO antigenSalmonella typhimurium

Identifiers

PMID26745982
OpenAlexW2231041528

What OpenQuestion holds

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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.