Evidence map›Paper›PMID 20704730›Full record

ArticleJournal of inflammation (London, England)2010

The inflammatory cytokine tumor necrosis factor modulates the expression of Salmonella typhimurium effector proteins.

Jun Ma, Yong-Guo Zhang, Yinglin Xia, Jun Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.3field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Wingless homolog Wnt11 suppresses bacterial invasion and inflammation in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2011
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  15. PPARα exacerbatesGut microbes
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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.

Jun Ma *Department of Medicine, Gastroenterology & Hepatology Division, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Yong-Guo Zhang *Department of Medicine, Gastroenterology & Hepatology Division, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Yinglin XiaDepartment of Biostatistics and Computational Biology, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Jun SunDepartment of Medicine, Gastroenterology & Hepatology Division, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.
University of Rochester · US

Funding

NF-kB /Beta-catenin interaction during intestinal inflammationK01DK075386 · NIDDK · UNIVERSITY OF ROCHESTER · PI SUN, JUN · 2007 to 2011
$651k
Enteric bacterial modulation of Vitamin D Receptor signaling in colitisR03DK089010 · NIDDK · UNIVERSITY OF ROCHESTER · PI SUN, JUN · 2010 to 2011
$154k
NIDDK NIH HHS K01 DK075386NIDDK NIH HHS R03 DK089010
6 · The paper itself

Abstract

Tumor necrosis factor alpha (TNF-alpha)is a host inflammatory factor. Bacteria increase TNF-alpha expression in a variety of human diseases including infectious diseases, inflammatory bowel diseases, and cancer. It is unknown, however, how TNF-alpha directly modulates bacterial protein expression during intestinal infection and chronic inflammation. In the current study, we hypothesize that Salmonella typhimurium senses TNF-alpha and show that TNF-alpha treatment modulates Salmonella virulent proteins (called effectors), thus changing the host-bacterial interaction in intestinal epithelial cells. We investigated the expression of 23 Salmonella effectors after TNF-alpha exposure. We found that TNF-alpha treatment led to differential effector expression: effector SipA was increased by TNF-alpha treatment, whereas the expression levels of other effectors, including gogB and spvB, decreased in the presence of TNF-alpha. We verified the protein expression of Salmonella effectors AvrA and SipA by Western blots. Furthermore, we used intestinal epithelial cells as our experimental model to explore the response of human intestinal cells to TNF-alpha pretreated Salmonella. More bacterial invasion was found in host cells colonized with Salmonella strains pretreated with TNF-alpha compared to Salmonella without TNF-alpha treatment. TNF-alpha pretreated Salmonella induced higher proinflammatory JNK signalling responses compared to the Salmonella strains without TNF-alpha exposure. Exposure to TNF-alpha made Salmonella to induce more inflammatory cytokine IL-8 in intestinal epithelial cells. JNK inhibitor treatment was able to suppress the effects of TNF-pretreated-Salmonella in enhancing expressions of phosphorylated-JNK and c-jun and secretion of IL-8. Overall, our study provides new insights into Salmonella-host interactions in intestinal inflammation.

Identifiers

PMID20704730
PMCPMC2925363
OpenAlexW2144617089

What OpenQuestion holds

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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.