Evidence map›Paper›PMID 22723263›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

Elevated lipopolysaccharide in the colon evokes intestinal inflammation, aggravated in immune modulator-impaired mice.

Eunok Im, Franz Martin Riegler, Charalabos Pothoulakis, Sang Hoon Rhee

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-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

45 citing papers in PubMed, 75 citations in OpenAlex.

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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 3 institutions in 3 countries.

Eunok ImSchool of Pharmacy, Pusan National University, Busan, Korea.
Franz Martin Riegler
Charalabos Pothoulakis
Sang Hoon Rhee
University of California, Los Angeles · USMedical University of Vienna · ATPusan National University · KR

Funding

Innate Immune Response and Intestinal InflammationK01DK079015 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RHEE, SANG HOON · 2008 to 2010
$450k
A Role for Neuropeptides in Intestinal AngiogenesisK01DK083336 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI IM, EUNOK · 2009 to 2011
$450k
NIDDK NIH HHS DK-072471NIDDK NIH HHS DK-079015NIDDK NIH HHS DK-083336
6 · The paper itself

Abstract

Frequency of gram-negative bacteria is markedly enhanced in inflamed gut, leading to augmented LPS in the intestine. Although LPS in the intestine is considered harmless and, rather, provides protective effects against epithelial injury, it has been suggested that LPS causes intestinal inflammation, such as necrotizing enterocolitis. Therefore, direct effects of LPS in the intestine remain to be studied. In this study, we examine the effect of LPS in the colon of mice instilled with LPS by rectal enema. We found that augmented LPS on the luminal side of the colon elicited inflammation in the small intestine remotely, not in the colon; this inflammation was characterized by body weight loss, increased fluid secretion, enhanced inflammatory cytokine production, and epithelial damage. In contrast to the inflamed small intestine induced by colonic LPS, the colonic epithelium did not exhibit histological tissue damage or inflammatory lesions, although intracolonic LPS treatment elicited inflammatory cytokine gene expression in the colon tissues. Moreover, we found that intracolonic LPS treatment substantially decreased the frequency of immune-suppressive regulatory T cells (CD4(+)/CD25(+) and CD4(+)/Foxp3(+)). We were intrigued to find that LPS-promoted intestinal inflammation is exacerbated in immune modulator-impaired IL-10(-/-) and Rag-1(-/-) mice. In conclusion, our results provide evidence that elevated LPS in the colon is able to cause intestinal inflammation and, therefore, suggest a physiological explanation for the importance of maintaining the balance between gram-negative and gram-positive bacteria in the intestine to maintain homeostasis in the gut.

Indexed as

Administration, RectalAnimalsCD4-Positive T-LymphocytesColonCytokinesEnemaGastroenteritisHomeodomain ProteinsHomeostasisInflammation MediatorsInterleukin-10Intestinal MucosaIntestinal SecretionsIntestine, SmallLipopolysaccharidesMiceCytokinesHomeodomain ProteinsIL10 protein, mouseInflammation MediatorsInterleukin-10lipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesRAG-1 protein

Identifiers

PMID22723263
PMCPMC3423140
OpenAlexW2106321006

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.