Linked Life Data

11053477

Source:http://linkedlifedata.com/resource/pubmed/id/11053477

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2000-11-6
pubmed:abstractText
Tubulointerstitial nephritis is the main manifestation of acute renal damage caused by leptospirosis, but the mechanism remains unexplored. Patients infected with LEPTOSPIRA: shermani in Taiwan disclosed tubular dysfunction particularly in the medullary thick ascending limb of loop of Henle (mTAL), and the related renal damage seems to be underestimated. To elucidate the mechanism of tubular damage, outer membrane protein extract from LEPTOSPIRA: was administered to a model of cultured mTAL cells derived from normal mice. The addition of outer membrane protein extract from L. shermani to cultured mTAL cells induced a significant nuclear DNA binding of the NF-kappa B transcription factor by electrophoresis mobility shift assay. Forty-eight h after adding the outer membrane protein extract (0.2 microg/ml) to the cultured cells, the expression of inducible nitric oxide mRNA increased by 4.2-fold, monocyte chemoattractant protein-1 by 3-fold, and tumor necrosis factor-alpha by 2.4-fold when compared with untreated cells examined by reverse transcription competitive-PCR. Supernatant nitrite, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha protein levels also increased by 1.8-, 7.1-, and 5-fold, respectively. An antiserum raised against L. shermani largely prevented these effects. Outer membrane protein extract from L. bratislava induced fewer effects than L. shermani, and the avirulent nonpathogenic L. biflexa serovar patoc did not induce significant effects in the mTAL cells. In conclusion, L. shermani infection may cause mTAL cell damage and inflammation through the NF-kappa B-associated pathway. Findings of this study may be important in understanding the pathogenesis of tubulointerstitial nephritis caused by these organisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2017-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11053477-Animals, pubmed-meshheading:11053477-Bacterial Outer Membrane Proteins, pubmed-meshheading:11053477-Cell Nucleus, pubmed-meshheading:11053477-Cell Survival, pubmed-meshheading:11053477-Cells, Cultured, pubmed-meshheading:11053477-Chemokine CCL2, pubmed-meshheading:11053477-DNA, pubmed-meshheading:11053477-Gene Expression Regulation, pubmed-meshheading:11053477-Horseshoe Crabs, pubmed-meshheading:11053477-Immune Sera, pubmed-meshheading:11053477-Kidney Medulla, pubmed-meshheading:11053477-Leptospira, pubmed-meshheading:11053477-Loop of Henle, pubmed-meshheading:11053477-Mice, pubmed-meshheading:11053477-NF-kappa B, pubmed-meshheading:11053477-Nitric Oxide Synthase, pubmed-meshheading:11053477-Nitric Oxide Synthase Type II, pubmed-meshheading:11053477-RNA, Messenger, pubmed-meshheading:11053477-Tumor Necrosis Factor-alpha
pubmed:year
2000
pubmed:articleTitle
Leptospira outer membrane protein activates NF-kappaB and downstream genes expressed in medullary thick ascending limb cells.
pubmed:affiliation
Division of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan, Republic of China. cwyang@ms1.hinet.net
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't