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Vol. 25, No. 6, 2005
Issue release date: November–December 2005
Section title: Original Report: Laboratory Investigation
Am J Nephrol 2005;25:570–578
(DOI:10.1159/000088990)

Tamm-Horsfall Protein Acts as a General Host-Defense Factor against Bacterial Cystitis

Raffi H.S. · Bates, Jr. J.M. · Laszik Z. · Kumar S.
Departments of aMedicine and bPathology, University of Oklahoma Health Sciences Center, Oklahoma City, Okla., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 5/20/2005
Accepted: 8/29/2005
Published online: 10/17/2005

Number of Print Pages: 9
Number of Figures: 9
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN

Abstract

Aims: Tamm-Horsfall protein (THP) is urine’s most abundant protein, but its biological function has remained elusive. Recently, THP-deficient (THP–/–) mice were shown to have difficulty clearing Escherichia coli from the urinary bladder. It has remained unclear if interaction between THP and E. coli is specific for E. coli or if THP has a versatile ability to clear a variety of bacteria from the bladder, and act as a broad host-defense mechanism against urinary tract infection (UTI). In this study, we examined the role of THP as a protective factor against UTI caused by bacteria other than E. coli, namely Klebsiella pneumoniae and Staphylococcus saprophyticus by determining if the THP–/– mouse has difficulty clearing these bacteria from its bladder. Methods: THP gene knockout mice were generated by the technique of homologous recombination. K. pneumoniae and S. saprophyticus were introduced transurethrally, in separate experiments, into the bladders of the THP–/– and genetically similar wild-type (THP+/+) mice. Urine was collected at periodic intervals and cultured to quantitate the degree of bacteriuria. Bladders were surgically removed and examined histomorphometrically to determine the intensity of inflammation. Results: Results showed that both with K. pneumoniae and with S. saprophyticus, the THP–/– mice had more severe bacteriuria in comparison with THP+/+ mice. The inflammatory changes in the bladder were also markedly more intense in THP–/– mice with each of the bacterial species. Conclusions: These findings support the hypothesis that THP helps eliminate K. pneumoniae and S. saprophyticus from the urinary tract and acts as a general host-defense factor against UTI.


  

Author Contacts

Satish Kumar, MD
Department of Medicine, Nephrology Section
The University of Oklahoma Health Sciences Center
920 S.L. Young Blvd, WP 2250, Oklahoma City, OK 73104 (USA)
Tel. +1 405 271 6842, Fax +1 405 271 6496, E-Mail satish-kumar@ouhsc.edu

  

Article Information

Received: May 10, 2005
Accepted: August 29, 2005
Published online: October 17, 2005
Number of Print Pages : 9
Number of Figures : 9, Number of Tables : 0, Number of References : 29

  

Publication Details

American Journal of Nephrology

Vol. 25, No. 6, Year 2005 (Cover Date: November-December 2005)

Journal Editor: Bakris, G. (Chicago, Ill.)
ISSN: 0250–8095 (Print), eISSN: 1421–9670 (Online)

For additional information: http://www.karger.com/ajn


Article / Publication Details

First-Page Preview
Abstract of Original Report: Laboratory Investigation

Received: 5/20/2005
Accepted: 8/29/2005
Published online: 10/17/2005

Number of Print Pages: 9
Number of Figures: 9
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN


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