Literature DB >> 18842674

Endogenous tissue-type plasminogen activator is protective during ascending urinary tract infection.

Joris J T H Roelofs1, Kasper M A Rouschop, Gwendoline J D Teske, Gerry T M Wagenaar, Nike Claessen, Jan J Weening, Tom van der Poll, Sandrine Florquin.   

Abstract

BACKGROUND: Acute pyelonephritis is one of the most common bacterial infections. Tissue-type plasminogen activator (tPA) is a potent fibrinolytic agent, but can play a role in inflammatory processes as well.
METHODS: We induced pyelonephritis in tPA(-/-) and C57BL/6 wild-type (WT) mice by intravesical inoculation with 10(10) CFU uropathogenic Escherichia coli 1677. The mice were killed after 24 and 48 h, after which bacterial outgrowth and cytokine levels in kidney homogenates were determined. Influx of neutrophils was quantified by myeloperoxidase-ELISA. Neutrophil phagocytosis and oxidative burst were measured.
RESULTS: The tPA(-/-) kidneys contained significantly higher numbers of E. coli CFU, accompanied by higher levels of interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha). The number of infiltrating neutrophils was similar in tPA(-/-) and WT mice at both time points, suggesting that tPA(-/-) neutrophils have a lower ability to eliminate E. coli. Phagocytosis of E. coli organisms was not diminished in tPA(-/-) neutrophils. Interestingly, tPA(-/-) neutrophils showed a significantly lower ability to generate an oxidative burst reaction upon stimulation with E. coli than WT neutrophils. Incubation with recombinant tPA reversed this effect completely.
CONCLUSIONS: These results show that deletion of the tPA-gene in mice leads to lower bactericidal potential of tPA(-/-) neutrophils, which results in significantly more bacterial outgrowth during experimental pyelonephritis.

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Year:  2008        PMID: 18842674     DOI: 10.1093/ndt/gfn562

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  5 in total

1.  S100A8/A9 is not involved in host defense against murine urinary tract infection.

Authors:  Mark C Dessing; Loes M Butter; Gwendoline J Teske; Nike Claessen; Chris M van der Loos; Thomas Vogl; Johannes Roth; Tom van der Poll; Sandrine Florquin; Jaklien C Leemans
Journal:  PLoS One       Date:  2010-10-14       Impact factor: 3.240

2.  Developmental loss, but not pharmacological suppression, of renal carbonic anhydrase 2 results in pyelonephritis susceptibility.

Authors:  John Ketz; Vijay Saxena; Samuel Arregui; Ashley Jackson; George J Schwartz; Takafumi Yagisawa; Robert L Fairchild; David S Hains; Andrew L Schwaderer
Journal:  Am J Physiol Renal Physiol       Date:  2020-05-11

Review 3.  Tissue plasminogen activator and inflammation: from phenotype to signaling mechanisms.

Authors:  Ling Lin; Kebin Hu
Journal:  Am J Clin Exp Immunol       Date:  2014-02-27

4.  Studies on Virulence and Extended-Spectrum β-Lactamase-Producing Uropathogenic Escherichia coli Isolates and Therapeutic Effect of Fosfomycin in Acute Pyelonephritis Mice.

Authors:  Lingchun Zhang; Fenfen Li; Xiaotian Li
Journal:  Biomed Res Int       Date:  2022-01-30       Impact factor: 3.411

5.  Lysis of cold-storage-induced microvascular obstructions for ex vivo revitalization of marginal human kidneys.

Authors:  Jenna R DiRito; Sarah A Hosgood; Melanie Reschke; Claire Albert; Laura G Bracaglia; John R Ferdinand; Benjamin J Stewart; Christopher M Edwards; Anand G Vaish; Sathia Thiru; David C Mulligan; Danielle J Haakinson; Menna R Clatworthy; W Mark Saltzman; Jordan S Pober; Michael L Nicholson; Gregory T Tietjen
Journal:  Am J Transplant       Date:  2020-07-05       Impact factor: 8.086

  5 in total

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