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Intrarenal Injection of Escherichia coli in a Rat Model of Pyelonephritis
06:09

Intrarenal Injection of Escherichia coli in a Rat Model of Pyelonephritis

Published on: July 18, 2017

Clarithromycin is an effective immunomodulator in experimental pyelonephritis caused by pan-resistant Klebsiella

Evangelos J Giamarellos-Bourboulis1, Vassiliki Tziortzioti, Pantelis Koutoukas

  • 14th Department of Internal Medicine, University of Athens, Medical School, Athens, Greece. giamarel@ath.forthnet.gr

The Journal of Antimicrobial Chemotherapy
|March 22, 2006
PubMed
Abstract

Insights

Clarithromycin treatment reduced inflammation and tissue damage in rabbits infected with pan-resistant Klebsiella pneumoniae. This antibiotic demonstrated immunomodulatory effects on blood monocytes, aiding in the host

Area of Science:

  • Infectious Diseases
  • Pharmacology
  • Immunology

Background:

  • Pan-resistant Klebsiella pneumoniae poses a significant therapeutic challenge.
  • Antibiotic resistance necessitates novel treatment strategies, including immunomodulatory approaches.

Purpose of the Study:

  • To evaluate clarithromycin's efficacy as an immunomodulatory agent against pan-resistant Klebsiella pneumoniae in a rabbit pyelonephritis model.
  • To investigate the impact of clarithromycin on systemic and local inflammatory markers.

Main Methods:

  • Acute pyelonephritis was induced in rabbits, followed by inoculation with pan-resistant K. pneumoniae.
  • Animals were treated with intravenous clarithromycin, amikacin, or both, simultaneously or 24 hours post-infection.
  • Key inflammatory markers including TNF-alpha, MDA, caspase-3 activity, and bacterial loads were assessed.

Main Results:

  • Clarithromycin administration, alone or with amikacin, reduced serum TNF-alpha levels and inflammatory cell infiltration in multiple organs.
  • Treatment with clarithromycin led to decreased monocyte caspase-3 activity and ex vivo TNF-alpha secretion.
  • While clarithromycin modulated the immune response, significant reductions in bacterial tissue loads were primarily observed with combination therapy.

Conclusions:

  • Intravenous clarithromycin effectively attenuated systemic inflammation and local tissue damage in experimental pan-resistant K. pneumoniae infection.
  • The immunomodulatory effects on blood monocytes appear to be a key mechanism underlying clarithromycin's therapeutic benefit.
  • Clarithromycin shows promise as an adjunctive therapy, potentially mitigating the host's inflammatory response to difficult-to-treat infections.

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