Antibiotic-Induced Release of Endotoxin in Chronically Bacteriuric Patients

Hurley, James C.; Wj, Louis; Tosolini, F. A.; Carlin, JB

doi:10.1128/aac.36.5.1170-c

Cited by 9 publications

(15 citation statements)

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“…In addition, antibiotic-induced endotoxin liberation has been demonstrated in patients treated for septicaemia, bacterial meningitis, and bacteriuria [54,55,56,57]. Two studies serially assessed endotoxin levels in patients with sepsis before and after treatment [55,57]; administration of antibiotics led to a shift from cellbound to free endotoxin and a 2-fold to 50-fold increase in free endotoxin levels [57].…”

Section: Antibiotic-induced Release Of Bacterial Cell Wall Componentsmentioning

confidence: 99%

Clinical implications of antibiotic-induced endotoxin release in septic shock

et al. 2002

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Antibiotic-induced release of bacterial cell wall components can have immediate adverse effects for the patient. This article reviews the data on endotoxin release after initiation of antibiotic therapy and its role in the pathogenesis of sepsis and septic shock. Antibiotics differ in their potential to liberate endotoxins from bacterial cell walls. When used for treatment of systemic Gram-negative infection, some classes of beta-lactam antibiotics lead to markedly increased levels of free endotoxins while treatment with carbapenems and aminoglycosides produces relatively low amounts of endotoxins. Antibiotics that induce the formation of long, aberrant bacterial cells before effectively killing the microorganisms show the highest degree of endotoxin liberation. There is increasing evidence from animal models and clinical studies of sepsis that the antibiotic-mediated release of biologically active cell wall components derived from Gram-positive, Gram-negative or fungal organisms is associated with a rapid clinical deterioration.

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Section: Antibiotic-induced Release Of Bacterial Cell Wall Componentsmentioning

confidence: 99%

Clinical implications of antibiotic-induced endotoxin release in septic shock

et al. 2002

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“…In meningococci, it was observed that isolates from patients had higher endotoxin-liberating activities than strains isolated from carriers (3). During normal growth, until the stationary phase, most endotoxin remains bound to the cell (4,25,65,69), and a stable ratio of bacterial counts and endotoxin concentration (total and shed) is usually observed (4,25,41,68,78).…”

Section: Endotoxinmentioning

confidence: 99%

“…Finally, in the only clinical study in which the endotoxinliberating potentials of antibiotics were compared in humans, no differences were found in the potential of ticarcillin, cephalothin, ceftazidime, gentamicin, or ciprofloxacin to induce endotoxin release in the urine of chronically bacteriuric patients (41).…”

Section: Studies In Animalsmentioning

confidence: 99%

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Clinical relevance of antibiotic-induced endotoxin release

Prins

Deventer

Kuijper

et al. 1994

Antimicrob Agents Chemother

138

101

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“…Having found that IAP expression within cell culture inhibited IL-8 induction by gram-negative bacteria, but also that exogenous IAP did not directly alter intact bacteria, we examined the effects of IAP on bacterial components. It is known that bacteria release proinflammatory components after invasion and after killing by antibiotics or heat (13,14,24,25,44). We therefore investigated whether the IAP enzyme would be able to alter the proinflammatory effects of heat-killed bacteria.…”

Section: Il-8 Induced By a Mixed Purulent Fluid Is Inhibited By Ciapmentioning

confidence: 98%

Identification of specific targets for the gut mucosal defense factor intestinal alkaline phosphatase

Chen

Malo

Moss

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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Intestinal alkaline phosphatase (IAP) is a small intestinal brush border enzyme that has been shown to function as a gut mucosal defense factor, but its precise mechanism of action remains unclear. We investigated the effects of IAP on specific bacteria and bacterial components to determine its molecular targets. Purulent fluid from a cecal ligation and puncture model, specific live and heat-killed bacteria (Escherichia coli, Salmonella typhimurium, and Listeria monocytogenes), and a variety of proinflammatory ligands (LPS, CpG DNA, Pam-3-Cys, flagellin, and TNF) were incubated with or without calf IAP (cIAP). Phosphate release was determined by using a malachite green assay. The various fluids were applied to target cells (THP-1, parent HT-29, and IAP-expressing HT-29 cells) and IL-8 secretion measured by ELISA. cIAP inhibited IL-8 induction by purulent fluid in THP-1 cells by >35% (P < 0.005). HT29-IAP cells had a reduced IL-8 response specifically to gram-negative bacteria; >90% reduction compared with parent cells (P < 0.005). cIAP had no effect on live bacteria but attenuated IL-8 induction by heat-killed bacteria by >40% (P < 0.005). cIAP exposure to LPS and CpG DNA caused phosphate release and reduced IL-8 in cell culture by >50% (P < 0.005). Flagellin exposure to cIAP also resulted in reduced IL-8 secretion by >40% (P < 0.005). In contrast, cIAP had no effect on TNF or Pam-3-Cys. The mechanism of IAP action appears to be through dephosphorylation of specific bacterial components, including LPS, CpG DNA, and flagellin, and not on live bacteria themselves. IAP likely targets these bacterially derived molecules in its role as a gut mucosal defense factor.

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Antibiotic-Induced Release of Endotoxin in Chronically Bacteriuric Patients

Cited by 9 publications

References 0 publications

Clinical implications of antibiotic-induced endotoxin release in septic shock

Clinical implications of antibiotic-induced endotoxin release in septic shock

Clinical relevance of antibiotic-induced endotoxin release

Identification of specific targets for the gut mucosal defense factor intestinal alkaline phosphatase

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