Continuous administration of PBP-2- and PBP-3-specific β-lactams causes higher cytokine responses in murine Pseudomonas aeruginosa and Escherichia coli sepsis | Zendy

Jacqueline Buijs | Zendy; Anthonius S. M. Dofferhoff | Zendy; Johan W. Mouton | Zendy; J.W.M. van der Meer | Zendy

Open Access

Continuous administration of PBP-2- and PBP-3-specific β-lactams causes higher cytokine responses in murine Pseudomonas aeruginosa and Escherichia coli sepsis

Author(s) -

Jacqueline Buijs,

Anthonius S. M. Dofferhoff,

Johan W. Mouton,

J.W.M. van der Meer

Publication year - 2007

Publication title -

journal of antimicrobial chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.124

H-Index - 194

eISSN - 1460-2091

pISSN - 0305-7453

DOI - 10.1093/jac/dkm073

Subject(s) - pseudomonas aeruginosa , escherichia coli , microbiology and biotechnology , sepsis , cytokine , enterobacteriaceae , biology , bacteria , pseudomonadaceae , immunology , gene , biochemistry , genetics

Initial antibiotic treatment of severe infections can lead to clinical deterioration due to sudden endotoxin release and concomitant exaggerated inflammatory response. Antibiotic-induced morphological changes may contribute to this phenomenon. High-dose ceftazidime, which inhibits penicillin-binding protein (PBP)-1 in Gram-negative bacteria, causes quick bacteriolysis and low endotoxin release. Low-dose ceftazidime leads to PBP-3 inhibition, which causes bacterial filament formation, associated with high endotoxin releases. PBP-2-specific antibiotics induce spheroplasts, again associated with low endotoxin release. We hypothesized that antibiotic type, concentration and regimen influence bacterial morphology, endotoxin levels and inflammatory response.

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