Comparison of the in vitro effects of amoxicillin and ampicillin on the polymorphonuclear neutrophil respiratory burst

Reynaert, Marie-Line; Hochart-Behra, Anne-Cécile; Behra-Miellet, Josette; Gressier, Bernard; Mine, Louis; Dine, T.; Luyckx, M.; Dubreuil, L.; Brunet, C.

doi:10.1093/jac/dkn545

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…Similarly, a previous study has demonstrated that ampicillin and carbenicillin were both unable to induce MN formation in in vivo rat bone marrow assay [Stemp et al, 1989]. AMO is structurally different from ampicillin by the addition of a hydroxyl to the amino-benzyl group of its side chain [Reynaert et al, 2009]. However, this difference does not lead to a significant distinction between the genotoxic potential of these analogs.…”

Section: Discussionmentioning

confidence: 89%

“…Recent studies on DNA repair kinetics have shown that 5 mM AMO concentration which is far higher than the expected human clinical exposure levels was able to induce DNA single-strand breaks via oxidative mechanisms (ROS) in human peripheral lymphocytes; however, concentrations lower than 5 mM hardly evoked any effect in the same experimental design [Arabski et al, 2005;Li et al, 2007]. Furthermore, AMO has been shown to induce the production of the superoxide (O 2 2 ) radicals in polymorphic nuclear neutrophils in the absence of a metabolic activation [Reynaert et al, 2009]. On the other hand, AMO was negative in Green Screen Assay (GSA) [Cahill et al, 2004].…”

Section: Discussionmentioning

confidence: 99%

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Cytogenetic genotoxicity of amoxicillin

İstifli

Topaktaş

2009

Environ and Mol Mutagen

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Amoxicillin (AMO), a drug used in the treatment of infections caused by susceptible bacteria, has been evaluated for its ability to induce genotoxicity in human peripheral blood lymphocytes. The potential genotoxic effects of AMO were investigated in vitro by the sister chromatid exchange (SCE), chromosomal aberration (CA), and micronucleus (MN) tests. The cells were treated with 400, 600, 800, and 1,000 microg/ml AMO in the presence and absence of a metabolic activator (S9 mix), respectively. In this study, AMO did not induce SCEs or CAs in human peripheral blood lymphocytes both in the presence and absence of the metabolic activator. AMO concentration-dependently decreased the proliferation index (PI) in the absence of the metabolic activation for 24-hr treatment period. Mitotic index (MI) was generally found to have been reduced when compared with the negative control but not with the solvent control in cultures treated with AMO for 24 hr. AMO did not decrease the PI and MI in the presence of the metabolic activator. Furthermore, AMO neither induced the formation of MN nor decreased the nuclear division index in human peripheral blood lymphocytes both in the presence and absence of the metabolic activator. According to the present results, we suggest that AMO does not pose genotoxic risk for patients who are under therapy against bacterial infections.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Cytogenetic genotoxicity of amoxicillin

İstifli

Topaktaş

2009

Environ and Mol Mutagen

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“…While most classes of antibiotics do not affect neutrophil function (e.g., beta-lactams, fluoroquinolones [11][12][13]) it has been shown for some classes of antibiotics that they may affect ROS production. Among the substance classes identified are sulfonamides (sulfa drugs), which have been demonstrated to impede the respiratory burst of neutrophils [14,15].…”

Section: Introductionmentioning

confidence: 99%

Glycopeptide Antibiotics Impair Neutrophil Effector Functions

Ettel¹,

Sehgal²,

Harrison³

et al. 2023

Int Arch Allergy Immunol

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Introduction: Neutrophilic granulocytes represent the first line of defense against microorganisms. Granulocytes phagocytose microorganisms and specifically synthesize oxygen radicals against them, which eventually kills the invaders. Methods: Neutrophilic granulocytes were isolated from peripheral blood of healthy volunteer donors. Putative interference of new-generation antibiotics with neutrophil function was tested using a collection of granulocyte-stimulating agents and Amplex™ Red-based plate assay and flow cytometry-based respiratory burst assays. In addition, phagocytosis of E. coli, IL-8 production, bactericidal activity, and CD62L expression of granulocytes were evaluated. Results: Of note, we found that the two glycopeptide antibiotics dalbavancin and teicoplanin inhibited ROS production upon granulocyte activation via different signaling pathways in a dose-dependent manner. Dalbavancin also blocked the PMA-induced shedding of CD62L. In contrast, the oxazolidinone antibiotics tedizolid and linezolid had no effect on neutrophil function, while the combination of ceftazidime/avibactam dose dependently inhibited the fMLP/Cytochalasin B-induced granulocyte burst in a dose-dependent manner. Additionally, we showed that dalbavancin and teicoplanin as well as sulfametrole/trimethoprim and ceftazidime/avibactam inhibited baseline and PMA-induced IL-8 production by neutrophilic granulocytes. Moreover, dalbavancin impaired the bactericidal activity of neutrophilic granulocytes. Conclusion: We here identified hitherto unknown inhibitory effects of several classes of antibiotics on the effector functions of neutrophilic granulocytes.

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