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ORIGINAL RESEARCH |
From the Department of Biochemical Sciences and Advanced Therapy, Section of Obstetrics and Gynaecology, the Department of Biology, and the Department of Clinical and Experimental Medicine, Section of Nuclear Medicine, University of Ferrara, Ferrara, Italy.
Address reprint requests to: Prof Fortunato Vesce, Department of Biomedical Sciences and Advanced Therapy, Section of Obstetrics and Gynaecology, University of Ferrara, 44100 Ferrara, Italy; e-mail: ves{at}dns.unife.it.
OBJECTIVE: To test the effect of ampicillin on amniotic interleukin-6 (IL-6) and prostaglandin E2 (PGE2) release.
METHODS: In an in vitro study, IL-6 and PGE2 release from amnion-like Wistar Institute Susan Hayflick cells was assayed under basal conditions, as well as after incubation with ampicillin. In an in vivo study, amniotic fluid IL-6 was assayed in a total of 212 patients submitted to genetic amniocentesis during the 17th week of their singleton physiological pregnancy. The study population was subdivided as follows: 92 patients sampled before ampicillin administration, 70 patients sampled 4 hours after administration of 1 g ampicillin, and 50 patients sampled 12 hours after administration of 1 g ampicillin.
RESULTS: At doses ranging from 10-7 to 10-4 M, ampicillin decreased IL-6 release from Wistar Institute Susan Hayflick cells. The drug effect was already statistically significant (-30%; P < .05) at the lowest concentration tested (10-7 M), reaching the maximum (-50%) at 10-6 M after 4 hours of incubation. Moreover, ampicillin concentrations ranging from 10-7 to 10-4 M decreased PGE2 release from Wistar Institute Susan Hayflick cells; maximal inhibition was reached at 10-6 M after 4 hours (-40%; P < .05). Finally, IL-6 levels measured in amniotic fluid of patients sampled 4 hours after ampicillin administration proved strongly and significantly reduced when compared with those sampled either before or 12 hours after treatment (P < .001).
CONCLUSION: The capacity of ampicillin to directly decrease amniotic IL-6 and PGE2 release should be considered in the management of bacterial and nonbacterial inflammatory complications of pregnancy mediated by the cytokine and prostanoid interaction.
LEVEL OF EVIDENCE: III
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