Browsing by Subject "Erythromycin"

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    MicroRNA 21 is a homeostatic regulator of macrophage polarization and prevents prostaglandin E2-mediated M2 generation
    (PLoS, 2015-02-23) Wang, Zhuo; Brandt, Stephanie; Medeiros, Alexandra; Wang, Soujuan; Wu, Hao; Dent, Alexander; Serezani, C. Henrique; Department of Microbiology and Immunology, IU School of Medicine
    Macrophages dictate both initiation and resolution of inflammation. During acute inflammation classically activated macrophages (M1) predominate, and during the resolution phase alternative macrophages (M2) are dominant. The molecular mechanisms involved in macrophage polarization are understudied. MicroRNAs are differentially expressed in M1 and M2 macrophages that influence macrophage polarization. We identified a role of miR-21 in macrophage polarization, and found that cross-talk between miR-21 and the lipid mediator prostaglandin E2 (PGE2) is a determining factor in macrophage polarization. miR-21 inhibition impairs expression of M2 signature genes but not M1 genes. PGE2 and its downstream effectors PKA and Epac inhibit miR-21 expression and enhance expression of M2 genes, and this effect is more pronounced in miR-21-/- cells. Among potential targets involved in macrophage polarization, we found that STAT3 and SOCS1 were enhanced in miR-21-/- cells and further enhanced by PGE2. We found that STAT3 was a direct target of miR-21 in macrophages. Silencing the STAT3 gene abolished PGE2-mediated expression of M2 genes in miR-21-/- macrophages. These data shed light on the molecular brakes involved in homeostatic macrophage polarization and suggest new therapeutic strategies to prevent inflammatory responses.
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    A retrospective comparison of antibiotic regimens for preterm premature rupture of membranes
    (Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2014-09) Pierson, Rebecca C.; Gordon, Sashana S.; Haas, David M.; Department of Obstetrics & Gynecology, IU School of Medicine
    OBJECTIVE: To evaluate whether the use of ampicillin and azithromycin leads to a similar latency period in preterm premature rupture of membranes as ampicillin and erythromycin and whether the substitution of azithromycin for erythromycin effects rates of other outcomes. METHODS: We performed a retrospective cohort study of women with preterm premature rupture of membranes between 24 and 34 completed weeks of gestation and compared two groups: those who received ampicillin and erythromycin and those who received ampicillin and azithromycin. Primary outcome was length of latency (defined as time from first antibiotic dose to delivery) and secondary outcomes were rates of chorioamnionitis, cesarean delivery, Apgar scores, birth weight, neonatal death, neonatal sepsis, and neonatal respiratory distress syndrome. RESULTS: Of 168 women who met inclusion criteria, 75 received ampicillin and erythromycin and 93 received ampicillin and azithromycin. There was no difference in latency between groups: 9.6±13.2 days (erythromycin) compared with 9.4±10.0 (azithromycin) days (P=.40). Secondary outcomes did not differ between groups. We had 80% power to detect a difference of 5 days. CONCLUSION: Among women with preterm premature rupture of membranes between 24 and 34 completed weeks of gestation, substitution of azithromycin for erythromycin in the recommended antibiotic regimen did not affect latency or any other measured maternal or fetal outcomes. LEVEL OF EVIDENCE: III.