Azithromycin suppresses activation of nuclear factor-kappa B and synthesis of pro-inflammatory cytokines in tracheal aspirate cells from premature infants

Zubair H. Aghai, Aruna Kode, Judy G. Saslow, Tarek Nakhla, Sabeena Farhath, Gary E. Stahl, Riva Eydelman, Louise Strande, Paola Leone, Irfan Rahman

    Research output: Contribution to journalArticlepeer-review

    98 Scopus citations

    Abstract

    Nuclear factor-kappaB (NF-κB) plays a central role in regulating key proinflammatory mediators. The activation of NF-κB is increased in tracheal aspirate (TA) cells from premature infants developing bronchopulmonary dysplasia (BPD). We studied the effect of azithromycin (AZM) on the suppression of NF-κB activation and the synthesis of pro-inflammatory cytokines IL-6 and IL-8 by TA cells obtained from premature infants. Tracheal aspirate cells were stimulated with tumor necrosis factor-alpha (TNF-α) and incubated with AZM. The nuclear NF-κB-DNA binding activity, the levels of inhibitory kappaB-alpha (IκB-α) in the cytoplasmic fraction and IL-6 and IL-8 release in the cell culture media were measured. Stimulation of TA cells by TNF-α increased the activation of NF-κB, which was suppressed by the addition of AZM. Increased activation of NF-κB was also associated with increased levels of pro-inflammatory cytokines (IL-6 and IL-8). AZM significantly reduced the IL-6 and IL-8 production to the levels similar to control. TNF-α stimulation also increased the degradation of IκB-α, which was restored with the addition of AZM. Our data suggest that AZM therapy may be an effective alternative to steroids in reducing lung inflammation and prevention of BPD in ventilated premature infants.

    Original languageEnglish (US)
    Pages (from-to)483-488
    Number of pages6
    JournalPediatric Research
    Volume62
    Issue number4
    DOIs
    StatePublished - Oct 2007

    All Science Journal Classification (ASJC) codes

    • Pediatrics, Perinatology, and Child Health

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