April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Inhibition Of Bacterial Lipase Secretion By Azithromycin
Author Affiliations & Notes
  • Sobhan Nandi
    Pharmacology, University of North Carolina, Chapel Hill, North Carolina
  • Kurt Brubaker
    Medical Affairs, Inspire, Durham, North Carolina
  • Jose L. Boyer
    Research and Development, Inspire Pharmaceuticals Inc, Durham, North Carolina
  • Robert A. Nicholas
    Pharmacology, University of North Carolina, Chapel Hill, North Carolina
  • Footnotes
    Commercial Relationships  Sobhan Nandi, Inspire Pharmaceuticals (F); Kurt Brubaker, Inspire Pharmaceuticals (E, C, P); Jose L. Boyer, Inspire Pharmaceuticals (E, P); Robert A. Nicholas, Inspire Pharmaceuticals (F)
  • Footnotes
    Support  Inspire Pharmaceuticals Sponsored Research Agreement
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1491. doi:
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      Sobhan Nandi, Kurt Brubaker, Jose L. Boyer, Robert A. Nicholas; Inhibition Of Bacterial Lipase Secretion By Azithromycin. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1491.

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Abstract

Purpose: : Conjunctival-, eyelid- and skin-colonizing bacteria such as Staphylococcus epidermidis and S. aureus produce extracellular lipases, which hydrolyze the lipids (triacylglycerols, cholesteryl esters and wax esters) in the meibum to free fatty acids, mono- and diacylglycerols that likely contribute to the inflammation and tear film instability associated with Blepharitis. Topical administration of azithromycin (AZM) results in its high deposition and sustained levels in rabbit and human ocular tissues. We investigated the efficacy of AZM and other antibiotics (relative to their MICs) to inhibit the expression of bacterial lipases and proteases expressed by S. epidermidis and S. aureus.

Methods: : Saturated cultures of S. epidermidis (ATCC 14990) and S. aureus (ATCC 12600 and an erythromycin- and clindamycin-resistant clinical isolate) were resuspended in fresh growth media with no antibiotic or with increasing concentrations of AZM, and incubated for two hours. Media cleared of bacteria was assessed for the levels of lipases, proteases and beta-lactamase using fluorogenic lipid and protein substrates and a chromogenic beta-lactam antibiotic. MICs were determined by macrodilution in Nutrient Broth. Viability of bacteria following incubation with AZM was assessed by colony counting.

Results: : Whereas AZM had no effect on colony counts throughout the entire range of concentrations examined, AZM was effective at inhibiting secretion of bacterial lipases, proteases, and beta-lactamase at concentrations below the MIC. The IC50s of AZM for inhibition of lipase secretion were 2- and 8-fold lower than the MICs for inhibition of cell growth of S. aureus, and S. epidermidis, respectively. A clinical isolate of S. aureus, highly resistant to AZM nonetheless showed significant inhibition of lipase secretion at concentrations of antibiotic 8-fold lower than the MIC (MIC=32 mg/ml; IC50=4 mg/ml).

Conclusions: : AZM was effective at inhibiting virulence factor secretion even when present at levels below that required to inhibit cell growth. When combined with its distribution and pharmacokinetic properties, AZM shows promise as a highly effective inhibitor of virulence factors that are associated with Blepharitis.

Keywords: antibiotics/antifungals/antiparasitics • inflammation • cornea: tears/tear film/dry eye 
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