April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Effect of Topical Azithromycin on Innate Immune Responses in Experimental Keratitis
Author Affiliations & Notes
  • Z. Sadrai
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • A. R. Hajrasouliha
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • S. K. Chauhan
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • D. R. Saban
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • M. H. Dastjerdi
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • R. Dana
    Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  Z. Sadrai, None; A.R. Hajrasouliha, None; S.K. Chauhan, None; D.R. Saban, None; M.H. Dastjerdi, None; R. Dana, None.
  • Footnotes
    Support  Commercial relationship: Research support from Inspire Pharmaceuticals (R. Dana)
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 5536. doi:
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      Z. Sadrai, A. R. Hajrasouliha, S. K. Chauhan, D. R. Saban, M. H. Dastjerdi, R. Dana; Effect of Topical Azithromycin on Innate Immune Responses in Experimental Keratitis. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5536.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Azithromycin (AZM) is a broad-spectrum macrolide antibiotic which may have endogenous anti-inflammatory properties similar to other macrolides via suppression of NF-kB signal transduction pathway. This study aimed to determine the potential immunomodulatory effects of AZM on corneal inflammation.

Methods: : 6-8 week old BALB/c mice underwent thermal cautery to the corneal surface to induce inflammation and leukocyte influx. Corneas were treated topically either with AZM ophthalmic solution 1% (AzaSite®; Inspire Pharmaceuticals, Inc, NC, USA) or the relevant vehicle, twice per day. Corneas were harvested at various time-points (day 1, 3, 7, 10, and 14) to characterize the inflammatory infiltrates via FACS analysis, and to quantitate relevant chemokines/cytokines via real time PCR.

Results: : AZM treatment significantly decreased the overall influx of total bone marrow-derived (CD45+) cells on day 7 by nearly 40%. The majority of the reduction in the CD45+ cells appeared to be found among the CD11b+ (macrophage) and CD11c+ (dendritic cell) subsets, but not among Gr-1+ cells (neutrophils). Moreover, pro-inflammatory chemokines CXCL10 and CCL5, and IL-1beta levels were significantly reduced (p<0.05) on day 7 with AZM treatment.

Conclusions: : Topical AZM reduces infiltration of macrophages and dendritic cells considerably in inflamed corneas. This was further supported by an associated reduction in CXCL10 and CCL5, as well as IL-1beta. In addition to its anti-microbial properties, topical AZM holds anti-inflammatory properties in a mouse model of keratitis.

Keywords: cornea: basic science • keratitis • drug toxicity/drug effects 
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