Meibomian gland dysfunction (MGD) is believed to be the leading cause of dry eye disease (DED), which affects tens of millions of Americans.1 Of particular interest, the most common pharmaceutical treatment for the management of MGD in the United States is the off-label use of topical azithromycin.2 This macrolide antibiotic is presumed to be effective because of its anti-inflammatory and antibacterial actions, which may suppress the MGD-associated posterior blepharitis and growth of bacteria on the eyelid.3 However, to our knowledge, no published, peer-reviewed data demonstrate that azithromycin has the ability to act directly on the human meibomian gland to enhance this tissue’s function and to ameliorate the pathophysiology of MGD.
Cells were treated with ethanol vehicle or azithromycin in serum-containing media for 7 days. Results are representative of 3 separate experiments. A, Appearance of cellular lipids. Cells were fixed and stained with LipidTOX green neutral lipid stain and 4’,6-diamidino-2-phenylindole (DAPI; red nuclear stain) (Invitrogen Corp) (original magnification ×400). B, LipidTOX staining intensity. Means are reported as fold-change compared with control values on the same day. Error bars indicate standard error. C, Cellular morphology. Images were taken prior to LipidTOX staining. Azithromycin-induced cellular maturation and vesicle accumulation were often followed by cell disruption and vesicle release (arrowhead, day 7) (original magnification ×200).aSignificantly greater than control (P < .005).
Cells were cultured in the absence (A) or presence (B) of serum for up to 7 days. Cell numbers at day 0 represent the baseline, and data are reported as mean ± standard error. Similar results were found in 2 additional studies.aSignificantly less than control (P < .005).
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