Affiliations 

  • 1 Department of Biological Sciences, Faculty of Science and Technology, Sunway University, Selangor, Malaysia
  • 2 Department of Biological and Biomedical Sciences, Aga Khan University, Karachi, Pakistan
  • 3 Division of Pediatric Infectious Diseases, Vanderbilt University School of Medicine, Nashville, USA
  • 4 Department of Biological Sciences, Faculty of Science and Technology, Sunway University, Selangor, Malaysia. Electronic address: [email protected]
Exp Parasitol, 2016 Jul 2;168:45-50.
PMID: 27381503 DOI: 10.1016/j.exppara.2016.06.011

Abstract

Non-steroidal anti-inflammatory drug, Diclofenac, targeting COX have shown promise in the treatment of Acanthamoeba keratitis, but the underlying mechanisms remain unknown. Using various NSAIDs, Diclofenac sodium, Indomethacin, and Acetaminophen, here we determined the effects of NSAIDs on the biological properties of Acanthamoeba castellanii belonging to the T4 genotype. Using amoebicidal assays, the results revealed that Diclofenac sodium, and Indomethacin affected growth of A. castellanii. In contrast, none of the compounds tested had any effect on the viability of A. castellanii. Importantly, all NSAIDs tested abolished A. castellanii encystation. This is a significant finding as the ability of amoebae to transform into the dormant cyst form presents a significant challenge in the successful treatment of infection. The NSAIDs inhibit production of cyclo-oxegenase, which regulates the synthesis of prostaglandins suggesting that cyclooxygenases (COX-1 and COX-2) and prostaglandins play significant role(s) in Acanthamoeba biology. As NSAIDs are routinely used in the clinical practice, these findings may help design improved preventative strategies and/or of therapeutic value to improve prognosis, when used in combination with other anti-amoebic drugs.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.