Tigecycline inhibits proliferation of Acanthamoeba castellanii

Acanthamoeba is an opportunistic protozoan parasite responsible for different diseases in humans, such as granulomatous amoebic encephalitis and amoebic keratitis. Tigecycline, a third-generation tetracycline antibiotic, has potential activity to treat most of the antibiotic resistant bacterial infe...

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Bibliographic Details
Published in:Parasitology research (1987) 2015-03, Vol.114 (3), p.1189-1195
Main Authors: Jha, Bijay Kumar, Seo, Incheol, Kong, Hyun-Hee, Suh, Seong-Il, Suh, Min-Ho, Baek, Won-Ki
Format: Article
Language:English
Subjects:
Acanthamoeba - drug effects
Acanthamoeba castellanii
Acanthamoeba castellanii - drug effects
adenosine triphosphate
Animals
Anti-Bacterial Agents - pharmacology
Antibiotics
bacterial infections
Biomedical and Life Sciences
Biomedicine
Cell proliferation
cell viability
Dosage and administration
Dose-Response Relationship, Drug
doxycycline
Encephalitis
encystment
eukaryotic cells
growth retardation
Health aspects
humans
Immunology
keratitis
Medical Microbiology
Microbiology
Minocycline - analogs & derivatives
Minocycline - pharmacology
Original Paper
Oxazines
parasites
parasitology
Prevention
Protozoans
tetracycline
tigecycline
trophozoites
Trophozoites - drug effects
Xanthenes
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Summary:Acanthamoeba is an opportunistic protozoan parasite responsible for different diseases in humans, such as granulomatous amoebic encephalitis and amoebic keratitis. Tigecycline, a third-generation tetracycline antibiotic, has potential activity to treat most of the antibiotic resistant bacterial infections. The effects of tigecycline in eukaryotic cells as well as parasites are less well studied. In the present study, we tested the effects of tigecycline on trophozoites of Acanthamoeba castellanii. The inhibitory effect of tigecycline on Acanthamoeba was determined by resazurin reduction and trypan blue exclusion assays. We found that tigecycline significantly inhibited the growth of Acanthamoeba (46.4 % inhibition at the concentration of 100 μM) without affecting cell viability and induction of encystation, whereas other tetracycline groups of antibiotics such as tetracycline and doxycycline showed no inhibitory effects. Furthermore, tigecycline decreased cellular adenosine triphosphate (ATP) level by 26 % than the control and increased mitochondrial mass, suggesting mitochondrial dysfunction in tigecycline-treated cells. These findings suggest that mitochondrial dysfunction with decreased ATP production might play an important mechanism of tigecycline in suppression of Acanthamoeba proliferation.
ISSN:0932-0113
1432-1955
DOI:10.1007/s00436-014-4302-1