Epinecidin-1: A marine fish antimicrobial peptide with therapeutic potential against Trichomonas vaginalis infection in mice.

Trichomoniasis is caused by infection with the protozoan parasite Trichomonas vaginalis, and prolonged persistence may lead to serious ill effects in patients. Thus, the development of new therapeutic strategies to combat drug-resistant T. vaginalis would be clinically beneficial. Antimicrobial peptides (AMPs) comprise an emerging class of molecules that may serve as effective alternatives to antibiotics. In this report, we demonstrate that the synthetic fish AMP, Epinecidin-1 (Epi-1), acts against T. vaginalis both in vitro and in vivo. Under in vitro conditions, Epi-1 disrupted the membrane of metronidazole-resistant T. vaginalis and completely killed the pathogen. To mimic human infection in vivo, estradiol-stimulated mice with vaginal Lactobacillus acidophilus colonization were infected with T. vaginalis, followed by treatment with Epi-1, Vigill, metronidazole or furazolidone. After seven days, the T. vaginalis content was effectively decreased in Epi-1 treated mice, as measured by acridine orange staining of wet smears and tissue biopsies, as well as qPCR of vaginal discharge DNA. Taken together, our results demonstrate that Epi-1 is a strong candidate for development as an alternative therapeutic for T. vaginalis infection.

Nucleophosmin modulates the alleviation of atopic dermatitis caused by the marine-derived compound dihydroaustrasulfone alcohol

Atopic dermatitis (AD) is a chronic inflammatory skin disease, and its prevalence is increasing. AD usually elicits skin barrier dysfunction, dry skin and itching. As the mechanisms of AD remain unknown, there is an urgent need to find effective therapies. Because of the diversity and complexity of marine environments, the discovery of drugs from marine organisms as novel therapeutic agents for human diseases has seen renewed interest. Dihydroaustrasulfone alcohol (WA-25), the synthetic precursor of austrasulfone, which is a natural product isolated from a Formosan soft coral, has been shown to possess many therapeutic effects in our previous studies. However, the detailed mechanisms and therapeutic effects of WA-25 on AD are incompletely understood. We performed in vitro and in vivo studies to examine the effects of WA-25 on AD. We showed that WA-25 blocks inflammation and oxidative stress. Simultaneously, we also found that WA-25 reduces the AD scores and AD-induced transepidermal water loss (TEWL), scratching behavior, and alloknesis. WA-25 is more effective in cases of AD than are the drugs that are currently used clinically. Importantly, we also found that when nucleophosmin (NPM) was inhibited or when its expression was reduced, the anti-inflammatory and anti-AD effects of WA-25 were blocked. These data suggest that NPM plays dual roles in inflammation and AD. Overall, these results suggest that WA-25 is a potential anti-inflammatory and AD therapeutic agent that is modulated by NPM.