The role of diclofenac sodium in the dimorphic transition in Candida albicans

Ghalehnoo, Zahra Rashki; Rashki, Ahmad; Najimi, Mohsen; Domínguez, Ángel

doi:10.1016/j.micpath.2009.12.003

Cited by 36 publications

(25 citation statements)

References 57 publications

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“…Sodium Diclofenacshowed lower MIC against C. albicans and C. glabrata while ibuprofen showed lower MIC against C. krusei in comparison to other NSAIDs. By testing their effect on germ tube formation, it was found that Sodium Diclofenacat 500 µg/ml inhibit germ tube formation while ketoprofen and ibuprofen inhibit it to lesser extent that agree with many studies [40,41,42].…”

Section: Discussionsupporting

confidence: 86%

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Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of Candida spp.

Ashraf¹,

Yousri²,

Taha³

et al. 2015

AJMR

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Candida spp. are the most common cause of fungal diseases and the fourth commonest cause of nosocomial invasive infections which are considered in many cases as life threatening. Among Candida spp., C. albicans is the most common cause of many fungal diseases, but non-albicans spp. infections are in increase. Nonsteroidal anti-inflammatory drugs have previously been shown to have antifungal activity. In this study we determine the antifungal activity of the tested NSAIDs using agar well diffusion method, their effect on the dimorphic transition of C. albicans by testing their ability to form germ tube in the presence of human serum. Determining the effect of NSAIDs on the adherence to plastic surfaces and on the mature biofilms formed by the tested Candida spp.. The results indicated that Sodium Diclofenac showed lower MIC against C. albicans and C. glabrata while Ibuprofen had lower MIC against C. krusei. upon examining the effect of Diclofenac sodium, Ibuprofen and ketoprofen on biofilm formed on polyurethane segments by Scanning electron microscope (SEM), a damage to membranes of the tested species was observed. Sodium Diclofenac showed the highest inhibitory effect on the adherence (51.1-76.9% at MIC and 56.6-83.3% at 2XMIC) of C. albicans and C. glabrata but Ibuprofen showed a higher inhibitory effect against the adherence of C. krusei. For mature biofilms, the highest disruptive effect on mature biofilms formed by all tested Candida Spp. .06% at 2XMIC) was observed by Diclofenac sodium. Sodium Diclofenac inhibited dimorphic transition of C. albicans but a decrease in germ tube formation was shown by others. In conclusion, the tested drugs showed antifungal, anti-adherent and antibiofilm activity that make them useful in the treatment of fungal infection and the prevention of biofilm formation on the surface of medical devices.

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Section: Discussionsupporting

confidence: 86%

“…Ghalehnoo et al, [41] and Bink et al, [42] have documented the effect of diclofenac on C. albicans biofilms or on cells grown on solid media. The second study [42] showed inhibition of the yeast-to-hyphae transition by diclofenac on solid YPD media.…”

Section: Discussionmentioning

confidence: 99%

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of Candida spp.

Ashraf¹,

Yousri²,

Taha³

et al. 2015

AJMR

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“…Agents in this class are available for the treatment of pain and inflammation. However, the activity of this drug class is not limited to mammalian systems, as they have also been shown to disrupt filamentation and biofilm formation in C. albicans , likely though inhibition of prostaglandin E2 synthesis (96, 97). To examine the impact of disrupting this pathway in vivo , rats received diclofenac treatment in the setting of subcutaneous catheter implant infection (95).…”

Section: In Vivo Models Of Fungal Biofilms and Drug Discoverymentioning

confidence: 99%

Fungal Biofilms: In Vivo Models for Discovery of Anti-Biofilm Drugs

Nett

Andes

2015

Microbiol Spectr

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SUMMARY During infection, fungi frequently transition to a biofilm lifestyle, proliferating as communities of surface-adherent aggregates of cells. Phenotypically, cells in a biofilm are distinct from free-floating cells. Their high tolerance of antifungals and ability to withstand host defenses are two characteristics that foster resilience. Biofilm infections are particularly difficult to eradicate and most available antifungals have minimal activity. Therefore, the discovery of novel compounds and innovative strategies to treat fungal biofilms is of great interest. Although many fungi have been observed to form biofilms, the most well-studied is Candida albicans. Animal models have been developed to simulate common Candida device-associated infections, including those involving vascular catheters, dentures, urinary catheters, and subcutaneous implants. Models have also reproduced the most common mucosal biofilm infections, oropharyngeal and vaginal candidiasis. These models incorporate the anatomical site, immune components, and fluid dynamics of clinical niches and have been instrumental in the study of drug resistance and investigation of novel therapies. This chapter describes the significance of fungal biofilm infections, the animal models developed for biofilm study, and how these models have contributed to development of new strategies for eradication of fungal biofilm infections.

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“…While C. albicans does not possess a COX homolog, the fatty acid desaturase OLE2 and the multicopper oxidase FET3 were found to play a role in prostaglandin synthesis (40). Concurrently, several COX inhibitors, including diclofenac sodium, indomethacin, ibuprofen, resveratrol, and eicosatetraynoic acid (ETYA), were shown to block the Y-H transition induced in serum-containing, Lee's or Spider medium at 37°C (3,44,108,136). It is not clear whether or not COX inhibitors affected filamentation by blocking prostaglandin synthesis, given that a direct association between reduced prostaglandin levels and reduced hypha formation was not shown and that C. albicans does not encode a COX homolog.…”

Section: Fatty Acids Eicosanoids and Cyclooxygenase Inhibitorsmentioning

confidence: 99%

“…Moreover, COX inhibitors appeared to reduce viability of C. albicans cells, which may account for their hypha-inhibiting activities (3,36,102). For instance, diclofenac sodium and resveratrol blocked hyphal development but also affected cellular growth (44,108).…”

Section: Fatty Acids Eicosanoids and Cyclooxygenase Inhibitorsmentioning

confidence: 99%

Modulation of Morphogenesis in Candida albicans by Various Small Molecules

2011

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The pathogenic yeast Candida albicans, a member of the mucosal microbiota, is responsible for a large spectrum of infections, ranging from benign thrush and vulvovaginitis in both healthy and immunocompromised individuals to severe, life-threatening infections in immunocompromised patients. A striking feature of C. albicans is its ability to grow as budding yeast and as filamentous forms, including hyphae and pseudohyphae. The yeast-to-hypha transition contributes to the overall virulence of C. albicans and may even constitute a target for the development of antifungal drugs. Indeed, impairing morphogenesis in C. albicans has been shown to be a means to treat candidiasis. Additionally, a large number of small molecules such as farnesol, fatty acids, rapamycin, geldanamycin, histone deacetylase inhibitors, and cell cycle inhibitors have been reported to modulate the yeast-to-hypha transition in C. albicans. In this minireview, we take a look at molecules that modulate morphogenesis in this pathogenic yeast. When possible, we address experimental findings regarding their mechanisms of action and their therapeutic potential. We discuss whether or not modulating morphogenesis constitutes a strategy to treat Candida infections.

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The role of diclofenac sodium in the dimorphic transition in Candida albicans

Cited by 36 publications

References 57 publications

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of <i>Candida spp</i><i>.</i>

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of <i>Candida spp</i><i>.</i>

Fungal Biofilms: In Vivo Models for Discovery of Anti-Biofilm Drugs

Modulation of Morphogenesis in Candida albicans by Various Small Molecules

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