Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine

Detalhes bibliográficos
Autor(a) principal: Mishra,Nripendra Nath
Data de Publicação: 2014
Outros Autores: Ali,Shakir, Shukla,Praveen K.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Infectious Diseases
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702014000300287
Resumo: Candida albicans utilizes arachidonic acid (AA) released during the course of infection (Candidiasis) from phospholipids of infected host cell membranes and synthesizes extracellular prostaglandin(s) which play an important role in hyphae formation and host cell damage. C. albicans biofilms secrete significantly more prostaglandin(s) and evidence suggests that Candida biofilms have dramatically reduced susceptibility to majority of antifungal drugs. AA influences the saturation level of lipids and fluidity of yeast cell membranes. Therefore the aim of this study was to evaluate the effect of AA alone or in combination with antifungal agents on biofilm formation and production of prostaglandin (PGE2) in C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, and C. albicans amphotericin B resistant strain (AmBR). Maximum biofilm formation was found to be in the case of C. albicans compared to C. non-albicans species. However, among the non-albicans species C. tropicalis exhibited highest biofilm formation. Treatment with AA in combination with subinhibitory concentrations of fluconazole and terbinafine separately exhibited significant (p < 0.05) reduction in biofilm formation against C. glabrata, C. parapsilosis, C. tropicalis and AmBR as compared to their individual effect. Further, these two antifungal agents in combination with AA caused an increase in production of prostaglandin from fungal cell itself which was significant (p < 0.05) in case of all the strains tested.
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spelling Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafineArachidonic acidCandida albicansAmBRCandida tropicalisProstaglandin E2FDACandida albicans utilizes arachidonic acid (AA) released during the course of infection (Candidiasis) from phospholipids of infected host cell membranes and synthesizes extracellular prostaglandin(s) which play an important role in hyphae formation and host cell damage. C. albicans biofilms secrete significantly more prostaglandin(s) and evidence suggests that Candida biofilms have dramatically reduced susceptibility to majority of antifungal drugs. AA influences the saturation level of lipids and fluidity of yeast cell membranes. Therefore the aim of this study was to evaluate the effect of AA alone or in combination with antifungal agents on biofilm formation and production of prostaglandin (PGE2) in C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, and C. albicans amphotericin B resistant strain (AmBR). Maximum biofilm formation was found to be in the case of C. albicans compared to C. non-albicans species. However, among the non-albicans species C. tropicalis exhibited highest biofilm formation. Treatment with AA in combination with subinhibitory concentrations of fluconazole and terbinafine separately exhibited significant (p < 0.05) reduction in biofilm formation against C. glabrata, C. parapsilosis, C. tropicalis and AmBR as compared to their individual effect. Further, these two antifungal agents in combination with AA caused an increase in production of prostaglandin from fungal cell itself which was significant (p < 0.05) in case of all the strains tested.Brazilian Society of Infectious Diseases2014-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702014000300287Brazilian Journal of Infectious Diseases v.18 n.3 2014reponame:Brazilian Journal of Infectious Diseasesinstname:Brazilian Society of Infectious Diseases (BSID)instacron:BSID10.1016/j.bjid.2013.09.006info:eu-repo/semantics/openAccessMishra,Nripendra NathAli,ShakirShukla,Praveen K.eng2015-10-26T00:00:00Zoai:scielo:S1413-86702014000300287Revistahttps://www.bjid.org.br/https://old.scielo.br/oai/scielo-oai.phpbjid@bjid.org.br||lgoldani@ufrgs.br1678-43911413-8670opendoar:2015-10-26T00:00Brazilian Journal of Infectious Diseases - Brazilian Society of Infectious Diseases (BSID)false
dc.title.none.fl_str_mv Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
title Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
spellingShingle Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
Mishra,Nripendra Nath
Arachidonic acid
Candida albicans
AmBR
Candida tropicalis
Prostaglandin E2
FDA
title_short Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
title_full Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
title_fullStr Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
title_full_unstemmed Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
title_sort Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine
author Mishra,Nripendra Nath
author_facet Mishra,Nripendra Nath
Ali,Shakir
Shukla,Praveen K.
author_role author
author2 Ali,Shakir
Shukla,Praveen K.
author2_role author
author
dc.contributor.author.fl_str_mv Mishra,Nripendra Nath
Ali,Shakir
Shukla,Praveen K.
dc.subject.por.fl_str_mv Arachidonic acid
Candida albicans
AmBR
Candida tropicalis
Prostaglandin E2
FDA
topic Arachidonic acid
Candida albicans
AmBR
Candida tropicalis
Prostaglandin E2
FDA
description Candida albicans utilizes arachidonic acid (AA) released during the course of infection (Candidiasis) from phospholipids of infected host cell membranes and synthesizes extracellular prostaglandin(s) which play an important role in hyphae formation and host cell damage. C. albicans biofilms secrete significantly more prostaglandin(s) and evidence suggests that Candida biofilms have dramatically reduced susceptibility to majority of antifungal drugs. AA influences the saturation level of lipids and fluidity of yeast cell membranes. Therefore the aim of this study was to evaluate the effect of AA alone or in combination with antifungal agents on biofilm formation and production of prostaglandin (PGE2) in C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, and C. albicans amphotericin B resistant strain (AmBR). Maximum biofilm formation was found to be in the case of C. albicans compared to C. non-albicans species. However, among the non-albicans species C. tropicalis exhibited highest biofilm formation. Treatment with AA in combination with subinhibitory concentrations of fluconazole and terbinafine separately exhibited significant (p < 0.05) reduction in biofilm formation against C. glabrata, C. parapsilosis, C. tropicalis and AmBR as compared to their individual effect. Further, these two antifungal agents in combination with AA caused an increase in production of prostaglandin from fungal cell itself which was significant (p < 0.05) in case of all the strains tested.
publishDate 2014
dc.date.none.fl_str_mv 2014-06-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702014000300287
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702014000300287
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1016/j.bjid.2013.09.006
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Brazilian Society of Infectious Diseases
publisher.none.fl_str_mv Brazilian Society of Infectious Diseases
dc.source.none.fl_str_mv Brazilian Journal of Infectious Diseases v.18 n.3 2014
reponame:Brazilian Journal of Infectious Diseases
instname:Brazilian Society of Infectious Diseases (BSID)
instacron:BSID
instname_str Brazilian Society of Infectious Diseases (BSID)
instacron_str BSID
institution BSID
reponame_str Brazilian Journal of Infectious Diseases
collection Brazilian Journal of Infectious Diseases
repository.name.fl_str_mv Brazilian Journal of Infectious Diseases - Brazilian Society of Infectious Diseases (BSID)
repository.mail.fl_str_mv bjid@bjid.org.br||lgoldani@ufrgs.br
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