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Pharmacodynamic and Immunomodulatory Effects of Micafungin on Host Responses against Biofilms of Candida parapsilosis in Comparison to Those of Candida albicans.

TitlePharmacodynamic and Immunomodulatory Effects of Micafungin on Host Responses against Biofilms of Candida parapsilosis in Comparison to Those of Candida albicans.
Publication TypeJournal Article
Year of Publication2018
AuthorsSimitsopoulou, M., Chlichlia K., Kyrpitzi D., Walsh T. J., & Roilides E.
JournalAntimicrob Agents Chemother
Volume62
Issue8
Date Published2018 Aug
ISSN1098-6596
Abstract

Micafungin (MFG) demonstrates potent activity against biofilms of and , the most frequent opportunistic fungal pathogens. Little is known about its immunopharmacologic effect on antibiofilm activity of phagocytic cells following exposure to biofilms. In this study, we investigated the effects of MFG on human neutrophil-mediated damage of and biofilms by XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] and the potential mechanisms underlying the immunomodulatory MFG activities on cultured monocyte-derived THP-1 cells in response to these biofilms by reverse transcription-PCR and sandwich and multiplex enzyme-linked immunosorbent assay. Preexposure of to subinhibitory MFG concentrations significantly enhanced neutrophil-mediated biofilm damage, an effect that appears to be species specific since a comparable effect was not observed with drug-pretreated biofilms. Human THP-1 cells responded to both biofilms through Toll-like receptor 2 (TLR2) and TLR4 upregulation, modest TLR6 involvement, and enhanced NLRP3 activation, whereas the signal was relayed to the nucleus via NF-κB p65 activation. MFG caused 2- to 3-fold lower TLR2 and TLR4 mRNA levels than those caused by either organism. biofilms induced a robust proinflammatory response, whereas biofilms either alone or in the presence of MFG caused increased interleukin-1β (IL-1β) production, but small amounts of IL-8, IL-23, and tumor necrosis factor alpha. In conclusion, MFG may condition THP-1 cells toward an inflammatory response through TLR2/TLR4 recruitment. Inflammatory signals observed with biofilms are considerably reduced upon exposure of THP-1 cells to biofilms, possibly enhancing fungal survival and increasing biofilm pathogenicity.

DOI10.1128/AAC.00478-18
Alternate JournalAntimicrob. Agents Chemother.
PubMed ID29866877
PubMed Central IDPMC6105855

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