Antibiofilm Activity and Biocompatibility of Temporin-SHa: A Promising Antimicrobial Peptide for Control of Fluconazole-Resistant Candida albicans

Author:

Dias Luana Mendonça12ORCID,Cilli Eduardo Maffud3ORCID,Medeiros Karine Sousa1,Brasil Maria Carolina Oliveira de Arruda3,Marin Lina Maria2ORCID,Siqueira Walter L.2ORCID,Pavarina Ana Claudia1ORCID

Affiliation:

1. Department of Dental Materials and Prosthodontics, School of Dentistry, São Paulo State University (UNESP), Araraquara 16015-050, Brazil

2. College of Dentistry, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada

3. Department of Biochemistry and Organic Chemistry, Institute of Chemistry, São Paulo State University (UNESP), Araraquara 14800-060, Brazil

Abstract

The aim of the study was to investigate the effect of antimicrobial peptides (AMPs) Hylin−a1, KR−12-a5, and Temporin-SHa in Candida albicans as well as the biocompatibility of keratinocytes spontaneously immortalized (NOK-si) and human gingival fibroblasts (FGH) cells. Initially, the susceptible (CaS—ATCC 90028) and fluconazole-resistant (CaR—ATCC 96901) C. albicans strains were grown to evaluate the effect of each AMP in planktonic culture, biofilm, and biocompatibility on oral cells. Among the AMPs evaluated, temporin−SHa showed the most promising results. After 24 h of Temporin-SHa exposure, the survival curve results showed that CaS and CaR suspensions reduced 72% and 70% of cell viability compared to the control group. The minimum inhibitory/fungicide concentrations (MIC and MFC) showed that Temporin−SHa was able to reduce ≥50% at ≥256 µg/mL for both strains. The inhibition of biofilm formation, efficacy against biofilm formation, and total biomass assays were performed until 48 h of biofilm maturation, and Temporin-SHa was able to reduce ≥50% of CaS and CaR growth. Furthermore, Temporin−SHa (512 µg/mL) was classified as non-cytotoxic and slightly cytotoxic for NOK-si and FGH, respectively. Temporin−SHa demonstrated an anti-biofilm effect against CaS and CaR and was biocompatible with NOK-si and FGH oral cells in monolayer.

Funder

São Paulo Research Foundation

Canadian Institutes of Health Research

Natural Sciences and Engineering Research Council

Publisher

MDPI AG

Subject

Virology,Microbiology (medical),Microbiology

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