Pathogenicity and intestinal barrier disruptive ability of Malassezia furfur in an alternative model host Caenorhabditis elegans is partially alleviated by Lacticaseibacillus rhamnosus

Abstract

Malassezia furfur is associated with various diseases; however, the mechanisms underlying its pathogenicity remain largely unknown. In the present study, Caenorhabditis elegans was used as the model host to evaluate M. furfur pathogenicity. Additionally, effects of lactic acid bacteria against M. furfur pathogenicity were evaluated. Compared to Escherichia coli OP50 (OP, control), both live and heat-killed M. furfur reduced the lifespan and body size of C. elegans, although heat-killed M. furfur was less effective than live M. furfur in lifespan shortening. Furthermore, unlike heat-killed M. furfur, live M. furfur disrupted the nematode intestinal barrier. nsy-1 and sek-1 loss-of-function mutants were susceptible to M. furfur, suggesting their involvement in the defense against M. furfur infection. Expression of genes involved in host defense and of those coding for C-type lectin domain-containing proteins and antimicrobial peptides was upregulated in M. furfur-infected C. elegans. Lacticaseibacillus rhamnosus (LR) significantly ameliorated lifespan shortening and body size reduction in M. furfur-infected C. elegans and protected against intestinal barrier disruption, suggesting that LR protects nematodes from M. furfur virulence. This study highlights M. furfur pathogenicity and intestinal barrier disruptive ability in C. elegans and suggests that the M. furfur virulence is partially attenuated by LR. ImportanceInfection with Malassezia furfur shortens the lifespan and disrupts the intestinal barrier in the model host C. elegans. The probiotic Lacticaseibacillus rhamnosus (LR) attenuates M. furfur virulence, thus partially protecting the intestinal tract. Signaling of the innate immune response to M. furfur in C. elegans is mediated by nsy-1 and sek-1, suggesting that the expression of genes involved in the biological defense response may be regulated downstream of nsy-1 and sek-1. This study enhances our understanding of the diseases associated with M. furfur and offers insights into potential preventive and therapeutic methods using probiotics.