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\begin{document}

\title{Epidermal barrier impairment predisposes for excessive growth of the
allergy-associated yeast Malassezia on murine skin}



\author[1]{Salomé LeibundGut-Landmann}%
\author[1]{Fiorella Ruchti}%
\author[2]{Pascale Zwicky}%
\author[2]{Burkhard Becher}%
\author[3]{Sandrine Dubrac}%
\affil[1]{Universitat Zurich Vetsuisse-Fakultat}%
\affil[2]{Universitat Zurich Institut fur Experimentelle Immunologie}%
\affil[3]{Landeskrankenhaus Innsbruck Universitatsklinik fur Dermatologie Venerologie und Allergologie}%


\vspace{-1em}



  
  \date{May 24, 2024}


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\begin{abstract}
The skin barrier is vital for protection against environmental threats
including insults caused by skin-resident microbes. Dysregulation of
this barrier is a hallmark of atopic dermatitis (AD) and ichthyosis,
with variable consequences for host immune control of colonizing
commensals and opportunistic pathogens. While \emph{Malassezia} is the
most abundant commensal fungus of the skin, little is known about the
host control of this fungus in inflammatory skin diseases. Here we show
that in barrier-impaired skin, \emph{Malassezia} acquires enhanced
fitness and overt growth properties. By using four distinct and
complementary murine models of atopic dermatitis and ichthyosis we
provide evidence that structural and metabolic changes in the
dysfunctional epidermal barrier environment provide increased
accessibility and an altered lipid profile, to which the lipid-dependent
yeast adapts for enhanced nutrient assimilation. These findings reveal
fundamental insights into the implication of the mycobiota in the
pathogenesis of common skin barrier disorders.%
\end{abstract}%



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