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Review
. 2024 Jun 17;10(6):426.
doi: 10.3390/jof10060426.

Inbred Mouse Models in Cryptococcus neoformans Research

Minna Ding  1 , Kirsten Nielsen  1
Affiliations
Review

Inbred Mouse Models in Cryptococcus neoformans Research

Minna Ding et al. J Fungi (Basel). .

Abstract

Animal models are frequently used as surrogates to understand human disease. In the fungal pathogen Cryptococcus species complex, several variations of a mouse model of disease were developed that recapitulate different aspects of human disease. These mouse models have been implemented using various inbred and outbred mouse backgrounds, many of which have genetic differences that can influence host response and disease outcome. In this review, we will discuss the most commonly used inbred mouse backgrounds in C. neoformans infection models.

Keywords: Cryptococcus neoformans; cryptococcal immune reconstitution inflammatory syndrome; cryptococcal meningitis; damage-response framework; fungus; host immune responses; host–pathogen interactions; human fungal pathogen; inbred mouse models; latent C. neoformans infection.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Damage-response framework parabola in Cryptococcus infections. Y-axis shows disease outcome and X-axis shows host immune status, whereby a dysregulated immune response and immunocompromised state is hypothesized to promote fungal dissemination (cryptococcal meningitis), and dysregulated Th1 activity and immunocompetent state is hypothesized to promote pathogenic host inflammation or immune reconstitution inflammatory syndrome (cryptococcal IRIS). And, a balanced Th1/Th2 response is hypothesized to control C. neoformans infection (latency). Cryptococcal meningitis can be modeled by lethal C. neoformans infection [9,10,11,12,13,14,15,16]; latency can be modeled by the latent C. neoformans model using clinical isolates [25]; and cryptococcal IRIS can be modeled by either intravenous injection of a high inoculum dose of C. deneoformans [17], or adoptive transfer of CD4 T-cells into C. deneoformans 1841 [18] or C. neoformans H99 [19] infected RAG1-/- mice. Figure adapted from (Pirofski and Casadevall, 2017 [3]; Skipper et al., 2019 [4]).
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