A comparative study of IL-33 and its receptor ST2 in a C57BL/6 J mouse model of pulmonary Cryptococcus neoformans infection

Wang, Zhengxia; Ma, Qiyun; Jiang, Jingxian; Yang, Xiaofan; Zhang, Enrui; Yuan, Tao; Hu, Huidi; Huang, Mao; Ji, Ningfei; Zhang, Mingshun

doi:10.1007/s00430-022-00755-4

Cited by 5 publications

(3 citation statements)

References 36 publications

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“…Compared to wild-type mice, IL-33R subunit T1/ ST2-deficient mice infected with C. neoformans showed decreased fungal burden in the lungs, spleen, and brain and improved survival. Wang et al also found that, in the early stages of C. neoformans infection, the load of pulmonary fungi in IL-33 −/− and ST2 − / − mice decreased with an increase in neutrophil infiltration (44). These results indicate that IL-33-dependent signal transduction contributes to the expansion of congenital type 2 immunity and the subsequent Th2-biased lung immunopathology, thereby promoting the growth and transmission of C. neoformans (45).…”

Section: Cytokines and Correlation With Immunitymentioning

confidence: 91%

Adaptive immunology of Cryptococcus neoformans infections—an update

et al. 2023

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The fungal genus Cryptococcus comprises a group of pathogens with considerable phenotypic and genotypic diversity that can lead to cryptococcosis in both healthy and immunocompromised individuals. With the emergence of the HIV pandemic, cryptococcosis, mainly meningoencephalitis, afflicts HIV-infected patients with severe dysfunction of T cells. It has also been reported in recipients of solid organ transplantation and in patients with autoimmune diseases who take immunosuppressive agents long-term, as well as in those with unidentified immunodeficiency. The clinical outcome of the disease is primarily determined by the immune response resulting from the interplay between the host immune system and the pathogen. Most human infections are caused by Cryptococcus neoformans, and nearly all immunological studies have focused on C. neoformans. This review provides an updated understanding of the role of adaptive immunity during infection with C. neoformans in human and animal models over the past half-decade.

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Section: Cytokines and Correlation With Immunitymentioning

confidence: 91%

Adaptive immunology of Cryptococcus neoformans infections—an update

et al. 2023

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“…In addition, regulatory CD4 T-cells (Tregs) expressing ST2 are immunosuppressive and accumulate during the early phases of C. deneoformans 52D infection (up to 7 days post-infection), but are then replaced by more inflammatory Tregs as the infection progresses (past 14 days post-infection) [ 72 ]. Interestingly, these findings were only partially replicated in C57BL/6J mice, where only IL-33 deficiency, but not ST2 deficiency, results in decreased fungal burden and a reduction in Th2 cytokines during C. neoformans H99 infection [ 73 ]. While the differences in host response between BALB/c and C57BL/6J mice are likely multifactorial, these studies suggest that IL-33 and its receptor ST2 may be a key factor in driving the differential host response between BALB/c and C57BL/6J mice and should be considered when choosing an appropriate inbred mouse model.…”

Section: Balb/c Inbred Mouse Strainmentioning

confidence: 99%

Inbred Mouse Models in Cryptococcus neoformans Research

Ding,

Nielsen

2024

JoF

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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.

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“…For example, in Alternaria-challenged mice, data show that deletion of ST2 decreases the type 2 immune response with complete elimination of pulmonary eosinophilia [73,74]. ST2-deficient mice also exhibited a better survival and lower fungal burden with decreased early production of IL-5 and IL-13 in invasive cryptococcosis [75][76][77]. These observations have also been linked to humans, where it was found that steroid-resistant pediatric asthma patients with fungal sensitization showed higher levels of airway IL-33 [78].…”

Section: Epithelial Cell-derived Cytokines As Initiators Of Fungal Ty...mentioning

confidence: 99%

Novel mechanistic insights underlying fungal allergic inflammation

Zheng,

Dang

2023

PLoS Pathog

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The worldwide prevalence of asthma and allergic disorders (allergic rhinitis, atopic dermatitis, food allergy) has been steadily rising in recent decades. It is now estimated that up to 20% of the global population is afflicted by an allergic disease, with increasing incidence rates in both high- and low-income countries. The World Allergy Organization estimates that the total economic burden of asthma and allergic rhinitis alone is approximately $21 billion per year. While allergic stimuli are a complex and heterogenous class of inputs including parasites, pollens, food antigens, drugs, and metals, it has become clear that fungi are major drivers of allergic disease, with estimates that fungal sensitization occurs in 20–30% of atopic individuals and up to 80% of asthma patients. Fungi are eukaryotic microorganisms that can be found throughout the world in high abundance in both indoor and outdoor environments. Understanding how and why fungi act as triggers of allergic type 2 inflammation will be crucial for combating this important health problem. In recent years, there have been significant advances in our understanding of fungi-induced type 2 immunity, however there is still much we don’t understand, including why fungi have a tendency to induce allergic reactions in the first place. Here, we will discuss how fungi trigger type 2 immune responses and posit why this response has been evolutionarily selected for induction during fungal encounter.

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A comparative study of IL-33 and its receptor ST2 in a C57BL/6 J mouse model of pulmonary Cryptococcus neoformans infection

Cited by 5 publications

References 36 publications

Adaptive immunology of Cryptococcus neoformans infections—an update

Adaptive immunology of Cryptococcus neoformans infections—an update

Inbred Mouse Models in Cryptococcus neoformans Research

Novel mechanistic insights underlying fungal allergic inflammation

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