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Early Il-33 Action on Myeloid Cells is Critical In Resistance to Systemic Candida Albicans Infection

H. Cho1, S. Park1, B. Kwon2, H. Park1, Y. Kim3, J. Lee4, J. Park4, K. Park4, K. Yoo4

1Department of Surgery, University of Ulsan College of Medicine, Ulsan, Korea, Republic of, 2School of Biological Sciences, University of Ulsan, Ulsan, Korea, Republic of, 3Biomedical research center, Ulsan University Hospital, Ulsan, Korea, Republic of, 4Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan, Korea, Republic of

Meeting: 2022 American Transplant Congress

Abstract number: 1234

Keywords: Epithelial cells, Fungal infection, Kidney, Mice, knockout

Topic: Basic Science » Basic Science » 08 - Innate Immunity; Chemokines, Cytokines, Complement

Session Information

Session Name: Innate Immunity; Chemokines, Cytokines, Complement

Session Type: Poster Abstract

Date: Monday, June 6, 2022

Session Time: 7:00pm-8:00pm

 Presentation Time: 7:00pm-8:00pm

Location: Hynes Halls C & D

*Purpose: Invasive candidiasis could be a cause of morbidity and mortality in immunocompromised patients with organ or bone marrow transplantation. In this study, we systematically analyzed the in vivo functions of endogenous IL-33 using Il33-/- mice and in vitro immune cell culture.

*Methods: WT and IL-33-deficient mice were infected with C. albicans via intravenous injection. Innate immune responses of the kidney were investigated using various immunological techniques.

*Results: Tubular epithelial cells mainly secreted IL-33 in response to systemic C. albicans infection. Il33-/- mice showed increased mortality and morbidity, which were due to impaired fungal clearance. IL-33 initiated an innate defense mechanism by co-stimulating dendritic cells to produce IL-23 after systemic C. albicans infection, which in turn promoted the phagocytosis of neutrophils through secretion of GM-CSF by NK cells. The susceptibility of Il33-/- mice was also associated with increased levels of IL-10 which were produced by Ly6G+ neutrophils and MHCII+F4/80+ macrophages and neutralization of IL-10 resulted in enhanced fungal clearance in Il33-/- mice. However, depletion of IL-10 overrided the effect of IL-33 on fungal clearance. In Il10-/- mouse kidneys, MHCII+F4/80+ macrophages were massively differentiated after C. albicans infection and these cells were superior to MHCII–F4/80+ macrophages that were preferentially differentiated in WT mouse kidneys, in killing of extracellular hyphal C. albicans.

*Conclusions: Our results identify IL-33 as critical early regulator controlling a serial downstream signaling events of innate defense to C. albicans infection.

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To cite this abstract in AMA style:

Cho H, Park S, Kwon B, Park H, Kim Y, Lee J, Park J, Park K, Yoo K. Early Il-33 Action on Myeloid Cells is Critical In Resistance to Systemic Candida Albicans Infection [abstract]. Am J Transplant. 2022; 22 (suppl 3). https://atcmeetingabstracts.com/abstract/early-il-33-action-on-myeloid-cells-is-critical-in-resistance-to-systemic-candida-albicans-infection/. Accessed May 29, 2025.

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