IFN-lambda is protective against lethal oral Toxoplasma gondii infection

Interferons are essential for innate and adaptive immune responses against a wide variety of pathogens. Interferon lambda (IFN-lambda) protects mucosal barriers during pathogen exposure. The intestinal epithelium is the first contact site for Toxoplasma gondii (T. gondii) with its hosts and the firs...

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Published inbioRxiv
Main Authors Murillo-Leon, Mateo, Bastidas-Quintero, Aura Maria, Endres, Niklas Sebastian, Schnepf, Daniel, Delgado-Betancourt, Estefania, Ohnemus, Annette, Taylor, Gregory A, Schwemmle, Martin, Staeheli, Peter, Steinfeldt, Tobias
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 24.02.2023
Subjects
Animal models
Chimeras
Epithelial cells
Epithelium
Gastrointestinal tract
Immune response
Infections
Interferon
Intestine
Leukocytes (neutrophilic)
Organoids
Pathogens
Protozoa
Toxoplasma gondii
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Summary:Interferons are essential for innate and adaptive immune responses against a wide variety of pathogens. Interferon lambda (IFN-lambda) protects mucosal barriers during pathogen exposure. The intestinal epithelium is the first contact site for Toxoplasma gondii (T. gondii) with its hosts and the first defense line that limits parasite infection. Knowledge of very early T. gondii infection events in the gut tissue is limited and a possible contribution of IFN-lambda has not been investigated so far. Here, we demonstrate with systemic interferon lambda receptor (IFNLR1) and conditional (Villin-Cre) knockout mouse models and bone marrow chimeras of oral T. gondii infection and mouse intestinal organoids a significant impact of IFN-lambda signaling in intestinal epithelial cells and neutrophils to T. gondii control in the gastrointestinal tract. Our results expand the repertoire of interferons that contribute to the control of T. gondii and may lead to novel therapeutic approaches against this world-wide zoonotic pathogen.Competing Interest StatementThe authors have declared no competing interest.
DOI:10.1101/2023.02.24.529861