IL-25, IL-33 and TSLP receptor are not critical for development of experimental murine malaria

Akiko Shibui; Ayako Takamori; Mohammed E M Tolba; Aya Nambu; Eri Shimura; Sachiko Yamaguchi; Chizu Sanjoba; Hajime Suto; Katsuko Sudo; Ko Okumura; Sumio Sugano; Hideaki Morita; Hirohisa Saito; Kenji Matsumoto; Susumu Nakae

doi:10.1016/j.bbrep.2015.12.007

IL-25, IL-33 and TSLP receptor are not critical for development of experimental murine malaria

Biochem Biophys Rep. 2015 Dec 14:5:191-195. doi: 10.1016/j.bbrep.2015.12.007. eCollection 2016 Mar.

Authors

Akiko Shibui^{1

2}, Ayako Takamori², Mohammed E M Tolba^{1

3}, Aya Nambu², Eri Shimura^{2

4}, Sachiko Yamaguchi², Chizu Sanjoba⁴, Hajime Suto⁵, Katsuko Sudo⁶, Ko Okumura⁵, Sumio Sugano¹, Hideaki Morita⁷, Hirohisa Saito⁷, Kenji Matsumoto⁷, Susumu Nakae^{2

8}

Affiliations

¹ Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo, Chiba 277-8561, Japan.
² Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
³ Department of Parasitology, Assiut University, Assiut 71515, Egypt.
⁴ Department of Molecular Immunology, School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan.
⁵ Atopy Research Center, Juntendo University, Tokyo 113-8412, Japan.
⁶ Animal Research Center, Tokyo Medical University, Tokyo 160-8402, Japan.
⁷ Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
⁸ Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Saitama 332-0012, Japan.

Abstract

IL-25, IL-33 and TSLP, which are produced predominantly by epithelial cells, can induce production of Th2-type cytokines such as IL-4, IL-5 and/or IL-13 by various types of cells, suggesting their involvement in induction of Th2-type cytokine-associated immune responses. It is known that Th2-type cytokines contribute to host defense against malaria parasite infection in mice. However, the roles of IL-25, IL-33 and TSLP in malaria parasite infection remain unclear. Thus, to elucidate this, we infected wild-type, IL-25^-/-, IL-33^-/- and TSLP receptor (TSLPR)^-/- mice with Plasmodium berghei (P. berghei) ANKA, a murine malaria strain. The expression levels of IL-25, IL-33 and TSLP mRNA were changed in the brain, liver, lung and spleen of wild-type mice after infection, suggesting that these cytokines are involved in host defense against P. berghei ANKA. However, the incidence of parasitemia and survival in the mutant mice were comparable to in the wild-type mice. These findings indicate that IL-25, IL-33 and TSLP are not critical for host defense against P. berghei ANKA.

Keywords: IL-25, interleukin-25; IL-33, interleukin-33; Interleukin-25; Interleukin-33; Malaria; Mouse; TSLPR, thymic stromal lymphoprotein receptor; Thymic stromal lymphoprotein.