Scientific article

Severe Neutrophil-Dominated Inflammation and Enhanced Myelopoiesis in IL-33-Overexpressing CMV/IL33 Mice

Published inThe Journal of immunology, vol. 194, no. 2, p. 750-760
Publication date2015

IL-33 is a cytokine of the IL-1 family, which signals through the ST2 receptor. Previous studies emphasized a role for IL-33 in shaping innate and adaptive immune responses. IL-33 was also reported to modulate myelopoiesis and myeloid cell activity. In this article, we describe IL-33-overexpressing CMV/IL33 and LysM/IL33 mice, which display an inflammatory phenotype associated with growth retardation and paw swelling. The phenotype of CMV/IL33 mice is dependent on activation of the ST2 receptor and is characterized by extensive neutrophil infiltration into different organs, including the paws. Local or systemic levels of proinflammatory mediators such as IL-1β, Cxcl-1, G-CSF, and IL-6 are increased. CMV/IL-33 mice also suffer from anemia, thrombocytosis, and a marked dysregulation of myelopoiesis, leading to an important increase in myeloid cell production or accumulation in bone marrow (BM), spleen, and peripheral blood. Consistently, recombinant IL-33 induced proliferation of myeloid lineage cells in BM-derived granulocyte cultures, whereas IL-33 knockout mice exhibited minor deficiencies in spleen and BM myeloid cell populations. Our observations reveal a neutrophil-dominated inflammatory phenotype in IL-33-overexpressing CMV/IL33 and LysM/IL33 mice, and highlight important regulatory effects of IL-33 on myelopoiesis in vitro and in vivo, where excessive IL-33 signaling can translate into the occurrence of a myeloproliferative disorder.

Citation (ISO format)
TALABOT FRISCHKNECHT-AYER, Dominique et al. Severe Neutrophil-Dominated Inflammation and Enhanced Myelopoiesis in IL-33-Overexpressing CMV/IL33 Mice. In: The Journal of immunology, 2015, vol. 194, n° 2, p. 750–760. doi: 10.4049/jimmunol.1402057
Main files (1)
Article (Published version)
ISSN of the journal0022-1767

Technical informations

Creation01/20/2015 9:34:00 AM
First validation01/20/2015 9:34:00 AM
Update time03/14/2023 10:45:12 PM
Status update03/14/2023 10:45:12 PM
Last indexation08/29/2023 2:28:44 PM
All rights reserved by Archive ouverte UNIGE and the University of GenevaunigeBlack