Interleukin-9 promotes early mast cell-mediated expulsion of Strongyloides ratti but is dispensable for generation of protective memory
Autor: | Wiebke Hartmann, Minka Breloer, Zane Orinska, Martina Reitz, Marie-Luise Brunn, Nikolas Rüdiger |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.medical_treatment lcsh:Medicine Biology Allergic inflammation 03 medical and health sciences Mice Immune system medicine Animals Immunologic Factors Interleukin 9 Mast Cells lcsh:Science Mice Knockout Receptors Interleukin-9 Mice Inbred BALB C Multidisciplinary lcsh:R Degranulation Interleukin-9 Strongyloides ratti Mast cell Acquired immune system Mice Inbred C57BL Disease Models Animal 030104 developmental biology Cytokine medicine.anatomical_structure Immunology Strongyloidiasis lcsh:Q Immunologic Memory |
Zdroj: | Scientific Reports, Vol 8, Iss 1, Pp 1-11 (2018) |
ISSN: | 2045-2322 |
DOI: | 10.1038/s41598-018-26907-2 |
Popis: | IL-9 is a cytokine with pleiotropic function that mediates allergic inflammation and immunity to intestinal helminth parasites. Accumulating evidence suggests that IL-9 acts via both, initiation and regulation of adaptive immune responses and direct activation of intestinal effector pathways. Here we use IL-9 receptor deficient mice on BALB/c and C57BL/6 genetic background to dissect effector and regulatory functions of IL-9 during infection with the parasitic nematode Strongyloides ratti. IL-9 receptor-deficient mice displayed increased intestinal parasite burden and prolonged infection irrespective of the genetic background of the mice. Increased parasite burden was correlated to a reciprocally reduced early degranulation of mucosal mast cells, reduced intestinal IL-13 expression and caused by IL-9 receptor deficiency on hematopoietic cells. We observed additional significant changes in the adaptive immune response to S. ratti infection in the absence of the IL-9 receptor that depended on the mouse strain. However, the generation of protective memory to a second infection was intact in IL-9 receptor-deficient mice, irrespective of the genetic background. In summary, our results support a central role for IL-9 as an early mast cell activating effector cytokine during intestinal helminth infection while non-redundant functions in the initiation and amplification of adaptive immune responses were not apparent. |
Databáze: | OpenAIRE |
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