Abstract
The development of deep venous thrombosis (DVT) is a sterile inflammatory process
related to cytokines, such as interleukin (IL)-6 or IL-17. IL-9 is a cytokine involved
in many inflammatory diseases, including cystic fibrosis, ulcerative colitis, psoriasis
and psoriatic arthritis. However, it remains unknown whether IL-9 is related to DVT.
In this study, we characterized the role and mechanism of IL-9 in DVT. Analysis of
the data of patients with and without DVT revealed that stasis, venous surgery as
well as elevated IL-9 and sP-selectin levels were related to the development of DVT.
We also showed for the first time that IL-9 receptor was expressed in mouse platelets,
and it dramatically promoted the aggregation rate and expression of P-selectin (CD62P)
in the presence of adenosine diphosphate, but otherwise exhibited no effect on platelets.
This study also revealed that Janus kinase 2/signal transducer and activator of transcription
3 (JAK2/STAT3) signalling pathway, not phosphoinositide 3-kinase/AKT pathway, was
involved in the process. We also showed in a mouse model of stasis that the thrombus
size (weight and length) and CD62P expression in the thrombus were higher and lower
in the IL-9 group and IL-9 antibody group, respectively, than in the control group.
All these findings indicated that IL-9 facilitated platelet function through the JAK2/STAT3
pathway, thus promoting the development of DVT.
Keywords
deep vein thrombosis - IL-9 - platelets - P-selectin
