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• W4386319078 abstract "Abstract Clonal hematopoiesis (CH) is suggested as an important risk factor for all-cause mortality and multiple chronic diseases including hematological neoplasms, cardiovascular diseases, and potentially a spectrum of autoimmune or immune-deficiency diseases. Mutations in TET2 are one of the first identified, most important and prevalent genetic drivers of CH. However, cooperative factors and mechanisms underlying TET2 -deficiency related CH (TedCH) remain largely unknown. Controversially, it is recently suggested that certain diseases take place prior to TedCH and promote TedCH on the contrary, indicating diseases in non-hematopoietic organs may act as environmental non-genetic drivers of CH. To clarify relationships between immune-dysfunctional diseases and CH, here we tested impact of various challenges on TedCH. We found that expedited TedCH depended on establishment of inflammatory environment. Primary or chimeric Tet2 -mutant mice spontaneously developed co-symptoms reminiscent of human chronic colitis and myeloid leukemia, which was exacerbated by feeding with DSS, an experimental inducer of ulcerative colitis. Single cell RNA-seq (scRNA-seq) analysis reveals in depth the damage of colon and bone marrow in the Tet2 -mutant mice in physiological condition or fed with DSS, along with increase of dysbacteriosis indicated by gut microbiome analysis. Results from colon scRNA-seq from both mouse and human highlight important roles of PTX3/IL-1β pro-inflammatory signaling in promoting colitis or leukemia. Finally, TedCH trajectory and inflammation in colon and bone marrow was ameliorated by treatment of IL-1R1 inhibitor Anakinra. Our study suggests that PTX3/IL-1β signaling and clonal hematopoiesis cooperates and plays important roles in gut-bone marrow axis and related diseases including colitis and leukemia. Highlights Certain environmental factors such as Dextran Sulfate Sodium (DSS), an experimental inducer of ulcerative colitis, promotes Tet2 -difficiency related clonal hematopoiesis (TedCH) Colitis and leukemia are spontaneously and simultaneously developed in Tet2 -defficient primary or chimeric mice, along with increased pathogenic gut microbiomes, indicating aberrant gut-bone marrow axis in the mutant mice. Single cell RNA-seq analysis reveals enhanced PTX3, a soluble pattern recognition molecule (PRM) and IL-1β pro-inflammatory signaling in colitis and leukemia. In vivo function of the PTX3/IL-1β pro-inflammatory signaling in TedCH is also indicated in human colitis and validated experimental settings." @default.
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• W4386319078 date "2023-08-31" @default.
• W4386319078 modified "2023-09-29" @default.
• W4386319078 title "Cooperative progression of colitis and leukemia modulated by clonal hematopoiesis via PTX3/IL-1β pro-inflammatory signaling" @default.
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• W4386319078 doi "https://doi.org/10.1101/2023.08.29.555330" @default.
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