Proceedings of the National Academy of Sciences of the United States of America · 2022
Reactive granulopoiesis depends on T-cell production of IL-17A and neutropenia-associated alteration of gut microbiota.
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Chen Xuanzhong, Hashimoto Daigo, Ebata Ko, Takahashi Shuichiro, Shimizu Yu, Shinozaki Ryuga, Hasegawa Yuta, Kikuchi Ryo, Senjo Hajime, Yoneda Kazuki, Zhang Zixuan, Harada Shinpei, Hayase Eiko, Ara Takahide, Ohigashi Hiroyuki, Iwakura Yoichiro, Nakamura Kiminori, Ayabe Tokiyoshi, Teshima Takanori
Аннотация
Granulopoiesis in the bone marrow adjusts cellular output as demand for neutrophils changes. Reactive granulopoiesis is induced by profound neutropenia, but its mechanism remains to be clarified. We herein explored its mechanisms using mouse models of syngeneic hematopoietic stem cell transplantation (SCT) and 5-fluorouracil-induced neutropenia. After SCT, T cell production of IL-17A was up-regulated. Neutrophil recovery was significantly delayed in IL-17A-deficient or T cell-deficient RAG1-/- mice, and adoptive transfer of wild-type (WT) T cells facilitated neutrophil engraftment. Gut decontamination with oral antibiotics suppressed T cell production of IL-17A and impaired neutrophil recovery. Transplantation of fecal microbiota collected from neutropenic, not naive, mice promoted neutrophil recovery in these mice, suggesting that neutropenia-associated microbiota had a potential to stimulate reactive granulopoiesis. Our study uncovered a cross talk between gut microbiota and neutropenia after SCT and chemotherapy.