Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
Chronic intermittent hypoxia sustains the low-grade inflammatory memory of monocytes via activation of myelopoiesis.
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Li Shi Qi, Wang Yi, Li Meng Yao, Zhang Liu, Chen Xi Xi, Lin Ying Ni, Zhou Li Na, Sun Xian Wen, Ding Yong Jie, Li Qing Yun
Аннотация
OBJECTIVE: Obstructive sleep apnea (OSA), characterized by chronic intermittent hypoxia (CIH), drives a chronic low-grade inflammatory state linked to multiple comorbidities. Monocytes play a pivotal role in the regulation of inflammatory responses. This study aimed to characterize the inflammatory profile of monocytes induced by CIH.
METHODS: Distribution and activation status of monocytes were analyzed in OSA versus healthy controls. In vivo, models of CIH were employed to assess the immediate and long-term effects on monocyte inflammatory profiles and bone marrow (BM) myelopoiesis.
RESULTS: Monocytes derived from OSA patients exhibited enhanced activation marker expression and cytokine secretion. In vivo, CIH provoked immediate inflammatory responses of peripheral monocytes, accompanied by increased abundance of hematopoietic stem and progenitor cells in the BM, resulting in enhanced myelopoiesis and increased circulating monocytes. After normoxic recovery, monocytes from CIH-exposed mice exhibited heightened inflammatory responses upon secondary challenge, which was associated with sustained, myeloid-biased myelopoiesis in the BM.
CONCLUSIONS: Our findings demonstrate that CIH sustains a low-grade inflammatory memory in monocytes, characterized by both basal activation and enhanced responsiveness to secondary stimulation. We identify the establishment of maladaptive myelopoiesis as a novel mechanism for the sustained inflammatory state in OSA, providing new insights into the pathogenesis of inflammatory responses and comorbidities associated with OSA.
METHODS: Distribution and activation status of monocytes were analyzed in OSA versus healthy controls. In vivo, models of CIH were employed to assess the immediate and long-term effects on monocyte inflammatory profiles and bone marrow (BM) myelopoiesis.
RESULTS: Monocytes derived from OSA patients exhibited enhanced activation marker expression and cytokine secretion. In vivo, CIH provoked immediate inflammatory responses of peripheral monocytes, accompanied by increased abundance of hematopoietic stem and progenitor cells in the BM, resulting in enhanced myelopoiesis and increased circulating monocytes. After normoxic recovery, monocytes from CIH-exposed mice exhibited heightened inflammatory responses upon secondary challenge, which was associated with sustained, myeloid-biased myelopoiesis in the BM.
CONCLUSIONS: Our findings demonstrate that CIH sustains a low-grade inflammatory memory in monocytes, characterized by both basal activation and enhanced responsiveness to secondary stimulation. We identify the establishment of maladaptive myelopoiesis as a novel mechanism for the sustained inflammatory state in OSA, providing new insights into the pathogenesis of inflammatory responses and comorbidities associated with OSA.