ArticleInflammation 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.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
objectiveObstructive 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.
methodsDistribution 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.
resultsMonocytes 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.
conclusionsOur 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.
Indexed as
Identifiers
42400619What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.