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In the past, proinflammatory CD11bLy6C monocytes were predominantly considered as a uniform population. However, recent investigations suggests that this population is far more diverse than previously thought. For example, in mouse models of and liver infections, it was shown that their absence had opposite effects. In the former model, it ameliorated parasite-dependent liver injury, whereas in the listeria model it exacerbated liver pathology. Here, we analyzed Ly6C monocytes from the liver of both infection models at transcriptome, protein, and functional levels. Paralleled by - and -specific differences in recruitment-relevant chemokines, both infections induced accumulation of Ly6C monocytes at infection sites. Transcriptomic analysis revealed a high similarity between monocytes from naïve and parasite-infected mice and a clear proinflammatory phenotype of listeria-induced monocytes. This was further reflected by the upregulation of M2-related transcription factors (e.g., ) and higher CD14 expression by Ly6C monocytes in the infection model. In contrast, monocytes from the listeria infection model expressed M1-related transcription factors (e.g., ) and showed higher expression of CD38, CD74, and CD86, as well as higher ROS production. Taken together, proinflammatory Ly6C monocytes vary considerably depending on the causative pathogen. By using markers identified in the study, Ly6C monocytes can be further subdivided into different populations.
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http://dx.doi.org/10.3390/cells11162539 | DOI Listing |
Environ Int
September 2025
State Key Laboratory of Environmental Chemistry and Toxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; College of Sciences, Northeastern University, Shenyang 110004, China; School of Environment, Hangzhou Institute for Advanced Study, Univ
Exposure to nanoplastics (NPs), a pervasive environmental pollutant, presents potential health risks. Pulmonary exposure to NPs has been shown to disrupt both pulmonary metabolic status and immune homeostasis, leading to concerns about their impact on respiratory health and systemic well-being. However, the underlying linkage and mechanisms remain elusive.
View Article and Find Full Text PDFInt Immunopharmacol
August 2025
School of Physical Education, Zhengzhou University, Zhengzhou, Henan Province, China. Electronic address:
Exercise has emerged as a powerful non-pharmacological intervention for mental health, yet its precise mechanisms in alleviating depression remain incompletely understood. Here, using a chronic unpredictable stress (CUS) mouse model, we demonstrate that prolonged stress induces hematopoietic stem cell (HSC) activation, leading to myeloid-biased hematopoiesis and an overproduction of Ly6C monocytes, which contribute to systemic and hippocampal inflammation. Notably, treadmill running exercise effectively mitigated depressive and anxiety-like behaviors in CUS mice by suppressing stress-induced HSC activation, restoring hematopoietic balance, and reducing peripheral Ly6C monocyte infiltration into the brain.
View Article and Find Full Text PDFCommun Biol
August 2025
School of Medicine and the Department of Human Biology, Haifa, University of Haifa, Haifa, Israel.
During the resolution of inflammation, Ly6CF4/80 monocytes differentiate to Ly6CF4/80 macrophages that exert apoptotic cell engulfment (efferocytosis) properties and consequently convert to interferon (IFN)-β-producing macrophages. Here, we report that exposure to IFN-β, or transforming growth factor (TGF)-β, or a deficiency in the pro-apoptotic protein ARTS, results in the conversion of mature macrophages to an Ly6CF4/80CCR2 phenotype in vivo and ex vivo. Deficiency in ARTS or caspase inhibition results in enhanced conversion of macrophages to the Ly6C phenotype.
View Article and Find Full Text PDFbioRxiv
August 2025
Department of Otolaryngology and Brain Health Institute, Rutgers University, Robert Wood Johnson Medical School, Piscataway, New Jersey, U.S.A., 08854 (present address).
Cochlear injury activates the resident macrophages (RM) and recruits the blood-circulating monocytes and monocyte-derived macrophages (Mo/Mo-M), but their specific functions in the injured cochlea are unknown. It is well established that the chemokine fractalkine receptor (CXCR1), expressed by cochlear macrophages, influences the density of those macrophages and promotes synaptic repair and spiral ganglion neuron survival in the injured cochlea. As CXCR1 is expressed on both RM and Mo/Mo-M, it remains unclear if CXCR1-expressing RM and Mo/Mo-M are distinct and differentially promote SGN survival after cochlear injury.
View Article and Find Full Text PDFMonocytes are key circulating effectors of vascular homeostasis, innate immunity and inflammation. Following their generation in mouse bone marrow, classical (Ly6C ) monocytes are mobilized into the blood circulation where they mature into non-classical (Ly6C ) patrolling monocytes or are recruited into peripheral tissues where they differentiate into tissue resident or inflammatory macrophages. Monocytes and macrophages express CSF1R (CD115), the receptor for lineage-specific growth factors CSF1 and IL34.
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