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Published on: April 6, 2022
CD38 Is Robustly Induced in Human Macrophages and Monocytes in Inflammatory Conditions
Stephanie A Amici1, Nicholas A Young2, Janiret Narvaez-Miranda1
1Division of Medical Laboratory Science, School of Health and Rehabilitation Sciences, College of Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, United States.
Abstract:
Macrophages and their monocyte precursors mediate innate immune responses and can promote a spectrum of phenotypes from pro-inflammatory to pro-resolving. Currently, there are few markers that allow for robust dissection of macrophage phenotype. We recently identified CD38 as a marker of inflammatory macrophages in murine in vitro and in vivo models. However, it is unknown whether CD38 plays a similar marker and/or functional role in human macrophages and inflammatory diseases. Here, we establish that CD38 transcript and protein are robustly induced in human macrophages exposed to LPS (±IFN-γ) inflammatory stimuli, but not with the alternative stimulus, IL-4. Pharmacologic and/or genetic CD38 loss-of-function significantly reduced the secretion of inflammatory cytokines IL-6 and IL-12p40 and glycolytic activity in human primary macrophages. Finally, monocyte analyses in systemic lupus erythematosus patients revealed that, while all monocytes express CD38, high CD38 expression in the non-classical monocyte subpopulation is associated with disease. These data are consistent with an inflammatory marker role for CD38 in human macrophages and monocytes.
Insights
CD38 identifies inflammatory macrophages in humans, similar to mouse models. Blocking CD38 reduces inflammatory markers and glycolytic activity in human macrophages, suggesting its role in inflammatory diseases like lupus.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages are key immune cells with diverse functions.
- Identifying specific macrophage phenotypes is crucial for understanding immune responses.
- CD38 was previously identified as a marker for inflammatory macrophages in mice.
Purpose of the Study:
- To investigate the role of CD38 in human macrophages and inflammatory diseases.
- To determine if CD38 functions similarly in human inflammatory conditions as observed in murine models.
Main Methods:
- Human primary macrophages were stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN-γ) or interleukin-4 (IL-4).
- CD38 expression was analyzed at transcript and protein levels.
- Pharmacologic and genetic approaches were used to inhibit CD38 function.
- Cytokine secretion and glycolytic activity were measured.
- Monocyte subpopulations from systemic lupus erythematosus (SLE) patients were analyzed for CD38 expression.
Main Results:
- CD38 expression was significantly upregulated in human macrophages stimulated with inflammatory cues (LPS ± IFN-γ), but not with IL-4.
- Inhibition of CD38 reduced the secretion of pro-inflammatory cytokines (IL-6, IL-12p40) and decreased glycolytic activity.
- High CD38 expression in non-classical monocytes correlated with disease activity in SLE patients.
Conclusions:
- CD38 serves as a marker for inflammatory macrophages in humans.
- CD38 plays a functional role in promoting inflammatory responses and glycolytic metabolism in human macrophages.
- CD38 may be a relevant biomarker in human inflammatory diseases, including systemic lupus erythematosus.
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