Based on CD14 and CD16 expression, human peripheral blood monocytes (MO) can be divided into a major CD14high CD16− population and two minor CD14high CD16+ and CD14dim CD16+ subpopulations. CD14dim CD16+ MO are well characterized and regarded as pro‐inflammatory because upon stimulation produce TNF‐α but little, if any, IL‐10. By contrast, little is known about CD14high CD16+ MO. We investigated the surface expression of selected determinants by CD16+ MO subpopulations, cytokine production, phagocytosis and antigen presentation. We found that both CD16+ subpopulations had a higher expression of HLA‐DR, CD86, CD54 and a lower expression of CD64 than CD14high CD16− population. In addition, CD14high CD16+ MO showed a higher expression of CD11b and TLR4 than CD14dim CD16+ and CD14high CD16− subpopulations. CD14high CD16+ MO exhibited an increased phagocytic activity and a decreased antigen presentation in comparison with CD14dim CD16+. As expected, lipopolysaccharide (LPS)‐stimulated CD14dim CD16+ MO produced TNF‐α but little IL‐10. By contrast, LPS‐stimulated CD14high CD16+ subpopulation produced significantly more IL‐10 than CD14dim CD16+ and CD14high CD16− MO. In conclusion, our data show that human peripheral blood CD16+ MO are heterogeneous in function and consist of two subpopulations: CD14dim CD16+ pro‐inflammatory and CD14high CD16+ with anti‐inflammatory potential.
Background: Internucleosomal DNA fragmentation is one of the hallmarks of apoptosis. Because the low molecular weight DNA fragments are extracted during cell staining in aqueous solutions, apoptotic cells can be identified on DNA content frequency histograms as cells with fractional (“sub‐G1”) DNA content. The aim of the present study was to explore whether in situ DNA fragmentation during apoptosis is discontinuous or progresses incessantly and if it is discontinuous, to define the resistant to cleavage fraction of DNA that remains stainable with the fluorochrome. Materials and Methods: The model of activation‐induced apoptosis of human lymphocytes was chosen as it provides uniform cell population with identical DNA content (DI = 1.00) that undergo apoptosis. Their apoptosis was induced by multivalent mitogen phytohemagglutinin (PHA) in the absence and presence of geldanamycin (GA), the benzoquinone ansamycin antibiotic which binds to Hsp90 (Heat Shock Protein 90) and alters its function. The cells were stained with acridine orange, the metachromatic fluorochrome that differentially stains cellular DNA and RNA. Results: A sharp, discrete peak representing the subpopulation of “sub‐G1” cells with highly reproducible DI = 0.42 ± 0.02 (CV = 5.5 ± 1.2) was observed on DNA content histograms of lymphocytes whose apoptosis was induced by PHA alone. Two distinct peaks, one representing cell subpopulations with DI = 0.42 (as above) and another, with DI = 0.79 ± 0.04 (CV = 5.8 ± 0.4), respectively, were seen in apoptotic cells from cultures stimulated with PHA in the presence of GA. The frequency of cells represented by the sub‐G1 peaks varied depending on time of induction of apoptosis and GA concentration. Conclusions: Apoptosis‐induced DNA fragmentation is discontinuous; approximately 42% of DNA is relatively stable and remains within the cell. The data suggest that the stable DNA is associated with nuclear matrix while the degradable fraction represents DNA in loop domains. A transient DNA stabilization is apparent in the presence of GA as evidenced by the presence of cell subpopulations with 79% of DNA retained in the cell. The observed discontinuity of DNA fragmentation appears to reflect sequential involvement of different nucleases and may also be modulated by chromatin structure. © 2007 International Society for Analytical Cytology.
Patients with AD differ in the ability to clear S. aureus from the skin during anti-inflammatory treatment, which appears to be related to the abnormalities in immunological parameters. Local antibiotic therapy should be considered only in patients with persistent S. aureus colonization.
Despite significant progress in cancer therapy, the outcome of the treatment is often unfavorable. Better treatment monitoring would not only allow an individual more effective, patient‐adjusted therapy, but also it would eliminate some of the side effects. Using a cytochrome c ELISA that was modified to increase sensitivity, we demonstrate that serum cytochrome c is a sensitive apoptotic marker in vivo reflecting therapy‐induced cell death burden. Furthermore, increased serum cytochrome c level is a negative prognostic marker. Cancer patients whose serum cytochrome c level was normal 3 years ago have a twice as high probability to be still alive, as judged from sera samples collected for 3 years, analyzed recently and matched with survival data. Moreover, we show that serum cytochrome c and serum LDH‐activity reflect different stages and different forms of cell death. Cellular cytochrome c release is specific for apoptosis, whereas increased LDH activity is an indicator of (secondary) necrosis. Whereas serum LDH activity reflects the “global” degree of cell death over a period of time, the sensitive cytochrome c‐based method allows confirmation of the individual cancer therapy‐induced and spontaneous cell death events. The combination of cytochrome c with tissue‐specific markers may provide the foundation for precise monitoring of apoptosis in vivo, by “lab‐on‐the‐chip” technology. © 2005 Wiley‐Liss, Inc.
The phenotype and function of peripheral blood monocytes change after trauma and during sepsis. The aim of the study was to evaluate monocyte expression of human leucocyte antigen (HLA)-DR and Fc receptor III (FcR III) (CD16) in neonates and small children with high risk of sepsis (hospitalized at the intensive care unit). The reduced proportion of CD14 HLA-DR monocytes was observed in all patients at the intensive care unit, while the increase of CD16 expression on monocytes was observed in the course of sepsis. The measurement of CD16 expression on monocytes also proved to be more useful for monitoring patient. The proportion of both CD14 dim CD16 and CD14 high CD16 monocytes increased during sepsis; however, monocytes showed reduced ability to phagocytose Escherichia coli, compromised ability to cooperate with T cells and reduced CD86 expression in parallel to HLA-DR depression. The reduced interleukin (IL)-1 but rather increased IL-10 production was associated with sepsis. The differences between CD14 CD16 monocytes of healthy donors and patients with sepsis are discussed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.