CD163 and CD206 expression does not correlate with tolerance and cytokine production in LPS-tolerant human monocytes.
Lipopolysaccharide (LPS)-tolerant monocytes produce small amounts of inflammatory cytokines, which is one of the characteristics of the alternative activated macrophages (AAM). These cells exhibited an increased expression of CD206 and CD163. Given the functional similarities of AAMs with the modulation of monocytes' functions observed during sepsis and LPS-tolerance, we evaluated whether the inhibition of inflammatory cytokine production by LPS-tolerant monocytes is associated with the phenotype of cells expressing CD206 and CD163.



We investigated whether tolerant human monocytes would modulate their expression of CD206 and CD163, markers of alternative activation, and whether the level of their expression would be related to cytokines detection. Tolerance to LPS was induced in peripheral blood mononuclear cell by pre-incubating the cells with increasing concentrations of LPS. The expression of CD206 and CD163 and intracellular TNF-α and IL-6 was determined 24 h after LPS challenge by flow cytometry.



No differences in CD163 expression were observed between tolerant and non-tolerant cells, while the expression of CD206, which was decreased following LPS stimulation in non-tolerized cells, was further reduced in tolerant cells. Decreased production of inflammatory cytokines was observed in the tolerized cells, regardless of the expression of CD163 and CD206, with the exception of IL-6 in CD206+ monocytes, which was similarly expressed in both tolerized and non-tolerized cells.



The effect of LPS in the expression of CD163 and CD206 on monocytes is not reverted in LPS tolerant cells, and the inhibition of inflammatory cytokines in tolerant cells is not related with modulation of these receptors. © 2016 International Clinical Cytometry Society.
Division of Infectious Diseases, Department of Medicine, Escola Paulista De Medicina, Hospital Sao Paulo, Universidade Federal De Sao Paulo, Sao Paulo, Brazil.
Amanda Barba
AB
Alves-Januzzi
Division of Infectious Diseases, Department of Medicine, Escola Paulista De Medicina, Hospital Sao Paulo, Universidade Federal De Sao Paulo, Sao Paulo, Brazil.
Milena Karina Colo
MKC
Brunialti
Division of Infectious Diseases, Department of Medicine, Escola Paulista De Medicina, Hospital Sao Paulo, Universidade Federal De Sao Paulo, Sao Paulo, Brazil.
Reinaldo
R
Salomao
D000328:Adult; D015703:Antigens, CD / Q000235:genetics* / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics* / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000235:genetics*; D037181:Lectins, C-Type / Q000235:genetics* / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008070:Lipopolysaccharides / Q000633:toxicity; D008213:Lymphocyte Activation / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000235:genetics* / Q000276:immunology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology; D011956:Receptors, Cell Surface / Q000235:genetics* / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D000098902:CD163 Antigen
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D016207:Cytokines; D037181:Lectins, C-Type; D008070:Lipopolysaccharides; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha
CD163; CD206; LPS tolerance; endotoxin; monocytes