The macrophage scavenger receptor CD163. Review
ABSTRACT Mature tissue macrophages form a first line of defense to recognize and eliminate potential pathogens; these specialized cells are capable of phagocytosis, degradation of self and foreign materials, establishment of cell-cell interactions, and the production of inflammatory mediators. Mature tissue macrophages express a variety of receptors, including the scavenger receptor cystein-rich (SRCR) superfamily members. CD163 is a member of the SRCR family class B and is expressed on most subpopulations of mature tissue macrophages. The best characterized function of CD163, which is essentially a homeostatic one, is related to the binding of Hemoglobin:Haptoglobin complexes. Furthermore, it has been suggested that CD163 positive macrophages or the soluble form of CD163 plays a role in the resolution of inflammation, as they are found in high numbers in inflamed tissue.
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- "(2) We normalized the DC T of A to B: DDC T = DC T(A) À DC T(B) , and (3) we calculated the expression ratio: 2 ÀDDCT = normalized expression ratio. Gene expression was measured using primers against interleukin (IL)-1b (P5 hippocampus), or IL-4, IL-10, and CD163 (splenocytes); IL-4 and IL-10 are anti-inflammatory cytokines demonstrated to be altered by helminths previously (Rook, 2009; Lesher et al., 2006), and CD163 is a macrophage marker associated with inflammation resolution (Fabriek et al., 2005). "
ABSTRACT: The incidence of autoimmune and inflammatory diseases has risen dramatically in post-industrial societies. "Biome depletion" - loss of commensal microbial and multicellular organisms such as helminths (intestinal worms) that profoundly modulate the immune system - may contribute to these increases. Hyperimmune-associated disorders also affect the brain, especially neurodevelopment, and increasing evidence links early-life infection to cognitive and neurodevelopmental disorders. We have demonstrated previously that rats infected with bacteria as newborns display life-long vulnerabilities to cognitive dysfunction, a vulnerability that is specifically linked to long-term hypersensitivity of microglial cell function, the resident immune cells of the brain. Here, we demonstrate that helminth colonization of pregnant dams attenuated the exaggerated brain cytokine response of their offspring to bacterial infection, and that combined with post-weaning colonization of offspring with helminths (consistent with their mothers treatment) completely prevented enduring microglial sensitization and cognitive dysfunction in adulthood. Importantly, helminths had no overt impact on adaptive immune cell subsets, whereas exaggerated innate inflammatory responses in splenic macrophages were prevented. Finally, helminths altered the effect of neonatal infection on the gut microbiome; neonatal infection with E. coli caused a shift from genera within the Actinobacteria and Tenericutes phyla to genera in the Bacteroidetes phylum in rats not colonized with helminths, but helminths attenuated this effect. In sum, these data point toward an inter-relatedness of various components of the biome, and suggest potential mechanisms by which this helminth might exert therapeutic benefits in the treatment of neuroinflammatory and cognitive disorders. Copyright © 2015. Published by Elsevier Inc.Brain Behavior and Immunity 07/2015; DOI:10.1016/j.bbi.2015.07.006 · 6.13 Impact Factor
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- "M2 macrophages specifically express higher levels of the scavenger receptor CD163, which functions as an anti-inflammatory signal and is a characteristic marker of the M2 macrophage phenotype . Macrophages from patients with respiratory diseases and some healthy smokers have a mixed phenotype and function. "
ABSTRACT: Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.PLoS ONE 09/2014; 9(9):e107063. DOI:10.1371/journal.pone.0107063 · 3.23 Impact Factor
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- "These cells located mostly in the interalveolar septa exhibit CD163-positivity as well. In human lung, CD163-positivity in both alveolar and interstitial mature macrophages was described . The expression of CD163 can be regulated by a variety of factors which have been studied extensively in vitro. "
ABSTRACT: Acute respiratory distress syndrome (ARDS) is a serious medical condition occurring in patients with polytrauma, pulmonary or non-pulmonary sepsis, pneumonia and many other circumstances. It causes inflammation of the lung parenchyma leading to impaired gas exchange with a systemic release of inflammatory mediators, causing consequential lung tissue injury, hypoxemia and frequently multiple organ failure. The aim of current study was to describe expression of inflammatory markers (myeloperoxidase, CD163 and vascular endothelial growth factor) by the cells in acute phase of ARDS. The lung samples of a 20-year-old man who had suffered a serious motorbike accident were obtained for histological examination. He died on the seventh day as a consequence of respiratory failure. Our results imply that expression of CD163 was restricted to activated alveolar macrophages and monocytes. Immunopositivityof MPO was observed in neutrophil granulocytes within lung alveoli and lung blood vessels. Myeloperoxidase positivity was observed in alveolar macrophages, too. Vascular endothelial growth factor was expressed in cytoplasm of neutrophil granulocytes, monocytes, small-sized alveolar macrophages and type II pneumocytes localized mostly inside lung alveoli. On the contrary, no positivity was observed in lung endothelial cells of blood vessels.International journal of clinical and experimental pathology 06/2014; 7(7). · 1.78 Impact Factor