<scp>CD</scp>163 and <scp>CD</scp>206 expression does not correlate with tolerance and cytokine production in <scp>LPS</scp>‐tolerant human monocytes

Alves-Januzzi, Amanda Barba; Brunialti, Milena Karina Coló; Salomão, Reinaldo

doi:10.1002/cyto.b.21321

Cited by 21 publications

(19 citation statements)

References 33 publications

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“…In contrast to our findings, it has been shown that CD163-positive macrophages under a double LPS stimulation paradigm display a higher intracellular content of TNF-α in comparison to their CD163-negative counterparts (Alves-Januzzi, et al, 2015). Here, we show that CD163 overexpression resulted in a reduction of released TNF-α.…”

Section: Discussioncontrasting

confidence: 99%

Macrophage-specific nanotechnology-driven CD163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions

et al. 2017

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M1 macrophages release pro-inflammatory factors during inflammation. They transition to an M2 phenotype and release anti-inflammatory factors to resolve inflammation. An imbalance in the transition from M1 to M2 phenotype in macrophages contributes to the development of persistent inflammation. CD163, a member of the scavenger receptor cysteine-rich family, is an M2 macrophage marker. The functional role of CD163 during the resolution of inflammation is not completely known. We postulate that CD163 contributes to the transition from M1 to M2 phenotype in macrophages. We induced CD163 gene in THP-1 and primary human macrophages using polyethylenimine nanoparticles grafted with a mannose ligand (Man-PEI). This nanoparticle specifically targets cells of monocytic origin via mannose receptors. Cells were challenged with a single or a double stimulation of lipopolysaccharide (LPS). A CD163 or empty plasmid was complexed with Man-PEI nanoparticles for cell transfections. Quantitative RT-PCR, immunocytochemistry, and ELISAs were used for molecular assessments. CD163-overexpressing macrophages displayed reduced levels of tumor necrosis factor-alpha (TNF)-α and monocytes chemoattractant protein (MCP)-1 after a single stimulation with LPS. Following a double stimulation paradigm, CD163-overexpressing macrophages showed an increase of interleukin (IL)-10 and IL-1ra, and a reduction of MCP-1. This anti-inflammatory phenotype was partially blocked by an anti-CD163 antibody (effects on IL-10 and IL-1ra). A decrease in the release of TNF-α, IL-1β, and IL-6 was observed in CD163-overexpressing human primary macrophages. The release of IL-6 was blocked by an anti-CD163 antibody in the CD163-overexpressing group. Our data show that the induction of the CD163 gene in human macrophages under inflammatory conditions produces changes in cytokine secretion in favor of an anti-inflammatory phenotype. Targeting macrophages to induce CD163 using cell-directed nanotechnology is an attractive and practical approach for inflammatory conditions that could lead to persistent pain, i.e. major surgeries, burns, rheumatoid arthritis, etc.

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Section: Discussioncontrasting

confidence: 99%

Macrophage-specific nanotechnology-driven CD163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions

et al. 2017

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“…Accordingly, human monocytes that are tolerant to LPS present inhibited inflammatory cytokine production but retain the ability to phagocytose bacteria and to generate reactive oxygen species (45,49). In our study, CD163 and CD206 expression, markers of alternative activated macrophages (M2), did not correlate with tolerance and cytokine production in LPS-tolerant human monocytes (50).…”

Section: The Pathophysiology Behind the Conceptcontrasting

confidence: 54%

Sepsis: evolving concepts and challenges

Salomão

Ferreira

Salomão

et al. 2019

Braz J Med Biol Res

245

176

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Sepsis remains a major cause of morbidity and mortality worldwide, with increased burden in low- and middle-resource settings. The role of the inflammatory response in the pathogenesis of the syndrome has supported the modern concept of sepsis. Nevertheless, a definition of sepsis and the criteria for its recognition is a continuous process, which reflects the growing knowledge of its mechanisms and the success and failure of diagnostic and therapeutic interventions. Here we review the evolving concepts of sepsis, from the “systemic inflammatory response syndrome triggered by infection” (Sepsis-1) to “a severe, potentially fatal, organic dysfunction caused by an inadequate or dysregulated host response to infection” (Sepsis-3). We focused in the pathophysiology behind the concept and the criteria for recognition and diagnosis of sepsis. A major challenge in evaluating the host response in sepsis is to characterize what is protective and what is harmful, and we discuss that, at least in part, the apparent dysregulated host response may be an effort to adapt to a hostile environment. The new criteria for recognition and diagnosis of sepsis were derived from robust databases, restricted, however, to developed countries. Since then, the criteria have been supported in different clinical settings and in different economic and epidemiological contexts, but still raise discussion regarding their use for the identification versus the prognostication of the septic patient. Clinicians should not be restricted to definition criteria when evaluating patients with infection and should wisely use the broad array of information obtained by rigorous clinical observation.

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“…Contradictory results have been reported on the expression levels of CD163 on endotoxin-tolerant monocytes. While some studies suggested that upregulated CD163 on monocytes is a marker of endotoxin tolerance [ 45 ], the others found no association between expression levels and tolerant state [ 46 ]. Decreased expression of anti-inflammatory CD163 by monocytes in T2DM provides additional evidence that innate immune response in these patients is disturbed.…”

Section: Discussionmentioning

confidence: 99%

Impaired Inflammatory Response to LPS in Type 2 Diabetes Mellitus

Khondkaryan

Margaryan

Poghosyan

et al. 2018

International Journal of Inflammation

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Type 2 diabetes mellitus (T2DM) is a severe health problem worldwide, reaching epidemic levels. High susceptibility to infections of T2DM patients indicates dysregulated immune responses to pathogens. However, innate immune responses, including monocyte functions, in T2DM are poorly investigated. Therefore, in this study we aimed to assess lipopolysaccharide- (LPS-) induced immune responses of circulating monocytes from T2DM patients. The results showed that monocytes from T2DM were hyporesponsive to LPS challenge as reflected by significantly suppressed secretion of TNFα (p < 0.01) and expression of CD11b (p < 0.001) and TLR4 (p < 0.001) compared to those in monocytes from healthy subjects. Furthermore, LPS-induced IL-10 levels were similar in diabetic and healthy supernatants, while expression levels of CD163 were found to be downregulated on monocytes from T2DM (p < 0.001) suggesting impaired ability of monocytes to switch their phenotype to anti-inflammatory. Taken together, our results suggest compromised function of monocytes in T2DM, which may explain, at least partly, high incidence of infection in these patients.

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CD163 and CD206 expression does not correlate with tolerance and cytokine production in LPS‐tolerant human monocytes

Abstract: 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.

Cited by 21 publications

References 33 publications

Macrophage-specific nanotechnology-driven CD163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions

Macrophage-specific nanotechnology-driven CD163 overexpression in human macrophages results in an M2 phenotype under inflammatory conditions

Sepsis: evolving concepts and challenges

Impaired Inflammatory Response to LPS in Type 2 Diabetes Mellitus

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