Soluble CD163 masks fibronectin-binding protein A-mediated inflammatory activation of<i>S</i><i>taphylococcus aureus</i>infected monocytes

Kneidl, Jessica; Mysore, Vijayashree; Geraci, Jennifer; Tuchscherr, Lorena; Löffler, Bettina; Holzinger, Dirk; Roth, Johannes; Barczyk-Kahlert, Katarzyna

doi:10.1111/cmi.12225

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…GC-induced CD163 has been reported as an innate immune sensor for certain bacteria in human monocytes ( E. coli, S. aureus ) (124). Further studies demonstrated that soluble CD163 can directly bind to fibronectin bound to the staphylococcal surface and this enhances phagocytosis and also killing of bacteria while preventing human monocytes from overwhelming inflammatory response during staphylococcal infections (125, 126). GC-mediated induction of efferocytosis by lung macrophages in mice was also associated with increased uptake of Streptococcus pneumoniae but reduced bactericidal functions of these cells (127).…”

Section: Gcs Effects On Phagocytosismentioning

confidence: 99%

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

2019

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Uncontrolled inflammation is a leading cause of many clinically relevant diseases. Current therapeutic strategies focus mainly on immunosuppression rather than on the mechanisms of inflammatory resolution. Glucocorticoids (GCs) are still the most widely used anti-inflammatory drugs. GCs affect most immune cells but there is growing evidence for cell type specific mechanisms. Different subtypes of monocytes and macrophages play a pivotal role both in generation as well as resolution of inflammation. Activation of these cells by microbial products or endogenous danger signals results in production of pro-inflammatory mediators and initiation of an inflammatory response. GCs efficiently inhibit these processes by down-regulating pro-inflammatory mediators from macrophages and monocytes. On the other hand, GCs act on “naïve” monocytes and macrophages and induce anti-inflammatory mediators and differentiation of anti-inflammatory phenotypes. GC-induced anti-inflammatory monocytes have an increased ability to migrate toward inflammatory stimuli. They remove endo- and exogenous danger signals by an increased phagocytic capacity, produce anti-inflammatory mediators and limit T-cell activation. Thus, GCs limit amplification of inflammation by repressing pro-inflammatory macrophage activation and additionally induce anti-inflammatory monocyte and macrophage populations actively promoting resolution of inflammation. Further investigation of these mechanisms should lead to the development of novel therapeutic strategies to modulate undesirable inflammation with fewer side effects via induction of inflammatory resolution rather than non-specific immunosuppression.

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Section: Gcs Effects On Phagocytosismentioning

confidence: 99%

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

2019

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“…sCD163 protects monocytes from hyperactivation during bacterial infections by dampening the secretion of the proinflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8 (38). The actions of sCD163 and TNF-α seem to be interconnected, and the sCD163/TNF-α ratio is higher in patients with uncomplicated malaria (39).…”

Section: Scd163 Expressionmentioning

confidence: 99%

Clinical significance of sCD163 and its possible role in asthma

Zhi

Gao

Xin

et al. 2017

Molecular Medicine Reports

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Macrophages exert important functions in the balance and efficiency of immune responses, and participate in innate and adaptive immunity. The proinflammatory actions of macrophages are implicated in autoimmune diseases. Unlike classically activated M1 macrophages, the alternatively activated cluster of differentiation (CD)163+ and CD206+ M2 macrophages are involved in tissue repair and wound healing, and use oxidative metabolism to support their long-term functions. CD163 is a member of the scavenger receptor superfamily, categorized into class B, and its soluble(s) form, sCD163, is a marker of activated M2 macrophages. CD163 is selectively expressed in cells of the monocyte and macrophage lineages; however, its biological role has yet to be elucidated. The expression of sCD163 is markedly induced by anti-inflammatory mediators, such as glucocorticoids and interleukin-10, whereas it is inhibited by proinflammatory mediators, such as interferon-γ. These findings suggest that CD163 may serve as a potential target for the therapeutic modulation of inflammatory responses. The concentration of sCD163 in blood is associated with acute and chronic inflammatory processes in autoimmune disorders of connective tissue, fat metabolism and cardiovascular diseases, and it can be used for the assessment of cancer prognosis. A role for sCD163 in the pathogenesis of asthma has also been proposed. The present review serves to present the available knowledge concerning the implication of sCD163 in the pathophysiological mechanisms of asthma, and evaluate its potential as a biomarker and possible therapeutic target for asthma.

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“…CD163 expression is up-regulated by glucocorticoids, IL-6, 10 and 12 and M-CSF (Macrophage colony-stimulating factor) and down-regulated by IL-4, interferon-c and TNF-α [22]. sCD163 diminishes the secretion of IL-1β and IL-6 and 8, and consequently prevents monocytes from hyperactivation [23]. Furthermore, activated M2 macrophages (which are CD163 + ) are involved in wound healing and tissue repair [24].…”

Section: Discussionmentioning

confidence: 99%

Regular Training Increases sTWEAK and Its Decoy Receptor sCD163–Does Training Trigger the sTWEAK/sCD163-Axis to Induce an Anti-Inflammatory Effect?

Schönbauer

Lichtenauer

Paar

et al. 2020

JCM

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Background: Low levels of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were reported in patients with coronary artery disease, heart failure, chronic kidney disease and diabetes mellitus. Soluble cluster differentiation 163 (sCD163) serum levels are related to M2 macrophages, having anti-inflammatory attributes. As sport is well-known for its anti-inflammatory and cardioprotective effects we aimed to investigate the influence of eight months of physical activity on serum sCD163 and sTWEAK levels. Methods: In total, 109 subjects with at least one cardiovascular risk factor were asked to perform endurance training within the calculated training pulse for eight months. Overall, 98 finished the study. The performance gain was measured/quantified by bicycle stress tests at the beginning and end of the observation period. The cohort was divided into four groups, dependent on their baseline performance and performance gain. sCD163 and sTWEAK were measured at baseline and after two, six and eight months by ELISA. Results: Those participants who had a performance gain of ≤2.9% (mean gain 12%) within eight months showed a significant increase in sTWEAK (group 2: from 133 to 200 pg/mL, p = 0.002 and group 4: from 166 to 212 pg/mL, p = 0.031) and sCD163 levels (group 2: from 255 to 348 ng/mL, p = 0.035 and group 4: from 247 to 288 ng/mL, p = 0.025) in contrast to subjects without performance gain (sTWEAK: group 1: from 161 to 177 pg/mL, p = 0.953 and group 3: from 153 to 176 pg/mL, p = 0.744; sCD163: group 1: from 289 to 256 ng/mL, p = 0.374 and group 4: from 291 to 271 ng/mL, p = 0.913). Baseline sCD163 correlated with erythrocyte count, hematocrit, ASAT and lipoprotein a, the presence of hypertension and a BMI > 30 kg/m2. Conclusion: Regular physical activity leads to a significant increase in sCD163 and sTWEAK levels of up to 37% and 50%, respectively. It is well-known that physical activity prevents or retards the onset and genesis of chronic inflammatory disease. One possible way of how training evolves its beneficial effect might be by modifying the inflammation status using the sTWEAK–sCD163 axis. Brief Summary: Regular physical activity leads to a significant increase in sTWEAK and sCD163 levels. Both factors are diminished in patients with chronic (inflammation-based) diseases, such as coronary artery disease, heart failure, pulmonary artery hypertension, chronic kidney disease and diabetes mellitus. It seems that the amounts of soluble TWEAK and CD163 are essential for a healthy balance and modulation between pro- and anti-inflammatory processes, and regular physical training could use the sCD163–sTWEAK axis to unfold its beneficial effect.

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Soluble CD163 masks fibronectin-binding protein A-mediated inflammatory activation ofStaphylococcus aureusinfected monocytes

Cited by 6 publications

References 42 publications

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

Clinical significance of sCD163 and its possible role in asthma

Regular Training Increases sTWEAK and Its Decoy Receptor sCD163–Does Training Trigger the sTWEAK/sCD163-Axis to Induce an Anti-Inflammatory Effect?

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