Monocyte differentiation and macrophage priming are regulated differentially by pentraxins and their ligands

Abstract

BackgroundCirculating bone marrow-derived monocytes can leave the blood, enter a tissue, and differentiate into M1 inflammatory, M2a remodeling/fibrotic, or M2c/Mreg resolving/immune-regulatory macrophages. Macrophages can also convert from one of the above types to another. Pentraxins are secreted proteins that bind to, and promote efficient clearance of, microbial pathogens and cellular debris during infection, inflammation, and tissue damage. The pentraxins C-reactive protein (CRP), serum amyloid P (SAP), and pentraxin-3 (PTX3) can also bind a variety of endogenous ligands. As monocytes and macrophages are exposed to differing concentrations of pentraxins and their ligands during infection, inflammation, and tissue damage, we assessed what effect pentraxins and their ligands have on these cells.ResultsWe found that many polarization markers do not discriminate between the effects of pentraxins and their ligands on macrophages. However, pentraxins, their ligands, and cytokines differentially regulate the expression of the hemoglobin-haptoglobin complex receptor CD163, the sialic acid-binding lectin CD169, and the macrophage mannose receptor CD206. CRP, a pentraxin generally thought of as being pro-inflammatory, increases the extracellular accumulation of the anti-inflammatory cytokine IL-10, and this effect is attenuated by GM-CSF, mannose-binding lectin, and factor H.ConclusionsThese results suggest that the presence of pentraxins and their ligands regulate macrophage differentiation in the blood and tissues, and that CRP may be a potent inducer of the anti-inflammatory cytokine IL-10.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-017-0214-z) contains supplementary material, which is available to authorized users.

Anti-inflammatory Mechanisms Triggered by Apoptotic Cells during Their Clearance

“…In addition to PS, late apoptotic neutrophils were shown to express also pentraxin 3 (PTX3) in their membranes ( 113 ). PTX3 was shown not only to enhance their phagocytic removal during inflammation ( 113 ) but also to induce the expression of CD169 in macrophages ( 114 ), a molecule that interferes with the development of an autoimmune response ( 115 ).…”

Melittin Induced G1 Cell Cycle Arrest and Apoptosis in Chago-K1 Human Bronchogenic Carcinoma Cells and Inhibited the Differentiation of THP-1 Cells into Tumour- Associated Macrophages

“…A n i m p o r t a n t m e c h a n i s m i n t h e t u m o u r microenvironment is the activation of circulating monocytes to enter the tumour, where they then differentiate and become tumour-associated macrophages (TAMs) under the influence of IL-4 and IL-10 secreted by the cancer cells (Pilling et al, 2017;Shao et al, 2016). Overall, TAMs may be a major component of the tumour microenvironment and are directly involved in tumour growth, infiltration, and metastasis.…”

HBV infection suppresses the expression of inflammatory macrophage miR‑210

“…A number of studies have shown that the expression of certain stress proteins (including heat shock proteins and C-reactive proteins) are increased during HBV infection (33,34). Moreover, these proteins may affect macrophage activation (35,36). Therefore, it was speculated that the expression of macrophage miR-210 may be affected by these stress proteins or other unknown factors during HBV infection.…”