scholarly journals Activated Platelets Convert CD14+CD16- Into CD14+CD16+ Monocytes With Enhanced FcγR-Mediated Phagocytosis and Skewed M2 Polarization

2021 ◽  
Vol 11 ◽  
Author(s):  
Su Jeong Lee ◽  
Bo Ruem Yoon ◽  
Hee Young Kim ◽  
Su-Jin Yoo ◽  
Seong Wook Kang ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Immune Defense ◽  
Innate Immune ◽  
Human Monocytes ◽  
Chronic Inflammatory Diseases ◽  
M2 Polarization ◽  
Activated Platelets ◽  
Cd16 Expression ◽  
Functional Features

Monocytes are important cellular effectors of innate immune defense. Human monocytes are heterogeneous and can be classified into three distinct subsets based on CD14 and CD16 expression. The expansion of intermediate CD14+CD16+ monocytes has been reported in chronic inflammatory diseases including rheumatoid arthritis (RA). However, the mechanism underlying induction of CD16 and its role in monocytes remains poorly understood. Here, we demonstrate that activated platelets are important for induction of CD16 on classical CD14+CD16- monocytes by soluble factors such as cytokines. Cytokine neutralization and signaling inhibition assays reveal that sequential involvement of platelet-derived TGF-β and monocyte-derived IL-6 contribute to CD16 induction on CD14+CD16- monocytes. Activated platelet-induced CD16 on monocytes participates in antibody-dependent cellular phagocytosis (ADCP) and its level is positively correlated with phagocytic activity. CD14+CD16- monocytes treated with activated platelets preferentially differentiate into M2 macrophages, likely the M2c subset expressing CD163 and MerTK. Lastly, the amount of sCD62P, a marker of activated platelets, is significantly elevated in plasma of RA patients and positively correlates with clinical parameters of RA. Our findings suggest an important role of activated platelets in modulating phenotypical and functional features of human monocytes. This knowledge increases understanding of the immunological role of CD14+CD16+ cells in chronic inflammatory diseases.

scholarly journals Breaking down chronic inflammatory diseases: the role of biglycan in promoting a switch between inflammation and autophagy

FEBS Journal ◽  
2019 ◽  
Vol 286 (15) ◽  
pp. 2965-2979 ◽  
Author(s):  
Heiko Roedig ◽  
Madalina Viviana Nastase ◽  
Malgorzata Wygrecka ◽  
Liliana Schaefer
Keyword(s):  
Inflammatory Diseases ◽  
Chronic Inflammatory Diseases

scholarly journals Amyloid Proteins and Peripheral Neuropathy

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1553 ◽  
Author(s):  
Mohammed M. H. Asiri ◽  
Sjoukje Engelsman ◽  
Niels Eijkelkamp ◽  
Jo W. M. Höppener
Keyword(s):  
Peripheral Neuropathy ◽  
Potential Role ◽  
Inflammatory Diseases ◽  
Amyloid Proteins ◽  
Chronic Inflammatory Diseases ◽  
Histopathological Feature ◽  
Common Diseases ◽  
Biological Defects

Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.

scholarly journals Myeloperoxidase Modulates Hydrogen Peroxide Mediated Cellular Damage in Murine Macrophages

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1255
Author(s):  
Chaorui Guo ◽  
Inga Sileikaite ◽  
Michael J. Davies ◽  
Clare L. Hawkins
Keyword(s):  
Hydrogen Peroxide ◽  
Hypochlorous Acid ◽  
Cell Function ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Cellular Damage ◽  
Enzymatic System ◽  
Therapeutic Approaches ◽  
Macrophage Cell

Myeloperoxidase (MPO) is involved in the development of many chronic inflammatory diseases, in addition to its key role in innate immune defenses. This is attributed to the excessive production of hypochlorous acid (HOCl) by MPO at inflammatory sites, which causes tissue damage. This has sparked wide interest in the development of therapeutic approaches to prevent HOCl-induced cellular damage including supplementation with thiocyanate (SCN−) as an alternative substrate for MPO. In this study, we used an enzymatic system composed of glucose oxidase (GO), glucose, and MPO in the absence and presence of SCN−, to investigate the effects of generating a continuous flux of oxidants on macrophage cell function. Our studies show the generation of hydrogen peroxide (H2O2) by glucose and GO results in a dose- and time-dependent decrease in metabolic activity and cell viability, and the activation of stress-related signaling pathways. Interestingly, these damaging effects were attenuated by the addition of MPO to form HOCl. Supplementation with SCN−, which favors the formation of hypothiocyanous acid, could reverse this effect. Addition of MPO also resulted in upregulation of the antioxidant gene, NAD(P)H:quinone acceptor oxidoreductase 1. This study provides new insights into the role of MPO in the modulation of macrophage function, which may be relevant to inflammatory pathologies.

scholarly journals An update on the role of gut microbiota in chronic inflammatory diseases, and potential therapeutic targets

2018 ◽  
Vol 12 (10) ◽  
pp. 969-983 ◽  
Author(s):  
Bobbi Laing ◽  
Matthew P. G. Barnett ◽  
Gareth Marlow ◽  
Noha Ahmed Nasef ◽  
Lynnette R. Ferguson
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Diseases ◽  
Therapeutic Targets ◽  
Chronic Inflammatory Diseases

scholarly journals The role of DMARDs in reducing the immunogenicity of TNF inhibitors in chronic inflammatory diseases

Rheumatology ◽  
2013 ◽  
Vol 53 (2) ◽  
pp. 213-222 ◽  
Author(s):  
M. Jani ◽  
A. Barton ◽  
R. B. Warren ◽  
C. E. M. Griffiths ◽  
H. Chinoy
Keyword(s):  
Inflammatory Diseases ◽  
Tnf Inhibitors ◽  
Chronic Inflammatory Diseases

scholarly journals Role of guanylate binding protein-1 in vascular defects associated with chronic inflammatory diseases

2011 ◽  
Vol 15 (7) ◽  
pp. 1582-1592 ◽  
Author(s):  
Matthias Hammon ◽  
Martin Herrmann ◽  
Oliver Bleiziffer ◽  
Galyna Pryymachuk ◽  
Laura Andreoli ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Binding Protein ◽  
Chronic Inflammatory Diseases ◽  
Guanylate Binding Protein

scholarly journals Microbiota in Healthy Skin and in Atopic Eczema

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Giuseppe Baviera ◽  
Maria Chiara Leoni ◽  
Lucetta Capra ◽  
Francesca Cipriani ◽  
Giorgio Longo ◽  
...  
Keyword(s):  
Atopic Eczema ◽  
Inflammatory Diseases ◽  
Normal Skin ◽  
Innate Immune ◽  
Microbiota Composition ◽  
Healthy Skin ◽  
Skin Microbiota ◽  
Disease States ◽  
The Relationship

The Italian interest group (IG) on atopic eczema and urticaria is member of the Italian Society of Allergology and Immunology. The aim of our IG is to provide a platform for scientists, clinicians, and experts. In this review we discuss the role of skin microbiota not only in healthy skin but also in skin suffering from atopic dermatitis (AD). A Medline and Embase search was conducted for studies evaluating the role of skin microbiota. We examine microbiota composition and its development within days after birth; we describe the role of specific groups of microorganisms that colonize distinct anatomical niches and the biology and clinical relevance of antimicrobial peptides expressed in the skin. Specific AD disease states are characterized by concurrent and anticorrelated shifts in microbial diversity and proportion ofStaphylococcus. These organisms may protect the host, defining them not as simple symbiotic microbes but rather as mutualistic microbes. These findings reveal links between microbial communities and inflammatory diseases such as AD and provide novel insights into global shifts of bacteria relevant to disease progression and treatment. This review also highlights recent observations on the importance of innate immune systems and the relationship with normal skin microflora for the maintenance of healthy skin.

scholarly journals The Role of IL-33 in Host Response toCandida albicans

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
C. Rodríguez-Cerdeira ◽  
A. Lopez-Bárcenas ◽  
B. Sánchez-Blanco ◽  
R. Arenas
Keyword(s):  
Defense Mechanisms ◽  
Fungal Pathogens ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Case Reports ◽  
Pathogenic Fungi ◽  
Cell Types ◽  
Immune Defense ◽  
Beneficial Role

Background. Interleukin (IL) 33 is a recently identified pleiotropic cytokine that influences the activity of multiple cell types and orchestrates complex innate and adaptive immune responses.Methods. We performed an extensive review of the literature published between 2005 and 2013 on IL-33 and related cytokines, their functions, and their regulation of the immune system followingCandida albicanscolonization. Our literature review included cross-references from retrieved articles and specific data from our own studies.Results. IL-33 (IL-1F11) is a recently identified member of the IL-1 family of cytokines. Accumulating evidence suggests a pivotal role of the IL-33/ST2 axis in host immune defense against fungal pathogens, includingC. albicans. IL-33 induces a Th2-type inflammatory response and activates both innate and adaptive immunity. Studies in animal models have shown that Th2 inflammatory responses have a beneficial role in immunity against gastrointestinal and systemic infections byCandidaspp.Conclusions. This review summarizes the most important clinical studies and case reports describing the beneficial role of IL-33 in immunity and host defense mechanisms against pathogenic fungi. The finding that the IL-33/ST2 axis is involved in therapeutic target has implications for the prevention and treatment of inflammatory diseases, including acute or chronic candidiasis.

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