Role of Histone Deacetylases in Monocyte Function in Health and Chronic Inflammatory Diseases

2021 ◽  
pp. 1-47
Author(s):  
Rosa María Tordera ◽  
María Cortés-Erice
Keyword(s):  
Histone Deacetylases ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Diseases ◽  
Monocyte Function

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 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 Osteoclasts contribute to early development of chronic inflammation by promoting dysregulated hematopoiesis and myeloid skewing

2020 ◽  
Author(s):  
Maria-Bernadette Madel ◽  
Lidia Ibáñez ◽  
Thomas Ciucci ◽  
Julia Halper ◽  
Majlinda Topi ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Myeloid Differentiation ◽  
Chronic Colitis ◽  
Therapeutic Blockade ◽  
Hematopoietic Stem ◽  
Chronic Inflammatory Diseases ◽  
Promising Target ◽  
Proliferation And Differentiation ◽  
Early Phases

ABSTRACTIncreased myelopoiesis is a hallmark of many chronic inflammatory diseases. However, the mechanisms involved in the myeloid skewing of hematopoiesis upon inflammation are still incompletely understood. Here, we identify an unexpected role of bone-resorbing osteoclasts in promoting hematopoietic stem cell (HSC) proliferation and differentiation towards myeloipoiesis in the early phases of chronic colitis. RNAseq analysis revealed that osteoclasts in colitis differ from control ones and overexpress genes involved in the remodeling of HSC niches. We showed that colitic osteoclasts modulate the interaction of HSCs with their niche and promote myeloid differentiation. Increased osteoclast activity was correlated with an augmentation of myelopoiesis in patients with chronic colitis. Therapeutic blockade of osteoclasts reduced HSC proliferation and myeloid skewing and resulted in a decreased inflammation and severity of colitis. Together, these data identify osteoclasts as potent regulators of HSCs and promising target in chronic colitis.

Chronic Inflammatory Diseases and Atherosclerotic Cardiovascular Disease: Innocent Bystanders or Partners in Crime?

2018 ◽  
Vol 24 (3) ◽  
pp. 281-290 ◽  
Author(s):  
Peter Riis Hansen
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Inflammatory Diseases ◽  
Atherosclerotic Cardiovascular Disease ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Chronic Inflammatory Diseases ◽  
Increased Risk ◽  
Shared Risk

Inflammation plays a significant role in atherosclerosis and cardiovascular disease (CVD). Patients with chronic inflammatory diseases are at increased risk of CVD, but it is debated whether this association is causal or dependent on shared risk factors, other exposures, genes, and/or inflammatory pathways. The current review summarizes epidemiological, clinical, and experimental data supporting the role of shared inflammatory mechanisms between atherosclerotic CVD and rheumatoid arthritis, psoriasis, inflammatory bowel disease, and periodontitis, respectively, and provides insights to future prospects in this area of research. Awareness of the role of inflammation in CVD in patients with chronic inflammatory diseases and the potential for anti-inflammatory therapy, e.g., with tumor necrosis factor-α inhibitors, to also reduce atherosclerotic CVD has evolved into guideline- based recommendations. These include regular CVD risk assessment, aggressive treatment of traditional CVD risk factors, and recognition of reduced CVD as an added benefit of strict inflammatory disease control. At present, chronic inflammatory diseases would appear to qualify as partners in crime and not merely innocent bystanders to CVD. However, definite incremental contributions of inflammation versus effects of the complex interplay with other CVD risk factors may never be fully elucidated and for the foreseeable future, inflammation is posed to maintain its current position as both a marker and a maker of CVD, with clinical utility both for identification of patient at risk of CVD and as target for therapy to reduce CVD.

Significance of gastroesophageal reflux disease in the formation of chronic rhinosinusitis

2021 ◽  
Vol 88 (2) ◽  
pp. 26-30
Author(s):  
V.E. Kokorina ◽  
Keyword(s):  
Gastroesophageal Reflux Disease ◽  
Gastroesophageal Reflux ◽  
Nasal Cavity ◽  
Gastric Juice ◽  
Paranasal Sinuses ◽  
Reflux Disease ◽  
Inflammatory Diseases ◽  
Clinical Manifestations ◽  
Chronic Inflammatory Diseases

The research conducted by the author establishes the role of gastroesophageal reflux disease (GERD) in the genesis of chronic inflammatory diseases of the nasal cavity and paranasal sinuses. The author notes the characteristic changes in the mucous membrane of the nasal cavity and paranasal sinuses during the application of gastric juice. The analysis of the dynamics of clinical manifestations of diseases of the nasal cavity and paranasal sinuses with various methods of GERD correction was carried out

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