Inflammation: The Cause of all Diseases 2.0

Topic Information

Dear Colleagues,

Inflammation refers to the defensive response of living tissue within the vascular system to inflammatory factors and local damage. When your body activates its immune system, it releases inflammatory cells. These cells attack external invaders, such as bacteria and viruses, or heal damaged tissue. Inflammatory reactions include symptoms such as redness, heat, and pain. Inflammation is the protective measure of the innate immune system to remove harmful stimuli or pathogens and promote repair, rather than targeting specific pathogens like the acquired immune system. Inflammation is also a symptom of many diseases. This Topic encourages contributors to explore the biological and clinical aspects of inflammation leading to disease causes, symptoms, and treatment. An understanding of these mechanisms can aid in the development of new therapeutic agents to eradicate these diseases. Topics welcome original research papers as well as critiques and opinion papers. Special clinical cases may also be included.

Prof. Dr. Vasso Apostolopoulos
Dr. Jack Feehan
Dr. Vivek P. Chavda
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cells cells	6.0	9.0	2012	16.6 Days	CHF 2700	Submit
Diseases diseases	3.7	-	2013	18.8 Days	CHF 1800	Submit
Healthcare healthcare	2.8	2.7	2013	19.5 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900	Submit
Vaccines vaccines	7.8	7.0	2013	19.2 Days	CHF 2700	Submit

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Published Papers (3 papers)

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All Cells Diseases Healthcare IJMS Vaccines

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20 pages, 636 KiB  

Open AccessReview

Target Role of Monocytes as Key Cells of Innate Immunity in Rheumatoid Arthritis

by Diana I. Salnikova, Nikita G. Nikiforov, Anton Y. Postnov and Alexander N. Orekhov

Diseases 2024, 12(5), 81; https://doi.org/10.3390/diseases12050081 - 25 Apr 2024

Viewed by 208

Abstract

Rheumatoid arthritis (RA) is a chronic, systemic, and inflammatory autoimmune condition characterized by synovitis, pannus formation (with adjacent bone erosion), and joint destruction. In the perpetuation of RA, fibroblast-like synoviocytes (FLSs), macrophages, B cells, and CD4⁺ T-cells—specifically Th1 and Th17 cells—play crucial [...] Read more.

Rheumatoid arthritis (RA) is a chronic, systemic, and inflammatory autoimmune condition characterized by synovitis, pannus formation (with adjacent bone erosion), and joint destruction. In the perpetuation of RA, fibroblast-like synoviocytes (FLSs), macrophages, B cells, and CD4⁺ T-cells—specifically Th1 and Th17 cells—play crucial roles. Additionally, dendritic cells, neutrophils, mast cells, and monocytes contribute to the disease progression. Monocytes, circulating cells primarily derived from the bone marrow, participate in RA pathogenesis. Notably, CCR2 interacts with CCL2, and CX3CR1 (expressed by monocytes) cooperates with CX3CL1 (produced by FLSs), facilitating the migration involved in RA. Canonical “classical” monocytes predominantly acquire the phenotype of an “intermediate” subset, which differentially expresses proinflammatory cytokines (IL-1β, IL-6, and TNF) and surface markers (CD14, CD16, HLA-DR, TLRs, and β1- and β2-integrins). However, classical monocytes have greater potential to differentiate into osteoclasts, which contribute to bone resorption in the inflammatory milieu; in RA, Th17 cells stimulate FLSs to produce RANKL, triggering osteoclastogenesis. This review aims to explore the monocyte heterogeneity, plasticity, antigenic expression, and their differentiation into macrophages and osteoclasts. Additionally, we investigate the monocyte migration into the synovium and the role of their cytokines in RA. Full article

(This article belongs to the Topic Inflammation: The Cause of all Diseases 2.0)

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23 pages, 1999 KiB  

Open AccessReview

Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease

by Maria Camacho-Encina, Laura K. Booth, Rachael E. Redgrave, Omowumi Folaranmi, Ioakim Spyridopoulos and Gavin D. Richardson

Cells 2024, 13(4), 353; https://doi.org/10.3390/cells13040353 - 17 Feb 2024

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Abstract

Cardiovascular diseases (CVDs), a group of disorders affecting the heart or blood vessels, are the primary cause of death worldwide, with an immense impact on patient quality of life and disability. According to the World Health Organization, CVD takes an estimated 17.9 million [...] Read more.

Cardiovascular diseases (CVDs), a group of disorders affecting the heart or blood vessels, are the primary cause of death worldwide, with an immense impact on patient quality of life and disability. According to the World Health Organization, CVD takes an estimated 17.9 million lives each year, where more than four out of five CVD deaths are due to heart attacks and strokes. In the decades to come, an increased prevalence of age-related CVD, such as atherosclerosis, coronary artery stenosis, myocardial infarction (MI), valvular heart disease, and heart failure (HF) will contribute to an even greater health and economic burden as the global average life expectancy increases and consequently the world’s population continues to age. Considering this, it is important to focus our research efforts on understanding the fundamental mechanisms underlying CVD. In this review, we focus on cellular senescence and mitochondrial dysfunction, which have long been established to contribute to CVD. We also assess the recent advances in targeting mitochondrial dysfunction including energy starvation and oxidative stress, mitochondria dynamics imbalance, cell apoptosis, mitophagy, and senescence with a focus on therapies that influence both and therefore perhaps represent strategies with the most clinical potential, range, and utility. Full article

(This article belongs to the Topic Inflammation: The Cause of all Diseases 2.0)

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13 pages, 611 KiB  

Open AccessArticle

Impact of Non-Surgical Periodontal Treatment on the Concentration and Level of MRP-8/14 (Calprotectin) as an Inflammatory Biomarker in Women with Periodontitis and Rheumatoid Arthritis: A Quasi-Experimental Study

by Elena Aurora Popoca-Hernández, Rita Elizabeth Martínez-Martínez, Roberto Fidencio González-Amaro, Perla del Carmen Niño-Moreno, José Luis Ayala-Herrera, Alberto Vinicio Jerezano-Domínguez, Leon Francisco Espinosa-Cristóbal, María de Lourdes Márquez-Corona, Irene Aurora Espinosa-de Santillana and Carlo Eduardo Medina-Solís

Diseases 2024, 12(1), 12; https://doi.org/10.3390/diseases12010012 - 01 Jan 2024

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Abstract

The aim of this study was to evaluate the impact of non-surgical periodontal treatment (NS-PT) on periodontal parameters and inflammatory biomarkers in the concentration and level of calprotectin (CLP) in women with periodontitis and rheumatoid arthritis (RA). In this quasi-experimental study, we evaluated [...] Read more.

The aim of this study was to evaluate the impact of non-surgical periodontal treatment (NS-PT) on periodontal parameters and inflammatory biomarkers in the concentration and level of calprotectin (CLP) in women with periodontitis and rheumatoid arthritis (RA). In this quasi-experimental study, we evaluated 30 women (mean age: 52.0 ± 5.8 years) with periodontitis and RA who had been diagnosed and treated for RA for more than 3 years and whose activity markers remained at similar values without significant reduction over three consecutive months. Patients underwent NS-PT, which included plaque control, scaling, and root planing. Serum and saliva samples, periodontal indices, RA activity markers, Disease Activity Score-28 (DAS28), the erythrocyte sedimentation rate (ESR), and the C-reactive protein (CRP) and CLP contents were measured at the beginning of the study and 6 and 12 weeks after NS-PT. Parametric and nonparametric tests were used in the analysis. The mean age was 52.0 ± 5.8 years. Compared to the baseline results, all periodontal indices were significantly reduced 6 and 12 weeks after NS-PT (p < 0.001). DAS28 was also significantly reduced after 12 weeks (p < 0.0001). Similarly, the serum CLP concentration decreased 6 and 12 weeks after NS-PT (p < 0.0001). Of the patients, 100% presented lower levels of CRP and ESR (p < 0.0001). Overall, NS-PT reduced inflammation and disease activity, highlighting the importance of oral health in the control and treatment of systemic diseases such as RA and confirming that NS-PT effectively reduces periodontitis activity and plays a key role in modulating RA activity. Therefore, NS-PT should be considered as an adjunct treatment for RA. Full article

(This article belongs to the Topic Inflammation: The Cause of all Diseases 2.0)

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