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	5.1	9.9	2012	17.5 Days	CHF 2700	Submit
Diseases diseases	2.9	0.8	2013	18.9 Days	CHF 1800	Submit
Healthcare healthcare	2.4	3.5	2013	20.5 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900	Submit
Vaccines vaccines	5.2	8.9	2013	17.6 Days	CHF 2700	Submit

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Published Papers (9 papers)

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Open AccessArticle

Combinatorial Genomic Biomarkers Associated with High Response in IgE-Dependent Degranulation in Human Mast Cells

by Issan Yee San Tam, Tak Hong Lee, Hang Yung Alaster Lau and See-Ying Tam

Cells 2024, 13(15), 1237; https://doi.org/10.3390/cells13151237 - 23 Jul 2024

Viewed by 258

Abstract

Mast cells are the major effector cells that mediate IgE-dependent allergic reactions. We sought to use integrated network analysis to identify genomic biomarkers associated with high response in IgE-mediated activation of primary human mast cells. Primary human mast cell cultures derived from 262 [...] Read more.

Mast cells are the major effector cells that mediate IgE-dependent allergic reactions. We sought to use integrated network analysis to identify genomic biomarkers associated with high response in IgE-mediated activation of primary human mast cells. Primary human mast cell cultures derived from 262 normal donors were categorized into High, Average and Low responder groups according to their activation response profiles. Transcriptome analysis was used to identify genes that were differentially expressed in different responder cultures in their baseline conditions, and the data were analyzed by constructing a personalized perturbed profile (PEEP). For upregulated genes, the construction of PEEP for each individual sample of all three responder groups revealed that High responders exhibited a higher percentage of “perturbed” samples whose PEEP values lay outside the normal range of expression. Moreover, the integration of PEEP of four selected upregulated genes into distinct sets of combinatorial profiles demonstrated that the specific pattern of upregulated expression of these four genes, in a tandem combination, was observed exclusively among the High responders. In conclusion, this combinatorial approach was useful in identifying a set of genomic biomarkers that are associated with high degranulation response in human mast cell cultures derived from the blood of a cohort of normal donors. Full article

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

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16 pages, 2652 KiB  

Open AccessArticle

Effects of Combustible Cigarettes and Heated Tobacco Products on Systemic Inflammatory Response in Patients with Chronic Inflammatory Diseases

by Nikolina Kastratovic, Natasa Zdravkovic, Ivan Cekerevac, Vanesa Sekerus, Carl Randall Harrell, Violeta Mladenovic, Aleksandar Djukic, Ana Volarevic, Marija Brankovic, Tijana Gmizic, Marija Zdravkovic, Jelica Bjekic-Macut, Nebojsa Zdravkovic, Valentin Djonov and Vladislav Volarevic

Diseases 2024, 12(7), 144; https://doi.org/10.3390/diseases12070144 - 5 Jul 2024

Viewed by 391

Abstract

Smoke derived from combustible cigarettes (CCs) contains numerous harmful chemicals that can impair the viability, proliferation, and activation of immune cells, affecting the progression of chronic inflammatory diseases. In order to avoid the detrimental effects of cigarette smoking, many CC users have replaced [...] Read more.

Smoke derived from combustible cigarettes (CCs) contains numerous harmful chemicals that can impair the viability, proliferation, and activation of immune cells, affecting the progression of chronic inflammatory diseases. In order to avoid the detrimental effects of cigarette smoking, many CC users have replaced CCs with heated tobacco products (HTPs). Due to different methods of tobacco processing, CC-sourced smoke and HTP-derived aerosols contain different chemical constituents. With the exception of nicotine, HTP-sourced aerosols contain significantly lower amounts of harmful constituents than CC-derived smoke. Since HTP-dependent effects on immune-cell-driven inflammation are still unknown, herein we used flow cytometry analysis, intracellular staining, and an enzyme-linked immunosorbent assay to determine the impact of CCs and HTPs on systemic inflammatory response in patients suffering from ulcerative colitis (UC), diabetes mellitus (DM), and chronic obstructive pulmonary disease (COPD). Both CCs and HTPs significantly modulated cytokine production in circulating immune cells, affecting the systemic inflammatory response in COPD, DM, and UC patients. Compared to CCs, HTPs had weaker capacity to induce the synthesis of inflammatory cytokines (IFN-γ, IL-1β, IL-5, IL-6, IL-12, IL-23, IL-17, TNF-α), but more efficiently induced the production of immunosuppressive IL-10 and IL-35. Additionally, HTPs significantly enhanced the synthesis of pro-fibrotic TGF-β. The continuous use of CCs and HTPs aggravated immune-cell-driven systemic inflammation in COPD and DM patients, but not in UC patients, suggesting that the immunomodulatory effects of CC-derived smoke and HTP-sourced aerosols are disease-specific, and need to be determined for specific immune-cell-driven inflammatory diseases. Full article

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

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14 pages, 543 KiB  

Open AccessArticle

Mild Systemic Inflammation Increases Erythrocyte Fragility

by Charlotte M. Stuart, Carmen Jacob, Aravinthan Varatharaj, Sarah Howard, Joe K. Chouhan, Jessica L. Teeling and Ian Galea

Int. J. Mol. Sci. 2024, 25(13), 7027; https://doi.org/10.3390/ijms25137027 - 27 Jun 2024

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Abstract

There is growing evidence that inflammation impairs erythrocyte structure and function. We assessed the impact of mild systemic inflammation on erythrocyte fragility in three different settings. In order to investigate causation, erythrocyte osmotic fragility was measured in mice challenged with a live attenuated [...] Read more.

There is growing evidence that inflammation impairs erythrocyte structure and function. We assessed the impact of mild systemic inflammation on erythrocyte fragility in three different settings. In order to investigate causation, erythrocyte osmotic fragility was measured in mice challenged with a live attenuated bacterial strain to induce low-grade systemic inflammation; a significant increase in erythrocyte osmotic fragility was observed. To gather evidence that systemic inflammation is associated with erythrocyte fragility in humans, two observational studies were conducted. First, using a retrospective study design, the relationship between reticulocyte-based surrogate markers of haemolysis and high-sensitivity C-reactive protein was investigated in 9292 healthy participants of the UK Biobank project. Secondly, we prospectively assessed the relationship between systemic inflammation (measured by the urinary neopterin/creatinine ratio) and erythrocyte osmotic fragility in a mixed population (n = 54) of healthy volunteers and individuals with long-term medical conditions. Both human studies were in keeping with a relationship between inflammation and erythrocyte fragility. Taken together, we conclude that mild systemic inflammation increases erythrocyte fragility and may contribute to haemolysis. Further research is needed to assess the molecular underpinnings of this pathway and the clinical implications in inflammatory conditions. Full article

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

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27 pages, 3818 KiB  

Open AccessArticle

Ileal Crohn’s Disease Exhibits Reduced Activity of Phospholipase C-β3-Dependent Wnt/β-Catenin Signaling Pathway

by Tomoaki Ando, Ikuo Takazawa, Zachary T. Spencer, Ryoji Ito, Yoshiaki Tomimori, Zbigniew Mikulski, Kenji Matsumoto, Tohru Ishitani, Lee A. Denson, Yu Kawakami, Yuko Kawakami, Jiro Kitaura, Yashi Ahmed and Toshiaki Kawakami

Cells 2024, 13(11), 986; https://doi.org/10.3390/cells13110986 - 5 Jun 2024

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Abstract

Crohn’s disease is a chronic, debilitating, inflammatory bowel disease. Here, we report a critical role of phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3-deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was [...] Read more.

Crohn’s disease is a chronic, debilitating, inflammatory bowel disease. Here, we report a critical role of phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3-deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-β3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/β-catenin signaling, which is essential for homeostasis and the regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and, potentially, protein–protein interaction levels. PLC-β3-deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of patients with ileal Crohn’s disease. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that a reduction in PLC-β3-mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease. Full article

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

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9 pages, 935 KiB  

Open AccessReview

Wernicke Encephalopathy Caused by Avoidance-Restrictive Food Intake Disorder in a Child: A Case-Based Review

by Ida Turrini, Clotilde Guidetti, Ilaria Contaldo, Silvia Pulitanò, Donato Rigante and Chiara Veredice

Diseases 2024, 12(6), 112; https://doi.org/10.3390/diseases12060112 - 24 May 2024

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Abstract

Background: Wernicke encephalopathy (WE) is an acute and potentially fatal neuropsychiatric disorder resulting from thiamine deficiency: its etiology and clinical presentation can be heterogeneous and arduously recognized, especially in children and adolescents. Case presentation: An 8-year-old girl arrived to the emergency room with [...] Read more.

Background: Wernicke encephalopathy (WE) is an acute and potentially fatal neuropsychiatric disorder resulting from thiamine deficiency: its etiology and clinical presentation can be heterogeneous and arduously recognized, especially in children and adolescents. Case presentation: An 8-year-old girl arrived to the emergency room with ataxic gait, nystagmus, and mental confusion after a 10-day history of repeated severe vomiting; her recent clinical history was characterized by restricted nutrition due to a choking phobia, which caused substantial weight loss. Brain magnetic resonance imaging revealed a bilaterally increased T2 signal in the medial areas of the thalami and cerebral periaqueductal region. Diagnosis of WE based on clinical and neuroradiological findings was established and confirmed after labwork showing low serum thiamine. Following psychiatric evaluation, the patient was also diagnosed with avoidance-restrictive food intake disorder (ARFID), which required starting cognitive behavioral therapy and introducing aripiprazole. The patient displayed improvement of the radiological findings after one month and complete resolution of her neurological symptoms and signs. Conclusions: Eating disorders like ARFID might forerun acute signs of WE; this possibility should be considered even in pediatric patients, especially when atypical neurological pictures or feeding issues come out. Full article

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

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18 pages, 6551 KiB  

Open AccessArticle

NADH Intraperitoneal Injection Prevents Lung Inflammation in a BALB/C Mice Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

by Nada Slama, Amina Abdellatif, Karima Bahria, Sara Gasmi, Maamar Khames, Abderrahmene Hadji, George Birkmayer, Mustapha Oumouna, Yassine Amrani and Karine Benachour

Cells 2024, 13(10), 881; https://doi.org/10.3390/cells13100881 - 20 May 2024

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Abstract

Cigarette smoke is one of the main factors in Chronic Obstructive Pulmonary Disease (COPD), a respiratory syndrome marked by persistent respiratory symptoms and increasing airway obstruction. Perturbed NAD+/NADH levels may play a role in various diseases, including lung disorders like COPD. In our [...] Read more.

Cigarette smoke is one of the main factors in Chronic Obstructive Pulmonary Disease (COPD), a respiratory syndrome marked by persistent respiratory symptoms and increasing airway obstruction. Perturbed NAD+/NADH levels may play a role in various diseases, including lung disorders like COPD. In our study, we investigated the preventive effect of NADH supplementation in an experimental model of COPD induced by cigarette smoke extract (CSE). N = 64 mice randomly distributed in eight groups were injected with NADH (two doses of 100 mg/kg or 200 mg/kg) or dexamethasone (2 mg/kg) before being exposed to CSE for up to 9 weeks. Additionally, NADH supplementation preserved lung antioxidant defenses by preventing the functional loss of key enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase, and the expression levels of glutathione (GSH) (n = 4, p < 0.001). It also reduced oxidative damage markers, such as malondialdehyde (MDA) and nitrites (n = 4, p < 0.001). A marked increase in tissue myeloperoxidase activity was assessed (MPO), confirming neutrophils implication in the inflammatory process. The latter was significantly ameliorated in the NADH-treated groups (p < 0.001). Finally, NADH prevented the CSE-induced secretion of cytokines such as Tumor Necrosis Factor alpha (TNF-α), IL-17, and IFN-y (n = 4, p < 0.001). Our study shows, for the first time, the clinical potential of NADH supplementation in preventing key features of COPD via its unique anti-inflammatory and antioxidant properties. Full article

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

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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 1595

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

Cited by 1 | Viewed by 2941

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 - 1 Jan 2024

Viewed by 2083

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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