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Advances in Understanding Molecular Basis of Inflammatory Diseases

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 18873

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Special Issue Editors

Dr. Laia Montell

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Guest Editor

Medical Science Liaison, R&D Department, Laboratories Reig Jofre, 08970 Barcelona, Spain
Interests: chronic inflammatory diseases; osteoarthritis; acne; antimicrobial resistance; nanotechnology; basic research

Dr. Francisco Fernández-Campos

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Guest Editor

R&D Department, Labiana Pharmaceuticals, 08757 Corbera Llobregat, Barcelona, Spain
Interests: nanotechnology; molecular mechanism of anti-inflammatory drugs; antibiotics and antifungals; drug delivery systems; topical inflammatory diseases; pharmacokinetics
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Dear Colleagues,

The past three decades have witnessed remarkable advances in our ability to target specific elements of the inflammatory response, fueled by advances in both biotechnology and disease knowledge.

At a molecular level, inflammation is a protective immune response mounted by the evolutionarily-conserved innate immune system to harmful stimuli, such as pathogens, dead cells, or irritants, and it is tightly regulated by the host. Insufficient inflammation can lead to the persistent infection of pathogens, while excessive inflammation can cause chronic or systemic inflammatory diseases. Innate immune function depends upon the recognition of pathogen-associated molecular patterns (PAMPs), derived from invading pathogens, and danger-associated molecular patterns (DAMPs), induced as a result of endogenous stress, by germline-encoded pattern-recognition receptors (PRRs). The activation of PRRs by PAMPs or DAMPs triggers downstream signaling cascades and leads to the production of type I interferon (interferon-α and interferon-β) and proinflammatory cytokines such as IL-1. Of note, DAMP-triggered inflammation, which is particularly important in inflammatory diseases, is termed sterile inflammation when it occurs in the absence of any foreign pathogens.

In terms of human disease, the properties of IL-1 itself remain the model for mediating inflammation. Several major advances in understanding the role of the different proinflammatory cytokines as signal molecules in the pathogenesis of inflammatory diseases have recently been achieved. A personalized therapy is also emerging in this field, focused on the relevant proteins responsible for the inflammatory pathway. Blocking IL-1 in the treatment of chronic inflammatory diseases is one of the aims. However, although the original IL-1 family only comprised IL-1α and IL-1β, the IL-1 family has expanded considerably, as well as the IL-1R family, whose specific roles in inflammatory response are still uncertain.

On the other hand, activation of the inflammasome is also a key function mediated by the innate immune system, and recent advances have greatly increased our understanding of the macromolecular activation of the inflammasome. Important advancements include the identification of additional inflammasome platforms and pathways that regulate the activation of inflammatory caspases. A better understanding of the mechanisms regulating caspase activation has supported initial efforts to modulate dysfunctional cell death and inflammation pathways in a suite of communicable, inflammatory, malignant, metabolic, and neurodegenerative diseases.

Therefore, major advances in understanding the molecular basis of these inflammatory diseases, such as inflammatory bowel disease, psoriasis, rheumatoid arthritis, asthma, or type 1 or 2 diabetes mellitus, will enable us to explore novel approaches to their treatment, together with providing new insights to their pathobiology.

Papers focused on (but not restricted to) the above cited diseases are welcome for submission to this Special Issue. Other diseases including a relevant inflammatory component (osteoarthritis, acne, areata alopecia, obesity, fatty liver disease, etc.) are also welcome.

Dr. Laia Montell
Dr. Francisco Fernández-Campos
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

proinflammatory cytokines
inflammasome
innate immune system
IL-1
caspases
rheumatoid arthritis
psoriasis
osteoarthritis
inflammatory bowel disease
type 1 and 2 diabetes mellitus
asthma

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14 pages, 2663 KiB

Open AccessArticle

An Elevated IL10 mRNA Combined with Lower TNFA mRNA Level in Active Rheumatoid Arthritis Peripheral Blood

by Georgi Vasilev, Viktoria Vasileva, Mariana Ivanova, Spaska Stanilova, Irena Manolova and Lyuba Miteva

Curr. Issues Mol. Biol. 2024, 46(3), 2644-2657; https://doi.org/10.3390/cimb46030167 - 20 Mar 2024

Viewed by 596

Abstract

We aimed to investigate the expression of pro-inflammatory cytokine genes TNFA, IL6, IL12B, IL23, IL18 and immunoregulatory genes FOXP3, TGFB1, and IL10 in the peripheral blood of patients with rheumatoid arthritis (RA) at messenger ribonucleic acid (mRNA) level. The total RNA was isolated from peripheral blood samples. Real-time quantitative PCR was used to perform TaqMan-based assays to quantify mRNAs from 8 target genes. IL23A was upregulated (1.7-fold), whereas IL6 (5-fold), FOXP3 (4-fold), and IL12B (2.56-fold) were downregulated in patients compared to controls. In addition, we found a strong positive correlation between the expression of FOXP3 and TNFA and a moderate correlation between FOXP3 and TGFB1. These data showed the imbalance of the T helper (Th) 1/Th17/ T regulatory (Treg) axis at a systemic level in RA. In cases with active disease, the IL10 gene expression was approximately 2-fold higher; in contrast, the expression of FOXP3 was significantly decreased (3.38-fold). The main part of patients with higher disease activity expressed upregulation of IL10 and downregulation of TNFA. Different disease activity cohorts could be separated based on IL10, TNFA and IL12B expression combinations. In conclusion, our results showed that active disease is associated with an elevated IL10 and lower TNFA mRNA level in peripheral blood cells of RA patients. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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12 pages, 2346 KiB

Open AccessArticle

A Potential Role for the Receptor for Advanced Glycation End-Products (RAGE) in the Development of Secondhand Smoke-Induced Chronic Sinusitis

by Hannah Robin, Courtney Trudeau, Adam Robbins, Emily Chung, Erum Rahman, Olivia Gangmark-Strickland, Frank W. Licari, Duane R. Winden, Dan L. Orr, Juan A. Arroyo and Paul R. Reynolds

Curr. Issues Mol. Biol. 2024, 46(1), 729-740; https://doi.org/10.3390/cimb46010047 - 13 Jan 2024

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Abstract

Chronic sinusitis (CS) is characterized by sinonasal inflammation, mucus overproduction, and edematous mucosal tissue. CS impacts one in seven adults and estimates suggest up to 15% of the general U.S. population may be affected. This research sought to assess a potential role for receptors for advanced glycation end-products (RAGE), an inflammatory receptor expressed in tissues exposed to secondhand smoke (SHS). Human sinus tissue sections were stained for RAGE and S100s, common RAGE ligands. Wild-type mice and mice that over-express RAGE in sinonasal epithelium (RAGE TG) were maintained in room air (RA) or exposed to secondhand smoke (SHS) via a nose-only delivery system five days a week for 6 weeks. Mouse sections were stained for RAGE and tissue lysates were assayed for cleaved caspase 3, cytokines, or matrix metalloproteases. We discovered increased RAGE expression in sinus tissue following SHS exposure and in sinuses from RAGE TG mice in the absence of SHS. Cleaved caspase-3, cytokines (IL-1β, IL-3, and TNF-α), and MMPs (-9 and -13) were induced by SHS and in tissues from RAGE TG mice. These results expand the inflammatory role of RAGE signaling, a key axis in disease progression observed in smokers. In this relatively unexplored area, enhanced understanding of RAGE signaling during voluntary and involuntary smoking may help to elucidate potential therapeutic targets that may attenuate the progression of smoke-related CS. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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19 pages, 1585 KiB

Open AccessArticle

Excess BAFF May Impact HIV-1-Specific Antibodies and May Promote Polyclonal Responses Including Those from First-Line Marginal Zone B-Cell Populations

by Kim Doyon-Laliberté, Matheus Aranguren, Josiane Chagnon-Choquet, Laurie-Anne Batraville, Olina Dagher, Jonathan Richard, Matteo Paniconi, Jean-Pierre Routy, Cécile Tremblay, Marie-Claude Quintal, Nathalie Brassard, Daniel E. Kaufmann, Andrés Finzi, Johanne Poudrier and Michel Roger

Curr. Issues Mol. Biol. 2024, 46(1), 25-43; https://doi.org/10.3390/cimb46010003 - 19 Dec 2023

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Abstract

We have previously shown that blood levels of B-cell Activating Factor (BAFF) rise relatively to disease progression status in the context of HIV-1 infection. Excess BAFF was concomitant with hyperglobulinemia and the deregulation of blood B-cell populations, notably with increased frequencies of a population sharing characteristics of transitional immature and marginal zone (MZ) B-cells, which we defined as marginal zone precursor-like” (MZp). In HIV-uninfected individuals, MZp present a B-cell regulatory (Breg) profile and function, which are lost in classic-progressors. Moreover, RNASeq analyses of blood MZp from classic-progressors depict a hyperactive state and signs of exhaustion, as well as an interferon signature similar to that observed in autoimmune disorders such as Systemic Lupus Erythematosus (SLE) and Sjögren Syndrome (SS), in which excess BAFF and deregulated MZ populations have also been documented. Based on the above, we hypothesize that excess BAFF may preclude the generation of HIV-1-specific IgG responses and drive polyclonal responses, including those from MZ populations, endowed with polyreactivity/autoreactivity. As such, we show that the quantity of HIV-1-specific IgG varies with disease progression status. In vitro, excess BAFF promotes polyclonal IgM and IgG responses, including those from MZp. RNASeq analyses reveal that blood MZp from classic-progressors are prone to Ig production and preferentially make usage of IGHV genes associated with some HIV broadly neutralizing antibodies (bNAbs), but also with autoantibodies, and whose impact in the battle against HIV-1 has yet to be determined. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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16 pages, 3496 KiB

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6-Hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline Demonstrates Anti-Inflammatory Properties and Reduces Oxidative Stress in Acetaminophen-Induced Liver Injury in Rats

by Evgenii D. Kryl’skii, Svetlana E. Kravtsova, Tatyana N. Popova, Larisa V. Matasova, Khidmet S. Shikhaliev and Svetlana M. Medvedeva

Curr. Issues Mol. Biol. 2023, 45(10), 8321-8336; https://doi.org/10.3390/cimb45100525 - 12 Oct 2023

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We examined the effects of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline on markers of liver injury, oxidative status, and the extent of inflammatory and apoptotic processes in rats with acetaminophen-induced liver damage. The administration of acetaminophen caused the accumulation of 8-hydroxy-2-deoxyguanosine and 8-isoprostane in the liver and serum, as well as an increase in biochemiluminescence indicators. Oxidative stress resulted in the activation of pro-inflammatory cytokine and NF-κB factor mRNA synthesis and increased levels of immunoglobulin G, along with higher activities of caspase-3, caspase-8, and caspase-9. The administration of acetaminophen also resulted in the development of oxidative stress, leading to a decrease in the level of reduced glutathione and an imbalance in the function of antioxidant enzymes. This study discovered that 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline reduced oxidative stress by its antioxidant activity, hence reducing the level of pro-inflammatory cytokine and NF-κB mRNA, as well as decreasing the concentration of immunoglobulin G. These changes resulted in a reduction in the activity of caspase-8 and caspase-9, which are involved in the activation of ligand-induced and mitochondrial pathways of apoptosis and inhibited the effector caspase-3. In addition, 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline promoted the normalization of antioxidant system function in animals treated with acetaminophen. As a result, the compound being tested alleviated inflammation and apoptosis by decreasing oxidative stress, which led to improved liver marker indices and ameliorated histopathological alterations. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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18 pages, 4777 KiB

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The Epigenetic Reader Protein SP140 Regulates Dendritic Cell Activation, Maturation and Tolerogenic Potential

by Mohammed Ghiboub, Matthew Bell, Dovile Sinkeviciute, Rab K. Prinjha, Menno P. J. de Winther, Nicola R. Harker, David F. Tough and Wouter J. de Jonge

Curr. Issues Mol. Biol. 2023, 45(5), 4228-4245; https://doi.org/10.3390/cimb45050269 - 11 May 2023

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Abstract

SP140 is an epigenetic reader protein expressed predominantly in immune cells. GWAS studies have shown an association between SP140 single nucleotide polymorphisms (SNPs) and diverse autoimmune and inflammatory diseases, suggesting a possible pathogenic role for SP140 in immune-mediated diseases. We previously demonstrated that treatment of human macrophages with the novel selective inhibitor of the SP140 protein (GSK761) reduced the expression of endotoxin-induced cytokines, implicating a role of SP140 in the function of inflammatory macrophages. In this study, we investigated the effects of GSK761 on in vitro human dendritic cell (DC) differentiation and maturation, assessing the expression of cytokines and co-stimulatory molecules and their capacity to stimulate T-cell activation and induce phenotypic changes. In DCs, lipopolysaccharide (LPS) stimulation induced an increase in SP140 expression and its recruitment to transcription start sites (TSS) of pro-inflammatory cytokine genes. Moreover, LPS-induced cytokines such as TNF, IL-6, and IL-1β were reduced in GSK761- or SP140 siRNA- treated DCs. Although GSK761 did not significantly affect the expression of surface markers that define the differentiation of CD14⁺ monocytes into immature DCs (iDCs), subsequent maturation of iDCs to mature DCs was significantly inhibited. GSK761 strongly reduced expression of the maturation marker CD83, the co-stimulatory molecules CD80 and CD86, and the lipid-antigen presentation molecule CD1b. Finally, when the ability of DCs to stimulate recall T-cell responses by vaccine-specific T cells was assessed, T cells stimulated by GSK761-treated DCs showed reduced TBX21 and RORA expression and increased FOXP3 expression, indicating a preferential generation of regulatory T cells. Overall, this study suggests that SP140 inhibition enhances the tolerogenic properties of DCs, supporting the rationale of targeting SP140 in autoimmune and inflammatory diseases where DC-mediated inflammatory responses contribute to disease pathogenesis. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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13 pages, 3044 KiB

Open AccessArticle

Integrin Subunit Alpha M, ITGAM Nonsynonymous SNP Is Associated with Knee Osteoarthritis among Thais: A Case-Control Study

by Kamphon Intharanut, Plaiwan Suttanon and Oytip Nathalang

Curr. Issues Mol. Biol. 2023, 45(5), 4168-4180; https://doi.org/10.3390/cimb45050265 - 09 May 2023

Cited by 1 | Viewed by 1105

Abstract

Knee osteoarthritis (OA), which is one of the most common degenerative joint diseases, presents a multifactorial etiology, involving multiple causative factors including genetic and environmental determinants. Four human neutrophil antigen (HNA) systems can be determined using each HNA allele by single-nucleotide polymorphisms (SNPs). However, there are no data on HNA polymorphisms and knee OA in Thailand, so we investigated the association of HNA SNPs and knee OA in the Thai population. In a case-control study, detection of HNA-1, -3, -4, and -5 alleles by polymerase chain reaction with sequence-specific priming (PCR-SSP) was performed in participants with and without symptomatic knee OA. Logistic regression models were used to estimate the odds ratio (OR) and 95% confidence interval (CI) between cases and controls. Among 200 participants, 117 (58.5%) had knee OA; 83 (41.5%) did not and were included as controls in this study. An integrin subunit alpha M (ITGAM) nonsynonymous SNP, rs1143679, was markedly associated with symptomatic knee OA. The ITGAM*01*01 genotype was identified as an important increased risk factor for knee OA (adjusted OR = 5.645, 95% CI = 1.799–17.711, p = 0.003). These findings may contribute to our understanding of the application prospects for therapeutic approaches to knee OA. Full article

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31 pages, 3629 KiB

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Inflammasome Molecular Insights in Autoimmune Diseases

by Monica Neamțu, Veronica Bild, Alexandru Vasincu, Oana Dana Arcan, Delia Bulea, Daniela-Carmen Ababei, Răzvan-Nicolae Rusu, Ioana Macadan, Ana Maria Sciucă and Andrei Neamțu

Curr. Issues Mol. Biol. 2024, 46(4), 3502-3532; https://doi.org/10.3390/cimb46040220 - 18 Apr 2024

Viewed by 665

Abstract

Autoimmune diseases (AIDs) emerge due to an irregular immune response towards self- and non-self-antigens. Inflammation commonly accompanies these conditions, with inflammatory factors and inflammasomes playing pivotal roles in their progression. Key concepts in molecular biology, inflammation, and molecular mimicry are crucial to understanding AID development. Exposure to foreign antigens can cause inflammation, potentially leading to AIDs through molecular mimicry triggered by cross-reactive epitopes. Molecular mimicry emerges as a key mechanism by which infectious or chemical agents trigger autoimmunity. In certain susceptible individuals, autoreactive T or B cells may be activated by a foreign antigen due to resemblances between foreign and self-peptides. Chronic inflammation, typically driven by abnormal immune responses, is strongly associated with AID pathogenesis. Inflammasomes, which are vital cytosolic multiprotein complexes assembled in response to infections and stress, are crucial to activating inflammatory processes in macrophages. Chronic inflammation, characterized by prolonged tissue injury and repair cycles, can significantly damage tissues, thereby increasing the risk of AIDs. Inhibiting inflammasomes, particularly in autoinflammatory disorders, has garnered significant interest, with pharmaceutical advancements targeting cytokines and inflammasomes showing promise in AID management. Full article

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25 pages, 1062 KiB

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Nerve Growth Factor and the Role of Inflammation in Tumor Development

by Giampiero Ferraguti, Sergio Terracina, Luigi Tarani, Francesca Fanfarillo, Sara Allushi, Brunella Caronti, Paola Tirassa, Antonella Polimeni, Marco Lucarelli, Luca Cavalcanti, Antonio Greco and Marco Fiore

Curr. Issues Mol. Biol. 2024, 46(2), 965-989; https://doi.org/10.3390/cimb46020062 - 23 Jan 2024

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Abstract

Nerve growth factor (NGF) plays a dual role both in inflammatory states and cancer, acting both as a pro-inflammatory and oncogenic factor and as an anti-inflammatory and pro-apoptotic mediator in a context-dependent way based on the signaling networks and its interaction with diverse cellular components within the microenvironment. This report aims to provide a summary and subsequent review of the literature on the role of NGF in regulating the inflammatory microenvironment and tumor cell growth, survival, and death. The role of NGF in inflammation and tumorigenesis as a component of the inflammatory system, its interaction with the various components of the respective microenvironments, its ability to cause epigenetic changes, and its role in the treatment of cancer have been highlighted in this paper. Full article

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16 pages, 307 KiB

Open AccessReview

Molecular Foundations of Inflammatory Diseases: Insights into Inflammation and Inflammasomes

by Mi Eun Kim and Jun Sik Lee

Curr. Issues Mol. Biol. 2024, 46(1), 469-484; https://doi.org/10.3390/cimb46010030 - 03 Jan 2024

Viewed by 1147

Abstract

Inflammatory diseases are a global health problem affecting millions of people with a wide range of conditions. These diseases, including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), osteoarthritis (OA), gout, and diabetes, impose a significant burden on patients and healthcare systems. A complicated interaction between genetic variables, environmental stimuli, and dysregulated immune responses shows the complex biological foundation of various diseases. This review focuses on the molecular mechanisms underlying inflammatory diseases, including the function of inflammasomes and inflammation. We investigate the impact of environmental and genetic factors on the progression of inflammatory diseases, explore the connection between inflammation and inflammasome activation, and examine the incidence of various inflammatory diseases in relation to inflammasomes. Full article

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13 pages, 1594 KiB

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Retinol-Binding Protein 4 and Visfatin Levels in Patients with Periodontitis and Obesity/Overweight: A Systematic Review and Meta-Analysis

by Yuwei Zhang, Ru Jia, Yifei Zhang, Rui Zou, Lin Niu and Shaojie Dong

Curr. Issues Mol. Biol. 2023, 45(12), 9838-9850; https://doi.org/10.3390/cimb45120614 - 07 Dec 2023

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Abstract

Prior studies demonstrated an equivocal conclusion about the association between the level of retinol-binding protein 4 (RBP4)/visfatin and periodontitis patients with obesity. The aim of our study (Prospero ID: CRD42023469058) was to systematically review the available articles linking the biofluid levels of RBP4/visfatin to the comorbidity of periodontitis and obesity. Clinical trials were screened in accordance with specific inclusion criteria from seven databases up to November 2023. A quality assessment was performed with the Newcastle–Ottawa Scale and ROBINS-I tools for observational and interventional trials, respectively. The standard mean difference (SMD) with a 95% confidence interval (CI) related to the RBP4 level was recorded; the other indicators related to the visfatin level were measured via the mean difference (MD) with the corresponding 95% CI, and Fisher’s Z transformation was measured to reveal the association using Review Manager 5.4. The current evidence was based on five observational studies and two interventional studies. All of them were included in the systematic review, and six of them were in the meta-analysis. Statistical analysis indicated that there was no significant difference in the circulating levels of RBP4 in the periodontitis patients with obesity or without, who were labeled as OP or NP, respectively (155 OP-107 NP: SMD = 1.38; 95% CI: −0.18–2.94, p = 0.08), as well as the periodontal healthy patients with a normal weight, who were labelled as NnP (116 OP-79 NnP: SMD = 6.76; 95% CI: −5.34–18.87, p = 0.27). Meanwhile, a significant higher level of serum visfatin was found in the OP patients than that of the NP (86 OP-45 NP: MD = 4.21; 95% CI: 2.65–5.77, p < 0.00001)/NnP (164 OP-88 NnP: MD = 13.02; 95% CI: 7.34–18.70, p < 0.00001) group. In addition, a positive association was observed between the serum RBP4 and body mass index/clinical attachment loss (CAL). And, then, there was a positive association between the serum visfatin and periodontal parameters, including the probing depth, CAL, and plaque index, as well as metabolic parameters, including the total cholesterol, triglycerides, fasting blood glucose, and low-density lipoprotein cholesterol. Here, the circulating RBP4 level was not independently related to the comorbidity of periodontitis and obesity, while serum visfatin was significantly associated with periodontitis and obesity. Notably, the positive association between circulating RBP4/visfatin and the periodontal parameters/metabolic parameters firmly suggested that the higher severity of the obese or periodontal status was associated with an elevated level of serum visfatin or RBP4 in the OP group. With more rigorous longitudinal research, the exact causations between RBP4/visfatin and the patients affected by obesity and periodontitis could be disentangled. RBP4 and visfatin might be novel, enlightening prospective bio-indexes for the targeted treatment of comorbidities. Full article

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16 pages, 932 KiB

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Influence of Breastfeeding on the State of Meta-Inflammation in Obesity—A Narrative Review

by Dominika Mazur, Małgorzata Satora, Anna K. Rekowska, Zuzanna Kabała, Aleksandra Łomża, Żaneta Kimber-Trojnar and Bożena Leszczyńska-Gorzelak

Curr. Issues Mol. Biol. 2023, 45(11), 9003-9018; https://doi.org/10.3390/cimb45110565 - 11 Nov 2023

Cited by 1 | Viewed by 851

Abstract

Obesity has become an emerging health issue worldwide that continues to grow in females of reproductive age as well. Obesity, as a multisystem and chronic disease, is associated with metabolic inflammation, which is defined as chronic low-grade systemic inflammation mediated by, i.a., adipose tissue macrophages. Lactation has been proven to have a beneficial influence on maternal health and could help restore metabolic balance, especially in the state of maternal obesity. In this review, we aimed to analyze the influence of breastfeeding on chronic low-grade meta-inflammation caused by obesity. We performed a comprehensive literature review using the PubMed, Science Direct, and Google Scholar electronic databases. For this purpose, we searched for “metabolic inflammation”; “meta-inflammation”; “obesity”; “breastfeeding”; “fetal programming”; “energy metabolism”; “postpartum”; “immunity”; “immune system”; and “inflammation” keyword combinations. While the clinical impact of breastfeeding on maternal and offspring health is currently well known, we decided to gain insight into more specific metabolic effects of adiposity, lipid, and glucose homeostasis, and immunological effects caused by the activity of cytokines, macrophages, and other immune system cells. Further research on the immunological and metabolic effects of breastfeeding in obese patients is key to understanding and potentially developing obesity therapeutic strategies. Full article

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16 pages, 680 KiB

Open AccessReview

Correlation between Hepatocyte Growth Factor (HGF) with D-Dimer and Interleukin-6 as Prognostic Markers of Coagulation and Inflammation in Long COVID-19 Survivors

by Bena Zaira, Trilis Yulianti and Jutti Levita

Curr. Issues Mol. Biol. 2023, 45(7), 5725-5740; https://doi.org/10.3390/cimb45070361 - 08 Jul 2023

Cited by 2 | Viewed by 1519

Abstract

In general, an individual who experiences the symptoms of Severe Acute Respiratory Syndrome Coronavirus 2 or SARS-CoV-2 infection is declared as recovered after 2 weeks. However, approximately 10–20% of these survivors have been reported to encounter long-term health problems, defined as ‘long COVID-19’, e.g., blood coagulation which leads to stroke with an estimated incidence of 3%, and pulmonary embolism with 5% incidence. At the time of infection, the immune response produces pro-inflammatory cytokines that stimulate stromal cells to produce pro-hepatocyte growth factor (pro-HGF) and eventually is activated into hepatocyte growth factor (HGF), which helps the coagulation process in endothelial and epithelial cells. HGF is a marker that appears as an inflammatory response that leads to coagulation. Currently, there is no information on the effect of SARS-CoV-2 infection on serum HGF concentrations as a marker of the prognosis of coagulation in long COVID-19 survivors. This review discusses the pathophysiology between COVID-19 and HGF, IL-6, and D-dimer. Full article

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24 pages, 670 KiB

Open AccessReview

Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

by Andrea Padoan, Giulia Musso, Nicole Contran and Daniela Basso

Curr. Issues Mol. Biol. 2023, 45(7), 5534-5557; https://doi.org/10.3390/cimb45070350 - 30 Jun 2023

Cited by 7 | Viewed by 2074

Abstract

In this review, the role of innate and adaptive immunity in the pathogenesis of inflammatory bowel diseases (IBD) is reported. In IBD, an altered innate immunity is often found, with increased Th17 and decreased Treg cells infiltrating the intestinal mucosa. An associated increase in inflammatory cytokines, such as IL-1 and TNF-α, and a decrease in anti-inflammatory cytokines, such as IL-10, concur in favoring the persistent inflammation of the gut mucosa. Autoinflammation is highlighted with insights in the role of inflammasomes, which activation by exogenous or endogenous triggers might be favored by mutations of NOD and NLRP proteins. Autoimmunity mechanisms also take place in IBD pathogenesis and in this context of a persistent immune stimulation by bacterial antigens and antigens derived from intestinal cells degradation, the adaptive immune response takes place and results in antibodies and autoantibodies production, a frequent finding in these diseases. Inflammation, autoinflammation and autoimmunity concur in altering the mucus layer and enhancing intestinal permeability, which sustains the vicious cycle of further mucosal inflammation. Full article

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13 pages, 861 KiB

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Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis

by Masaya Iwamuro, Takehiro Tanaka and Motoyuki Otsuka

Curr. Issues Mol. Biol. 2023, 45(7), 5263-5275; https://doi.org/10.3390/cimb45070334 - 21 Jun 2023

Cited by 4 | Viewed by 2692

Abstract

Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-α, IL-15, transforming growth factor-β1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm. Full article

(This article belongs to the Special Issue Advances in Understanding Molecular Basis of Inflammatory Diseases)

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