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Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 23047

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Special Issue Editor

Prof. Dr. Evgenii Gusev

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Guest Editor

Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences (IIP UB RAS), Laboratory for Immunology of Inflammation, 620049 Ekaterinburg, Russia
Interests: immunology of inflammation; systemic inflammation; typical pathological processes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent molecular studies and their generalizations have enabled a significant change in the traditional understanding of inflammation, as well as the role of pro-inflammatory mechanisms at the cellular, tissue and organism levels in pathology and in physiological functions.

The elementary functional unit of any pro-inflammatory process is cellular stress. Universal reactions on the cellular level (linked into a single system) include oxidative stress, cell response to the DNA damage, unfolded protein response to mitochondrial stress and endoplasmic reticulum stress, changes in autophagy, inflammasome formation, non-coding RNA response, and formation of a network of cellular stress signaling pathways.

The formation of a pro-inflammatory receptor and secretory phenotype in a large number of activated cells leads to the creation of a variant of the cytokine network and the development of tissue stress. Typical manifestations of this can be classified as classical forms of inflammation, low-grade inflammation and life-critical systemic inflammation of high intensity. Particular aspects of this problem are the study of the role of pro-inflammatory mechanisms in physiological functions, as well as role in malignancies, neurodegeneration, aging, metabolic dysfunctions, and many other processes that are not directly related to traditional concepts of inflammation.

Concurrently, in this Special Issue we are seeking reviews and original articles that focus on understanding all aspects of inflammatory processes in the norm and in pathology.

Prof. Dr. Evgenii Gusev
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

molecular mechanisms
cellular stress
signal pathways
canonical inflammation
low-grade inflammation
systemic inflammation
inflammatory diseases
cytokine network
metabolism
extreme physiology
inflammatory biomarkers

Published Papers (6 papers)

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Research

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23 pages, 2399 KiB

Open AccessArticle

Acute and Chronic Systemic Inflammation: Features and Differences in the Pathogenesis, and Integral Criteria for Verification and Differentiation

by Natalya Zotova, Yulia Zhuravleva, Valeriy Chereshnev and Evgenii Gusev

Int. J. Mol. Sci. 2023, 24(2), 1144; https://doi.org/10.3390/ijms24021144 - 6 Jan 2023

Cited by 10 | Viewed by 5977

Abstract

Currently, there is rationale for separating the systemic manifestations of classical inflammation from systemic inflammation (SI) itself as an independent form of the general pathological process underlying the pathogenesis of the most severe acute and chronic diseases. With this aim in view, we used integral scales of acute and chronic SI (ChSI), including the following blood plasma parameters: interleukins 6, 8, 10; tumor necrosis factor alpha; C-reactive protein; D-dimer; cortisol; troponin I; myoglobin. The presence of multiple organ dysfunction according to the SOFA score was also taken into account. The effectiveness of the scales was tested in groups of intensive care patients during different periods of acute trauma, sepsis, and septic shock. The ChSI scale was applicable under systemic autoimmune diseases, chronic purulent infections, chronic limb threatening ischemia, and end-stage renal disease of various genesis. The number of examined patients was 764 in total. The scales allowed us to verify specific phases of acute SI and identify pathogenetic risk factors of lethal outcomes, as well as the most severe variants of the chronic pathologies course. These scales are open adaptable systems (in terms of the nomenclature and choice of indicators). They are primarily intended for scientific research. However, the SI verification methodology presented in this paper may be useful for developing advanced criteria for assessing both the typical links in the pathogenesis of many diseases and the severity of the overall condition of patients for clinical practice. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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16 pages, 3268 KiB

Open AccessArticle

Immunomodulation via MyD88-NFκB Signaling Pathway from Human Umbilical Cord-Derived Mesenchymal Stem Cells in Acute Lung Injury

by Kang-Hsi Wu, Ju-Pi Li, Wan-Ru Chao, Yi-Ju Lee, Shun-Fa Yang, Ching-Chang Cheng and Yu-Hua Chao

Int. J. Mol. Sci. 2022, 23(10), 5295; https://doi.org/10.3390/ijms23105295 - 10 May 2022

Cited by 7 | Viewed by 1741

Abstract

Excess inflammatory processes play a key detrimental role in the pathophysiology of acute lung injury (ALI). Mesenchymal stem cells (MSCs) were reported to be beneficial to ALI, but the underlying mechanisms have not been completely understood. The present study aimed to examine the involvement of MyD88–NFκB signaling in the immunomodulation of MSCs in mice with lipopolysaccharides (LPS)-induced ALI. We found that serum concentrations of IL-6, TNF-α, MCP-1, IL-1β, and IL-8 were significantly decreased at 6 h after LPS-induced ALI in the MSC group (p < 0.05). For each of the five cytokines, the serum concentration of each individual mouse in either group declined to a similar level at 48 h. The intensity of lung injury lessened in the MSC group, as shown by histopathology and lung injury scores (p < 0.001). The expressions of MyD88 and phospho-NFκB in the lung tissue were significantly decreased in mice receiving MSCs as measured by Western blotting and immunohistochemistry. Our data demonstrated that human umbilical cord-derived MSCs could effectively alleviate the cytokine storm in mice after LPS-induced ALI and attenuated lung injury. Firstly, we documented the correlation between the down-regulation of MyD88–NFκB signaling and immunomodulatory effects of MSCs in the situation of ALI. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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12 pages, 2625 KiB

Open AccessArticle

Chronic Experimental Model of TNBS-Induced Colitis to Study Inflammatory Bowel Disease

by Inês Silva, João Solas, Rui Pinto and Vanessa Mateus

Int. J. Mol. Sci. 2022, 23(9), 4739; https://doi.org/10.3390/ijms23094739 - 25 Apr 2022

Cited by 13 | Viewed by 3381

Abstract

Background: Inflammatory bowel disease (IBD) is a world healthcare problem. In order to evaluate the effect of new pharmacological approaches for IBD, we aim to develop and validate chronic trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods: Experimental colitis was induced by the rectal administration of multiple doses of TNBS in female CD-1 mice. The protocol was performed with six experimental groups, depending on the TNBS administration frequency, and two control groups (sham and ethanol groups). Results: The survival rate was 73.3% in the first three weeks and, from week 4 until the end of the experimental protocol, the mice’s survival remained unaltered at 70.9%. Fecal hemoglobin presented a progressive increase until week 4 (5.8 ± 0.3 µmol Hg/g feces, p < 0.0001) compared with the ethanol group, with no statistical differences to week 6. The highest level of tumor necrosis factor-α was observed on week 3; however, after week 4, a slight decrease in tumor necrosis factor-α concentration was verified, and the level was maintained until week 6 (71.3 ± 3.3 pg/mL and 72.7 ± 3.6 pg/mL, respectively). Conclusions: These findings allowed the verification of a stable pattern of clinical and inflammation signs after week 4, suggesting that the chronic model of TNBS-induced colitis develops in 4 weeks. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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23 pages, 5212 KiB

Open AccessArticle

More Prominent Inflammatory Response to Pachyman than to Whole-Glucan Particle and Oat-β-Glucans in Dextran Sulfate-Induced Mucositis Mice and Mouse Injection through Proinflammatory Macrophages

by Pratsanee Hiengrach, Peerapat Visitchanakun, Malcolm A. Finkelman, Wiwat Chancharoenthana and Asada Leelahavanichkul

Int. J. Mol. Sci. 2022, 23(7), 4026; https://doi.org/10.3390/ijms23074026 - 5 Apr 2022

Cited by 13 | Viewed by 2249

Abstract

(1→3)-β-D-glucans (BG) (the glucose polymers) are recognized as pathogen motifs, and different forms of BGs are reported to have various effects. Here, different BGs, including Pachyman (BG with very few (1→6)-linkages), whole-glucan particles (BG with many (1→6)-glycosidic bonds), and Oat-BG (BG with (1→4)-linkages), were tested. In comparison with dextran sulfate solution (DSS) alone in mice, DSS with each of these BGs did not alter the weight loss, stool consistency, colon injury (histology and cytokines), endotoxemia, serum BG, and fecal microbiome but Pachyman–DSS-treated mice demonstrated the highest serum cytokine elicitation (TNF-α and IL-6). Likewise, a tail vein injection of Pachyman together with intraperitoneal lipopolysaccharide (LPS) induced the highest levels of these cytokines at 3 h post-injection than LPS alone or LPS with other BGs. With bone marrow-derived macrophages, BG induced only TNF-α (most prominent with Pachyman), while LPS with BG additively increased several cytokines (TNF-α, IL-6, and IL-10); inflammatory genes (iNOS, IL-1β, Syk, and NF-κB); and cell energy alterations (extracellular flux analysis). In conclusion, Pachyman induced the highest LPS proinflammatory synergistic effect on macrophages, followed by WGP, possibly through Syk-associated interactions between the Dectin-1 and TLR-4 signal transduction pathways. Selection of the proper form of BGs for specific clinical conditions might be beneficial. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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Review

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15 pages, 6758 KiB

Open AccessReview

Immunomodulation of Mesenchymal Stem Cells in Acute Lung Injury: From Preclinical Animal Models to Treatment of Severe COVID-19

by Ju-Pi Li, Kang-Hsi Wu, Wan-Ru Chao, Yi-Ju Lee, Shun-Fa Yang and Yu-Hua Chao

Int. J. Mol. Sci. 2022, 23(15), 8196; https://doi.org/10.3390/ijms23158196 - 25 Jul 2022

Cited by 11 | Viewed by 2449

Abstract

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been a major public health challenge worldwide. Owing to the emergence of novel viral variants, the risks of reinfections and vaccine breakthrough infections has increased considerably despite a mass of vaccination. The formation of cytokine storm, which subsequently leads to acute respiratory distress syndrome, is the major cause of mortality in patients with COVID-19. Based on results of preclinical animal models and clinical trials of acute lung injury and acute respiratory distress syndrome, the immunomodulatory, tissue repair, and antiviral properties of MSCs highlight their potential to treat COVID-19. This review article summarizes the potential mechanisms and outcomes of MSC therapy in COVID-19, along with the pathogenesis of the SARS-CoV-2 infection. The properties of MSCs and lessons from preclinical animal models of acute lung injury are mentioned ahead. Important issues related to the use of MSCs in COVID-19 are discussed finally. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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41 pages, 3031 KiB

Open AccessReview

Inflammation: A New Look at an Old Problem

by Evgenii Gusev and Yulia Zhuravleva

Int. J. Mol. Sci. 2022, 23(9), 4596; https://doi.org/10.3390/ijms23094596 - 21 Apr 2022

Cited by 27 | Viewed by 6444

Abstract

Pro-inflammatory stress is inherent in any cells that are subject to damage or threat of damage. It is defined by a number of universal components, including oxidative stress, cellular response to DNA damage, unfolded protein response to mitochondrial and endoplasmic reticulum stress, changes in autophagy, inflammasome formation, non-coding RNA response, formation of an inducible network of signaling pathways, and epigenetic changes. The presence of an inducible receptor and secretory phenotype in many cells is the cause of tissue pro-inflammatory stress. The key phenomenon determining the occurrence of a classical inflammatory focus is the microvascular inflammatory response (exudation, leukocyte migration to the alteration zone). This same reaction at the systemic level leads to the development of life-critical systemic inflammation. From this standpoint, we can characterize the common mechanisms of pathologies that differ in their clinical appearance. The division of inflammation into alternative variants has deep evolutionary roots. Evolutionary aspects of inflammation are also described in the review. The aim of the review is to provide theoretical arguments for the need for an up-to-date theory of the relationship between key human pathological processes based on the integrative role of the molecular mechanisms of cellular and tissue pro-inflammatory stress. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Cellular and Tissue Stress, Canonical and Non-classical Forms of Pro-inflammatory Processes in Health and Disease)

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