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Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 March 2021) | Viewed by 29747

Special Issue Editors

Dr. Nadia Ferlazzo

E-Mail Website
Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
Interests: oxidative stress; inflammation; neurological disorders; apoptosis; natural products; transglutaminase; DNA-based molecular markers
Dr. Monica Currò

E-Mail Website
Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
Interests: biomarkers; cancer biology; hyperhomocysteinemia; hypoxia; inflammation; neuroprotection; transglutaminase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Inflammation participates in host defenses against infectious agents and injury, but it also contributes to the development of many diseases that collectively represent the leading causes of disability and mortality worldwide. In particular, multiple lines of evidence have suggested that chronic diseases such as obesity, cardiovascular disease, type 2 diabetes mellitus, nonalcoholic fatty liver disease, autoimmunity, cancer, and neurodegenerative disorders recognize inflammation as a common trigger for pathophysiological conditions. However, the mechanisms underlying the inflammatory regulation of these disorders are not fully understood. The interplay of cells involved in the immune system and inflammatory mediators orchestrates molecular pathways that contribute to tissue injury, oxidative stress, remodeling of the extracellular matrix, angiogenesis, and fibrosis in target tissues.

As the control of inflammation seems to be an attractive target for healthcare improvement, a thorough knowledge of molecular profiles and the detection of new biomarkers of inflammatory processes can support the development of new approaches to early diagnosis, treatment, and monitoring of inflammation-related disorders, and also provide tools to predict disease susceptibility.

This Special Issue “Old and New Players in Inflammatory Disorders as Powerful Tools for Prevention, Diagnosis, and Treatment” welcomes original research and review articles in the field, with a focus on but not limited to molecular players in inflammation that hold the potential for making advancements in the management of inflammatory diseases.

Dr. Nadia Ferlazzo
Dr. Monica Currò
Guest Editors

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

  • Immunomodulatory effectors
  • Peripheral inflammation molecular profiles
  • Signal transduction
  • Oxidative stress-related inflammation
  • Chronic inflammation-associated oncogenic players
  • Gut microbiota–immunity axis
  • Anti-inflammatory agents
  • Promising biomarkers in inflammation-related diseases

Related Special Issue

Published Papers (6 papers)

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Research

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12 pages, 1749 KiB  
Article
Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist
by Eva Uchytilova, Diana Spicarova and Jiri Palecek
Int. J. Mol. Sci. 2021, 22(7), 3712; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073712 - 02 Apr 2021
Cited by 6 | Viewed by 1916
Abstract
Transient receptor potential vanilloid 1 (TRPV1) channels contribute to the development of several chronic pain states and represent a possible therapeutic target in many painful disease treatment. Proinflammatory mediator bradykinin (BK) sensitizes TRPV1, whereas noxious peripheral stimulation increases BK level in the spinal [...] Read more.
Transient receptor potential vanilloid 1 (TRPV1) channels contribute to the development of several chronic pain states and represent a possible therapeutic target in many painful disease treatment. Proinflammatory mediator bradykinin (BK) sensitizes TRPV1, whereas noxious peripheral stimulation increases BK level in the spinal cord. Here, we investigated the involvement of spinal TRPV1 in thermal and mechanical hypersensitivity, evoked by intrathecal (i.t.) administration of BK and an endogenous agonist of TRPV1, N-oleoyldopamine (OLDA), using behavioral tests and i.t. catheter implantation, and administration of BK-induced transient thermal and mechanical hyperalgesia and mechanical allodynia. All these hypersensitive states were enhanced by co-administration of a low dose of OLDA (0.42 µg i.t.), which was ineffective only under the control conditions. Intrathecal pretreatment with TRPV1 selective antagonist SB366791 prevented hypersensitivity induced by i.t. co-administration of BK and OLDA. Our results demonstrate that both thermal and mechanical hypersensitivity evoked by co-administration of BK and OLDA is mediated by the activation of spinal TRPV1 channels. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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17 pages, 1475 KiB  
Article
Neuraminidase Inhibitor Zanamivir Ameliorates Collagen-Induced Arthritis
by Bettina Sehnert, Juliane Mietz, Rita Rzepka, Stefanie Buchholz, Andrea Maul-Pavicic, Sandra Schaffer, Falk Nimmerjahn and Reinhard E. Voll
Int. J. Mol. Sci. 2021, 22(3), 1428; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031428 - 31 Jan 2021
Cited by 4 | Viewed by 3461
Abstract
Altered sialylation patterns play a role in chronic autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown the pro-inflammatory activities of immunoglobulins (Igs) with desialylated sugar moieties. The role of neuraminidases (NEUs), enzymes which are responsible for the cleavage of terminal [...] Read more.
Altered sialylation patterns play a role in chronic autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown the pro-inflammatory activities of immunoglobulins (Igs) with desialylated sugar moieties. The role of neuraminidases (NEUs), enzymes which are responsible for the cleavage of terminal sialic acids (SA) from sialoglycoconjugates, is not fully understood in RA. We investigated the impact of zanamivir, an inhibitor of the influenza virus neuraminidase, and mammalian NEU2/3 on clinical outcomes in experimental arthritides studies. The severity of arthritis was monitored and IgG titers were measured by ELISA. (2,6)-linked SA was determined on IgG by ELISA and on cell surfaces by flow cytometry. Zanamivir at a dose of 100 mg/kg (zana-100) significantly ameliorated collagen-induced arthritis (CIA), whereas zana-100 was ineffective in serum transfer-induced arthritis. Systemic zana-100 treatment reduced the number of splenic CD138+/TACI+ plasma cells and CD19+ B cells, which was associated with lower IgG levels and an increased sialylation status of IgG compared to controls. Our data reveal the contribution of NEU2/3 in CIA. Zanamivir down-modulated the T and B cell-dependent humoral immune response and induced an anti-inflammatory milieu by inhibiting sialic acid degradation. We suggest that neuraminidases might represent a promising therapeutic target for RA and possibly also for other antibody-mediated autoimmune diseases. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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15 pages, 1945 KiB  
Article
Spinal PAR2 Activation Contributes to Hypersensitivity Induced by Peripheral Inflammation in Rats
by Petra Mrozkova, Diana Spicarova and Jiri Palecek
Int. J. Mol. Sci. 2021, 22(3), 991; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22030991 - 20 Jan 2021
Cited by 5 | Viewed by 2045
Abstract
The mechanisms of inflammatory pain need to be identified in order to find new superior treatments. Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) are highly co-expressed in dorsal root ganglion neurons and implicated in pain development. Here, we examined [...] Read more.
The mechanisms of inflammatory pain need to be identified in order to find new superior treatments. Protease-activated receptors 2 (PAR2) and transient receptor potential vanilloid 1 (TRPV1) are highly co-expressed in dorsal root ganglion neurons and implicated in pain development. Here, we examined the role of spinal PAR2 in hyperalgesia and the modulation of synaptic transmission in carrageenan-induced peripheral inflammation, using intrathecal (i.t.) treatment in the behavioral experiments and recordings of spontaneous, miniature and dorsal root stimulation-evoked excitatory postsynaptic currents (sEPSCs, mEPSCs and eEPSCs) in spinal cord slices. Intrathecal PAR2-activating peptide (AP) administration aggravated the carrageenan-induced thermal hyperalgesia, and this was prevented by a TRPV1 antagonist (SB 366791) and staurosporine i.t. pretreatment. Additionally, the frequency of the mEPSC and sEPSC and the amplitude of the eEPSC recorded from the superficial dorsal horn neurons were enhanced after acute PAR2 AP application, while prevented with SB 366791 or staurosporine pretreatment. PAR2 antagonist application reduced the thermal hyperalgesia and decreased the frequency of mEPSC and sEPSC and the amplitude of eEPSC. Our findings highlight the contribution of spinal PAR2 activation to carrageenan-induced hyperalgesia and the importance of dorsal horn PAR2 and TRPV1 receptor interactions in the modulation of nociceptive synaptic transmission. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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Review

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21 pages, 1328 KiB  
Review
Role of Thioredoxin-Interacting Protein in Diseases and Its Therapeutic Outlook
by Naila Qayyum, Muhammad Haseeb, Moon Suk Kim and Sangdun Choi
Int. J. Mol. Sci. 2021, 22(5), 2754; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052754 - 09 Mar 2021
Cited by 59 | Viewed by 6542
Abstract
Thioredoxin-interacting protein (TXNIP), widely known as thioredoxin-binding protein 2 (TBP2), is a major binding mediator in the thioredoxin (TXN) antioxidant system, which involves a reduction-oxidation (redox) signaling complex and is pivotal for the pathophysiology of some diseases. TXNIP increases reactive oxygen species production [...] Read more.
Thioredoxin-interacting protein (TXNIP), widely known as thioredoxin-binding protein 2 (TBP2), is a major binding mediator in the thioredoxin (TXN) antioxidant system, which involves a reduction-oxidation (redox) signaling complex and is pivotal for the pathophysiology of some diseases. TXNIP increases reactive oxygen species production and oxidative stress and thereby contributes to apoptosis. Recent studies indicate an evolving role of TXNIP in the pathogenesis of complex diseases such as metabolic disorders, neurological disorders, and inflammatory illnesses. In addition, TXNIP has gained significant attention due to its wide range of functions in energy metabolism, insulin sensitivity, improved insulin secretion, and also in the regulation of glucose and tumor suppressor activities in various cancers. This review aims to highlight the roles of TXNIP in the field of diabetology, neurodegenerative diseases, and inflammation. TXNIP is found to be a promising novel therapeutic target in the current review, not only in the aforementioned diseases but also in prolonged microvascular and macrovascular diseases. Therefore, TXNIP inhibitors hold promise for preventing the growing incidence of complications in relevant diseases. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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18 pages, 907 KiB  
Review
From Rheumatoid Factor to Anti-Citrullinated Protein Antibodies and Anti-Carbamylated Protein Antibodies for Diagnosis and Prognosis Prediction in Patients with Rheumatoid Arthritis
by Chao-Yi Wu, Huang-Yu Yang, Shue-Fen Luo and Jenn-Haung Lai
Int. J. Mol. Sci. 2021, 22(2), 686; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020686 - 12 Jan 2021
Cited by 51 | Viewed by 8630
Abstract
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease mainly involving synovial inflammation and articular bone destruction. RA is a heterogeneous disease with diverse clinical presentations, prognoses and therapeutic responses. Following the first discovery of rheumatoid factors (RFs) 80 years ago, the identification [...] Read more.
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease mainly involving synovial inflammation and articular bone destruction. RA is a heterogeneous disease with diverse clinical presentations, prognoses and therapeutic responses. Following the first discovery of rheumatoid factors (RFs) 80 years ago, the identification of both anti-citrullinated protein antibodies (ACPAs) and anti-carbamylated protein antibodies (anti-CarP Abs) has greatly facilitated approaches toward RA, especially in the fields of early diagnosis and prognosis prediction of the disease. Although these antibodies share many common features and can function synergistically to promote disease progression, they differ mechanistically and have unique clinical relevance. Specifically, these three RA associating auto-antibodies (autoAbs) all precede the development of RA by years. However, while the current evidence suggests a synergic effect of RF and ACPA in predicting the development of RA and an erosive phenotype, controversies exist regarding the additive value of anti-CarP Abs. In the present review, we critically summarize the characteristics of these autoantibodies and focus on their distinct clinical applications in the early identification, clinical manifestations and prognosis prediction of RA. With the advancement of treatment options in the era of biologics, we also discuss the relevance of these autoantibodies in association with RA patient response to therapy. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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23 pages, 1045 KiB  
Review
Can We Treat Neuroinflammation in Alzheimer’s Disease?
by Sandra Sánchez-Sarasúa, Iván Fernández-Pérez, Verónica Espinosa-Fernández, Ana María Sánchez-Pérez and Juan Carlos Ledesma
Int. J. Mol. Sci. 2020, 21(22), 8751; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228751 - 19 Nov 2020
Cited by 40 | Viewed by 6095
Abstract
Alzheimer’s disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid depression and aggressiveness. Aging is the major factor contributing to AD; however, the [...] Read more.
Alzheimer’s disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid depression and aggressiveness. Aging is the major factor contributing to AD; however, the initial cause that triggers the disease is yet unknown. Scientific evidence demonstrates that AD, especially the late onset of AD, is not the result of a single event, but rather it appears because of a combination of risk elements with the lack of protective ones. A major risk factor underlying the disease is neuroinflammation, which can be activated by different situations, including chronic pathogenic infections, prolonged stress and metabolic syndrome. Consequently, many therapeutic strategies against AD have been designed to reduce neuro-inflammation, with very promising results improving cognitive function in preclinical models of the disease. The literature is massive; thus, in this review we will revise the translational evidence of these early strategies focusing in anti-diabetic and anti-inflammatory molecules and discuss their therapeutic application in humans. Furthermore, we review the preclinical and clinical data of nutraceutical application against AD symptoms. Finally, we introduce new players underlying neuroinflammation in AD: the activity of the endocannabinoid system and the intestinal microbiota as neuroprotectors. This review highlights the importance of a broad multimodal approach to treat successfully the neuroinflammation underlying AD. Full article
(This article belongs to the Special Issue Old and New Players in Inflammatory Disorders as Tools for Prevention, Diagnosis, and Treatment)
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