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Special Issue Editor

Dr. Nicki Panoskaltsis

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Guest Editor

Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: cytokine release syndrome/cytokine storm; hematopoiesis; acute myeloid leukemia; myeloid neoplasms; cancer immunotherapy; cancer immunology; immune pathogenesis of myeloid cancer; 3D bone marrow organoid cultures; in silico modeling for optimized immunochemotherapy of leukemia

Special Issue Information

Dear Colleagues,

Cytokine release syndrome (CRS), also known as cytokine storm, results from massive pro-inflammatory cytokine secretion in the absence of adequate immunomodulation. The resulting imbalance in cytokine and cellular homeostatic networks results in ongoing inflammation, tissue damage, short- and long-term cellular and organ dysfunction and death if left uncontrolled following immunotherapy, such as with TGN1412 and CART cells, or infection, such as COVID-19. It is unclear if all cytokine storms are the same regardless of cause, justifying similar treatments, or even if biomarkers for severity and long-term effects can be established.

The scope of this Special Issue of International Journal of Molecular Sciences, entitled “Cytokine Release Syndrome: From Cell Metabolism to Organ Dysfunction”, is to bring together cutting-edge primary research, reviews and commentaries with a focus on characterizing CRS using novel experimental models and multi-omics methodologies and integrating them with clinically relevant approaches for the prevention and treatment of short- and long-term secondary organ dysfunction in affected patients. The aim of this issue is to provide clarity on the features common to CRS regardless of the causative agent and to offer practical actionable biomarkers for targeted treatment.

Dr. Nicki Panoskaltsis
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

cytokine storm
cytokine release syndrome
CRS
immune-related adverse event
immunotherapy
COVID-19
SARS-CoV-2

Published Papers (2 papers)

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Research

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16 pages, 4248 KiB

Open AccessArticle

COVID-19: Immunohistochemical Analysis of TGF-β Signaling Pathways in Pulmonary Fibrosis

by Caroline Busatta Vaz de Paula, Seigo Nagashima, Vanessa Liberalesso, Mariana Collete, Felipe Paes Gomes da Silva, Alessandro Gonçalves Gomes Oricil, Giovanna Silva Barbosa, Guilherme Vieira Cavalcante da Silva, David Batista Wiedmer, Felipe da Silva Dezidério and Lucia Noronha

Int. J. Mol. Sci. 2022, 23(1), 168; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010168 - 24 Dec 2021

Cited by 55 | Viewed by 4729

Abstract

Acute respiratory distress syndrome (ARDS) followed by repair with lung remodeling is observed in COVID-19. These findings can lead to pulmonary terminal fibrosis, a form of irreversible sequelae. There is evidence that TGF-β is intimately involved in the fibrogenic process. When activated, TGF-β promotes the differentiation of fibroblasts into myofibroblasts and regulates the remodeling of the extracellular matrix (ECM). In this sense, the present study evaluated the histopathological features and immunohistochemical biomarkers (ACE-2, AKT-1, Caveolin-1, CD44v6, IL-4, MMP-9, α-SMA, Sphingosine-1, and TGF-β1 tissue expression) involved in the TGF-β1 signaling pathways and pulmonary fibrosis. The study consisted of 24 paraffin lung samples from patients who died of COVID-19 (COVID-19 group), compared to 10 lung samples from patients who died of H1N1pdm09 (H1N1 group) and 11 lung samples from patients who died of different causes, with no lung injury (CONTROL group). In addition to the presence of alveolar septal fibrosis, diffuse alveolar damage (DAD) was found to be significantly increased in the COVID-19 group, associated with a higher density of Collagen I (mature) and III (immature). There was also a significant increase observed in the immunoexpression of tissue biomarkers ACE-2, AKT-1, CD44v6, IL-4, MMP-9, α-SMA, Sphingosine-1, and TGF-β1 in the COVID-19 group. A significantly lower expression of Caveolin-1 was also found in this group. The results suggest the participation of TGF-β pathways in the development process of pulmonary fibrosis. Thus, it would be plausible to consider therapy with TGF-β inhibitors in those patients recovered from COVID-19 to mitigate a possible development of pulmonary fibrosis and its consequences for post-COVID-19 life quality. Full article

(This article belongs to the Special Issue Cytokine Release Syndrome: From Cell Metabolism to Organ Dysfunction)

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Review

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21 pages, 3747 KiB

Open AccessReview

Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway

by Yi-Wen Duan, Shao-Xia Chen, Qiao-Yun Li and Ying Zang

Int. J. Mol. Sci. 2022, 23(13), 7191; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137191 - 28 Jun 2022

Cited by 19 | Viewed by 4453

Abstract

The neuroimmune mechanism underlying neuropathic pain has been extensively studied. Tumor necrosis factor-alpha (TNF-α), a key pro-inflammatory cytokine that drives cytokine storm and stimulates a cascade of other cytokines in pain-related pathways, induces and modulates neuropathic pain by facilitating peripheral (primary afferents) and central (spinal cord) sensitization. Functionally, TNF-α controls the balance between cell survival and death by inducing an inflammatory response and two programmed cell death mechanisms (apoptosis and necroptosis). Necroptosis, a novel form of programmed cell death, is receiving increasing attraction and may trigger neuroinflammation to promote neuropathic pain. Chronic pain is often accompanied by adverse pain-associated emotional reactions and cognitive disorders. Overproduction of TNF-α in supraspinal structures such as the anterior cingulate cortex (ACC) and hippocampus plays an important role in pain-associated emotional disorders and memory deficits and also participates in the modulation of pain transduction. At present, studies reporting on the role of the TNF-α–necroptosis pathway in pain-related disorders are lacking. This review indicates the important research prospects of this pathway in pain modulation based on its role in anxiety, depression and memory deficits associated with other neurodegenerative diseases. In addition, we have summarized studies related to the underlying mechanisms of neuropathic pain mediated by TNF-α and discussed the role of the TNF-α–necroptosis pathway in detail, which may represent an avenue for future therapeutic intervention. Full article

(This article belongs to the Special Issue Cytokine Release Syndrome: From Cell Metabolism to Organ Dysfunction)

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