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Biomolecules
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Chemokines in Infectious and Non-infectious Diseases
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Chemokines in Infectious and Non-infectious Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (30 July 2021) | Viewed by 26209

Special Issue Editor

Dr. Jordi Camps

E-Mail Website
Guest Editor
Unitat de Recerca Biomèdica (Biomedical Research Unit), Universitat Rovira i Virgili, Hospital Sant Joan de Reus, Institut d’Investigació Sanitària Pere Virgili, Reus, Spain
Interests: oxidative stress; inflammation; metabolism; non-communicable diseases; infectious diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Infectious and non-infectious diseases share various metabolic and immunological alterations. Research on the factors that relate the immune system to metabolic alterations in disease is clinically important because it can allow the identification of therapeutic targets. It remains unclear how immunity affects systemic metabolism, but experimental evidence supports an intertwined relationship through interorgan metabolic crosstalk and mitochondrial dynamics, which is highlighted by the rapid evolution of the interdisciplinary field of immunometabolism. One of the consequences of these processes is metabolic stress leading to adaptive responses and altered cellular communication. Chemokines are small molecules (8–12 kDa) and can be divided based on the position of the N-terminal cysteine residues into four canonical subclasses: C, CC, CXC, and CX3C chemokines. These proteins can bind to specific heptahelical receptors and to a subclass of scavenging atypical chemokine receptors. In addition, a fifth subclass has been proposed to complement this superfamily, consisting of chemotactic cytokines that are missing the specific N-terminal cysteine residue. Chemokines have various functions that are involved in the maintenance of normal metabolism and affect immune and inflammatory reactions. Recently, the relationships among mitochondrial dysfunction, autophagy, and disease have been linked to chemokines. In this Special Issue, we aim to publish original research papers and reviews on chemokines in infectious and non-infectious diseases to fulfill our wish to provide an instrument for communication and dissemination of the most recent findings of the role that these proteins play in human diseases. Reports on chemokines and SARS-CoV-2 and COVID infection are strongly encouraged.

Dr. Jordi Camps
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. Biomolecules 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 2700 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

  • Immunometabolism
  • Infectious diseases
  • Inflammation
  • Non-communicable diseases

Published Papers (7 papers)

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Research

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14 pages, 2438 KiB  
Article
TNF-α Increases IP-10 Expression in MCF-7 Breast Cancer Cells via Activation of the JNK/c-Jun Pathways
by Shihab Kochumon, Amnah Al-Sayyar, Texy Jacob, Amal Hasan, Fahd Al-Mulla, Sardar Sindhu and Rasheed Ahmad
Biomolecules 2021, 11(9), 1355; https://doi.org/10.3390/biom11091355 - 13 Sep 2021
Cited by 5 | Viewed by 2974
Abstract
IP-10 (also called CXCL10) plays a significant role in leukocyte homing to inflamed tissues, and increased IP-10 levels are associated with the pathologies of various inflammatory disorders, including type 2 diabetes, atherosclerosis, and cancer. TNF-α is a potent activator of immune cells and [...] Read more.
IP-10 (also called CXCL10) plays a significant role in leukocyte homing to inflamed tissues, and increased IP-10 levels are associated with the pathologies of various inflammatory disorders, including type 2 diabetes, atherosclerosis, and cancer. TNF-α is a potent activator of immune cells and induces inflammatory cytokine expression in these cells. However, it is unclear whether TNF-α is able to induce IP-10 expression in MCF-7 breast cancer cells. We therefore determined IP-10 expression in TNF-α-treated MCF-7 cells and investigated the mechanism involved. Our data show that TNF-α induced/upregulated the IP-10 expression at both mRNA and protein levels in MCF-7 cells. Inhibition of JNK (SP600125) significantly suppressed the TNF-α-induced IP-10 in MCF-7 cells, while the inhibition of p38 MAPK (SB203580), MEK1/2 (U0126), and ERK1/2 (PD98059) had no significant effect. Furthermore, TNF-α-induced IP-10 expression was abolished in MCF-7 cells deficient in JNK. Similar results were obtained using MCF-7 cells deficient in c-Jun. Moreover, the JNK kinase inhibitor markedly reduced the TNF-α-induced JNK and c-Jun phosphorylation. The kinase activity of JNK induced by TNF-α stimulation of MCF-7 cells was significantly inhibited by SP600125. Altogether, our novel findings provide the evidence that TNF-α induces IP-10 expression in MCF-7 breast cancer cells via activation of the JNK/c-Jun signaling pathway. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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12 pages, 2378 KiB  
Article
Small Molecule CCR4 Antagonists Protect Mice from Aspergillus Infection and Allergy
by Silvia Bozza, Rossana Giulietta Iannitti, Marilena Pariano, Giorgia Renga, Claudio Costantini, Luigina Romani and Jagadeesh Bayry
Biomolecules 2021, 11(3), 351; https://doi.org/10.3390/biom11030351 - 25 Feb 2021
Cited by 3 | Viewed by 2395
Abstract
The ability to regulate the recruitment of immune cells makes chemokines and their receptors attractive drug targets in many inflammatory diseases. Based on its preferential expression on T helper type 2 (Th2) cells, C-C chemokine receptor type 4 (CCR4) has been widely studied [...] Read more.
The ability to regulate the recruitment of immune cells makes chemokines and their receptors attractive drug targets in many inflammatory diseases. Based on its preferential expression on T helper type 2 (Th2) cells, C-C chemokine receptor type 4 (CCR4) has been widely studied in the context of allergic diseases, but recent evidence on the expression of CCR4 in other cell types has considerably expanded the potential applications of CCR4 antagonism. However, the current number of approved indications, as well as the portfolio of CCR4-targeting drugs, are still limited. In the present study, we have assessed the potential therapeutic efficacy of a CCR4 small molecule antagonist, SP50, discovered via an in silico-based approach, against a variety of pre-clinical settings of infection with the fungus Aspergillus fumigatus. We show that SP50 efficiently worked as prophylactic vaccine adjuvant in immunocompetent mice, protected against invasive aspergillosis in immunosuppressed mice. Further, the CCR4 antagonist prevented allergic bronchopulmonary aspergillosis in susceptible mice, and in a murine model of cystic fibrosis, a genetic disorder characterized by chronic pulmonary inflammation and recurrent infections. In conclusion, our results extend the potential applications of CCR4 antagonism and prompt for the development of novel compounds with the potential to progress to clinical trials. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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16 pages, 6237 KiB  
Article
Biphasic Expression of Atypical Chemokine Receptor (ACKR) 2 and ACKR4 in Colorectal Neoplasms in Association with Histopathological Findings
by Paulina Lewandowska, Jaroslaw Wierzbicki, Marek Zawadzki, Anil Agrawal and Małgorzata Krzystek-Korpacka
Biomolecules 2021, 11(1), 8; https://doi.org/10.3390/biom11010008 - 23 Dec 2020
Cited by 8 | Viewed by 1885
Abstract
Facilitating resolution of inflammation using atypical chemokine receptors (ACKR) as an anticancer strategy is considered but requires a deeper understanding of receptor role in carcinogenesis. We aimed at transcriptional analysis (RTqPCR) of ACKR2 and ACKR4 expression in colorectal adenoma-adenocarcinoma sequence in paired normal-neoplastic [...] Read more.
Facilitating resolution of inflammation using atypical chemokine receptors (ACKR) as an anticancer strategy is considered but requires a deeper understanding of receptor role in carcinogenesis. We aimed at transcriptional analysis (RTqPCR) of ACKR2 and ACKR4 expression in colorectal adenoma-adenocarcinoma sequence in paired normal-neoplastic tissues from 96 polyps and 51 cancers. On average, ACKR2 was downregulated in neoplastic as compared to non-affected tissue in polyp (by 2.7-fold) and cancer (by 3.1-fold) patients. The maximal downregulation (by 8.2-fold) was observed in adenomas with the highest potential for malignancy and was gradually lessening through cancer stages I-IV, owing to increased receptor expression in tumors. On average, ACKR4 was significantly downregulated solely in adenocarcinomas (by 1.5-fold), less so in patients with lymph node metastasis, owing to a gradual decrease in ACKR4 expression among N0-N1-N2 cancers in non-affected tissue without changes in tumors. In adenomas, ACKR4 downregulation in neoplastic tissue increased with increasing potential for malignancy and contribution of villous growth pattern. ACKR4 expression increased in non-affected tissue with a concomitant decrease in pathological mucosa. In conclusion, the changes in ACKRs expression occur already in precancerous colorectal lesions, culminating in the adenomas with the highest potential for malignancy. Therefore, chemoprevention by manipulating ACKRs’ expression is worth exploration. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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Review

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26 pages, 2545 KiB  
Review
On the Role of Paraoxonase-1 and Chemokine Ligand 2 (C-C motif) in Metabolic Alterations Linked to Inflammation and Disease. A 2021 Update
by Jordi Camps, Helena Castañé, Elisabet Rodríguez-Tomàs, Gerard Baiges-Gaya, Anna Hernández-Aguilera, Meritxell Arenas, Simona Iftimie and Jorge Joven
Biomolecules 2021, 11(7), 971; https://doi.org/10.3390/biom11070971 - 01 Jul 2021
Cited by 19 | Viewed by 3632
Abstract
Infectious and many non-infectious diseases share common molecular mechanisms. Among them, oxidative stress and the subsequent inflammatory reaction are of particular note. Metabolic disorders induced by external agents, be they bacterial or viral pathogens, excessive calorie intake, poor-quality nutrients, or environmental factors produce [...] Read more.
Infectious and many non-infectious diseases share common molecular mechanisms. Among them, oxidative stress and the subsequent inflammatory reaction are of particular note. Metabolic disorders induced by external agents, be they bacterial or viral pathogens, excessive calorie intake, poor-quality nutrients, or environmental factors produce an imbalance between the production of free radicals and endogenous antioxidant systems; the consequence being the oxidation of lipids, proteins, and nucleic acids. Oxidation and inflammation are closely related, and whether oxidative stress and inflammation represent the causes or consequences of cellular pathology, both produce metabolic alterations that influence the pathogenesis of the disease. In this review, we highlight two key molecules in the regulation of these processes: Paraoxonase-1 (PON1) and chemokine (C-C motif) ligand 2 (CCL2). PON1 is an enzyme bound to high-density lipoproteins. It breaks down lipid peroxides in lipoproteins and cells, participates in the protection conferred by HDL against different infectious agents, and is considered part of the innate immune system. With PON1 deficiency, CCL2 production increases, inducing migration and infiltration of immune cells in target tissues and disturbing normal metabolic function. This disruption involves pathways controlling cellular homeostasis as well as metabolically-driven chronic inflammatory states. Hence, an understanding of these relationships would help improve treatments and, as well, identify new therapeutic targets. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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14 pages, 447 KiB  
Review
Chemokines in Severe Cutaneous Adverse Reactions (SCARs)
by Fumi Miyagawa and Hideo Asada
Biomolecules 2021, 11(6), 847; https://doi.org/10.3390/biom11060847 - 06 Jun 2021
Cited by 8 | Viewed by 3414
Abstract
Although the incidence of severe cutaneous adverse reactions (SCARs) to medications is very low, SCARs can result in disability or even death if they are not diagnosed and treated properly. As the rapid recognition of SCARs is essential, it is necessary to develop [...] Read more.
Although the incidence of severe cutaneous adverse reactions (SCARs) to medications is very low, SCARs can result in disability or even death if they are not diagnosed and treated properly. As the rapid recognition of SCARs is essential, it is necessary to develop diagnostic markers for them that can also be used to assess severity and predict outcomes in the early phase. In addition, it is important to identify novel therapeutic targets for SCARs. Chemokines are chemotactic cytokines that control the migratory patterns and locations of immune cells and usually exhibit markedly specific associations with certain human diseases. In Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN), the Th1-associated chemokines chemokine (C-X-C motif) ligand 9 (CXCL9) and CXCL10 predominate, while in drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS), the levels of the Th2-associated chemokines chemokine (C-C motif) ligand 17 (CCL17) and CCL22 are markedly elevated. We suggest that the distinct chemokine profiles of SJS/TEN and DIHS/DRESS can be used to aid their differential diagnosis. CXCL10 has also been reported to be associated with the development of long-term sequelae in DIHS/DRESS. This review focuses on the chemokines involved in the pathogenesis and adjuvant diagnosis of SCARs, particularly SJS/TEN and DIHS/DRESS, but also provides a brief overview of SCARs and the chemokine superfamily. As it is being increasingly recognized that an association exists between human herpesvirus 6 (HHV-6) and DIHS/DRESS, the possible roles of the chemokine/chemokine receptor homologs encoded by HHV-6 in the pathogenesis of DIHS/DRESS are also discussed. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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21 pages, 799 KiB  
Review
Cytokines and Chemokines in SARS-CoV-2 Infections—Therapeutic Strategies Targeting Cytokine Storm
by Alexandra Pum, Maria Ennemoser, Tiziana Adage and Andreas J. Kungl
Biomolecules 2021, 11(1), 91; https://doi.org/10.3390/biom11010091 - 12 Jan 2021
Cited by 65 | Viewed by 5924
Abstract
The recently identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, the cause of coronavirus disease (COVID-19) and the associated ongoing pandemic, frequently leads to severe respiratory distress syndrome and pneumonia with fatal consequences. Although several factors of this infection and its consequences [...] Read more.
The recently identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, the cause of coronavirus disease (COVID-19) and the associated ongoing pandemic, frequently leads to severe respiratory distress syndrome and pneumonia with fatal consequences. Although several factors of this infection and its consequences are not completely clear, the presence and involvement of specific chemokines is undoubtedly crucial for the development and progression of COVID-19. Cytokine storm and the often-resulting cytokine release syndrome (CRS) are pathophysiological hallmarks in COVID-19 infections related to its most severe and fatal cases. In this hyperinflammatory event, chemokines and other cytokines are highly upregulated and are therefore not fulfilling their beneficial function in the host response anymore but causing harmful effects. Here, we present the recent views on the involvement of chemokines and selected cytokines in COVID-19 and the therapeutics currently in clinical development targeting or interfering with them, discussing their potentials in the treatment of COVID-19 infections. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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17 pages, 919 KiB  
Review
Beta-Arrestins and Receptor Signaling in the Vascular Endothelium
by Claudia Lee, Gayathri Viswanathan, Issac Choi, Chanpreet Jassal, Taylor Kohlmann and Sudarshan Rajagopal
Biomolecules 2021, 11(1), 9; https://doi.org/10.3390/biom11010009 - 23 Dec 2020
Cited by 8 | Viewed by 4871
Abstract
The vascular endothelium is the innermost layer of blood vessels and is a key regulator of vascular tone. Endothelial function is controlled by receptor signaling through G protein-coupled receptors, receptor tyrosine kinases and receptor serine-threonine kinases. The β-arrestins, multifunctional adapter proteins, have the [...] Read more.
The vascular endothelium is the innermost layer of blood vessels and is a key regulator of vascular tone. Endothelial function is controlled by receptor signaling through G protein-coupled receptors, receptor tyrosine kinases and receptor serine-threonine kinases. The β-arrestins, multifunctional adapter proteins, have the potential to regulate all of these receptor families, although it is unclear as to whether they serve to integrate signaling across all of these different axes. Notably, the β-arrestins have been shown to regulate signaling by a number of receptors important in endothelial function, such as chemokine receptors and receptors for vasoactive substances such as angiotensin II, endothelin-1 and prostaglandins. β-arrestin-mediated signaling pathways have been shown to play central roles in pathways that control vasodilation, cell proliferation, migration, and immune function. At this time, the physiological impact of this signaling has not been studied in detail, but a deeper understanding of it could lead to the development of novel therapies for the treatment of vascular disease. Full article
(This article belongs to the Special Issue Chemokines in Infectious and Non-infectious Diseases)
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