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Stress, Immunity, and Tissue Microenvironment
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Stress, Immunity, and Tissue Microenvironment

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 July 2022) | Viewed by 16354

Special Issue Editors

Prof. Dr. Massimo Conese

E-Mail Website
Collection Editor
Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Interests: nose-to-brain delivery; applications of nanoparticles to drug delivery; Parkinson’s disease; mucopenetration; mesenchymal stem cells; exosomes; airway diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Arcangelo Liso

E-Mail Website
Collection Editor
Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy
Interests: immunity; cancer; inflammation; autoimmune diseases; infertility; infections
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The inflammatory response is activated by a complex network of exogenous and endogenous warning signals that bring about either repair and homeostasis or disease. The tissue microenvironment is essential in dictating these alternative responses by engendering cellular pathways of stress, such as those related to the endoplasmic reticulum and the mitochondria. The hyperthermic response (i.e., fever) seems to be the link among different cell types and molecular stressors, indicating that other inflammation-related events might be responsible for alterations in the microenvironment. This topic collection aims to unveil the composite roles of molecular stress responses in cancer, chronic inflammatory, and autoimmune diseases. It is undoubtful that an in-depth knowledge of these pathways will indicate how to bring forth both novel biomarkers and therapeutic approaches for these important diseases.

Assoc. Prof. Massimo Conese
Prof. Dr. Arcangelo Liso
Collection 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.

Related Special Issue

Published Papers (5 papers)

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Research

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15 pages, 1614 KiB  
Article
Identification of Ovine Serum miRNAs Following Bacterial Lipopolysaccharide Challenge
by Ankita Sharma, Umesh K. Shandilya, Tianna Sullivan, Danielle Naylor, Angela Canovas, Bonnie A. Mallard and Niel A. Karrow
Int. J. Mol. Sci. 2020, 21(21), 7920; https://doi.org/10.3390/ijms21217920 - 25 Oct 2020
Cited by 12 | Viewed by 2315
Abstract
Host–pathogen interactions are complex and influenced by host genetic and epigenetic modifications. Recently, the significance of microRNAs (miRNAs) in pathogenic infection and the regulation of immune response has been highlighted. However, information on miRNAs’ role in the course of inflammation is still very [...] Read more.
Host–pathogen interactions are complex and influenced by host genetic and epigenetic modifications. Recently, the significance of microRNAs (miRNAs) in pathogenic infection and the regulation of immune response has been highlighted. However, information on miRNAs’ role in the course of inflammation is still very limited in small ruminants. The present study was intended to identify changes in the expression of circulatory miRNAs post-lipopolysaccharide (LPS)-challenge. In this study, young ewes (n = 18) were challenged with Escherichia coli LPS (400 ng/kg i.v.) and blood samples were collected for serum miRNA isolation at two-time points; prior to challenge (T0), and 4 h (T4) post-challenge, reflecting the peak cortisol response. A total of 91 miRNAs were profiled, including 84 miRNAs on a commercial ovine miRNA-PCR array, and seven individual miRNAs. Forty five miRNAs were differentially expressed (DE) with 35 being up-regulated (Fold regulation, FR > 2) and 10 being down-regulated (FR < 1, p < 0.05) at T4. Among the up-regulated miRNAs, 14 were significantly (p < 0.05) induced, including oar-miRs: 369-3p, 495-3p, 376a-3p, 543-3p, 668-3p, 329a-3p, 655-3p, 411a-5p, and 154a-3p, which were located on ovine chromosome 18 forming four miRNA clusters within 10 kb. The elevated miRNAs belonged to different functional classes, playing roles in activating the hypothalamic-pituitary-adrenal axis; increasing cell survival and differentiation; and inducing inflammatory responses and targeted PI3K-Akt and MAPK signaling and chemokine signaling pathways. In summary, these results reveal the dynamic nature of ovine serum miRNAs during LPS-induced stress and highlight the potential role of identified miRNA-clusters on chromosome 18 to understand the regulation of the acute-phase response. Some of these identified circulating miRNAs may also serve as stress biomarkers for livestock in the future. Full article
(This article belongs to the Special Issue Stress, Immunity, and Tissue Microenvironment)
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10 pages, 953 KiB  
Communication
Insulin-Like Growth Factor Binding Protein 6 Is Secreted in Extracellular Vesicles upon Hyperthermia and Oxidative Stress in Dendritic Cells But Not in Monocytes
by Massimo Conese, Lorenzo Pace, Nicoletta Pignataro, Lucia Catucci, Antonio Ambrosi, Sante Di Gioia, Nicola Tartaglia and Arcangelo Liso
Int. J. Mol. Sci. 2020, 21(12), 4428; https://doi.org/10.3390/ijms21124428 - 22 Jun 2020
Cited by 7 | Viewed by 2168
Abstract
Recently, insulin-like growth factor binding protein 6 (IGFBP-6) has been shown to play a putative role in the immune system, as monocyte-derived dendritic cells (Mo-DCs) are stimulated by hyperthermia to express IGFBP-6 at both the mRNA and protein levels. However, the presence of [...] Read more.
Recently, insulin-like growth factor binding protein 6 (IGFBP-6) has been shown to play a putative role in the immune system, as monocyte-derived dendritic cells (Mo-DCs) are stimulated by hyperthermia to express IGFBP-6 at both the mRNA and protein levels. However, the presence of IGFBP-6 in extracellular vesicles (EVs) and whether other pro-inflammatory stimuli can induce IGFBP-6 expression in Mo-DCs are not known yet. In this brief report, we show that hyperthermia (39 °C) induces IGFBP-6 secretion associated with microvesicles and exosomes as early as 3 h. Moreover, free IGFBP-6 is found in conditioned media (CM) of hyperthermia- and H2O2-treated Mo-DCs, but not in CM obtained from monocytes similarly treated. These results show that diverse inflammatory stimuli can induce IGFBP-6 association with EVs and secretion in conditioned medium, indicating a role for IGFBP-6 in communication between immune cells. Full article
(This article belongs to the Special Issue Stress, Immunity, and Tissue Microenvironment)
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16 pages, 2449 KiB  
Article
The Heat Shock Protein HSP70 Promotes Th17 Genes’ Expression via Specific Regulation of microRNA
by Hanna Cwiklinska, Maria Cichalewska-Studzinska, Krzysztof W. Selmaj and Marcin P. Mycko
Int. J. Mol. Sci. 2020, 21(8), 2823; https://doi.org/10.3390/ijms21082823 - 17 Apr 2020
Cited by 8 | Viewed by 2967
Abstract
T helper cells type 17 (Th17) are orchestrators of autoimmune conditions, including multiple sclerosis (MS), but mechanisms of Th17 pathogenicity remain unknown. MicroRNAs (miRNA) are known to control T cells. To understand the function of miRNA in Th17, we have established a T [...] Read more.
T helper cells type 17 (Th17) are orchestrators of autoimmune conditions, including multiple sclerosis (MS), but mechanisms of Th17 pathogenicity remain unknown. MicroRNAs (miRNA) are known to control T cells. To understand the function of miRNA in Th17, we have established a T cell line, EL4-TCR+, that resembles the expression pattern of the Th17 cells. Subsequently, we have evaluated the crosstalk between miRNA and Th17 genes’ expression using a combination of gene expression profiling, gene expression manipulation, RNA and protein immunoprecipitation, as well as confocal microscopy. We have found that Th17-related miRNA were strongly expressed in EL4-TCR+ cells following the binding of the cluster of differentiation 3 (CD3) component of the T cell receptor (TCR). Furthermore, a specific inhibition of these miRNA resulted in downregulation of the critical Th17 genes’ expression. Surprisingly, this mechanism relied on the function of the stress signal regulator heat shock protein 70 (HSP70). Upon activation, HSP70 co-localized intracellularly with miRNA processing proteins. Precipitation of HSP70 resulted in enrichment of the Th17-associated miRNA. Finally, HSP70 inhibition led to downregulation of the Th17 genes’ expression and ameliorated development of autoimmune demyelination. Our study demonstrated that HSP70 facilitates specific miRNA function leading to Th17 genes’ expression, a mechanism linking stress and autoimmunity. Full article
(This article belongs to the Special Issue Stress, Immunity, and Tissue Microenvironment)
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20 pages, 4214 KiB  
Article
Proregenerative Activity of IL-33 in Gastric Tissue Cells Undergoing Helicobacter Pylori-Induced Apoptosis
by Weronika Gonciarz, Agnieszka Krupa and Magdalena Chmiela
Int. J. Mol. Sci. 2020, 21(5), 1801; https://doi.org/10.3390/ijms21051801 - 05 Mar 2020
Cited by 14 | Viewed by 2978
Abstract
Interleukin (IL)-33 is a proinflammatory mediator that alerts the host immune system to disorders in tissue homeostasis. Aim. To understand the role of IL-33 in modulating gastric tissue cell growth affected by Helicobacter pylori (H. pylori). Methods. IL-33 production in guinea pigs [...] Read more.
Interleukin (IL)-33 is a proinflammatory mediator that alerts the host immune system to disorders in tissue homeostasis. Aim. To understand the role of IL-33 in modulating gastric tissue cell growth affected by Helicobacter pylori (H. pylori). Methods. IL-33 production in guinea pigs (Caviae porcellus) experimentally infected with H. pylori was evaluated by ELISA or immunohistochemical staining. The proregenerative activity of IL-33 was evaluated using gastric epithelial cells and fibroblasts that were naive or transfected with IL-33 siRNA exposed to H. pylori glycine acid extract antigenic complex (GE), as well as by measuring cell migration, proliferation, metabolic activity and apoptosis. Animals infected by H. pylori responded with increased production of IL-33. Also, cells treated in vitro with GE released more IL-33 than cells that were unstimulated. Silencing IL-33 in cells resulted in downregulation of metabolic activity, adhesion, migration and proliferation, especially after treatment with H. pylori GE, as well as upregulation of cells apoptosis associated with caspase 3 increase and Bcl-xL decrease, suggesting proregenerative activity of IL-33. Interestingly, upregulation of cell proliferation by IL-33 was Erk independent. Our results indicate that IL-33 may protect gastric tissue from loss of homeostasis caused by deleterious effects of H. pylori components and the inflammatory response developed during infection. Full article
(This article belongs to the Special Issue Stress, Immunity, and Tissue Microenvironment)
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Review

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11 pages, 1999 KiB  
Review
Proteasome Inhibitors as a Possible Therapy for SARS-CoV-2
by Lucia Longhitano, Daniele Tibullo, Cesarina Giallongo, Giacomo Lazzarino, Nicola Tartaglia, Sara Galimberti, Giovanni Li Volti, Giuseppe Alberto Palumbo and Arcangelo Liso
Int. J. Mol. Sci. 2020, 21(10), 3622; https://doi.org/10.3390/ijms21103622 - 20 May 2020
Cited by 42 | Viewed by 5118
Abstract
The COVID-19 global pandemic is caused by SARS-CoV-2, and represents an urgent medical and social issue. Unfortunately, there is still not a single proven effective drug available, and therefore, current therapeutic guidelines recommend supportive care including oxygen administration and treatment with antibiotics. Recently, [...] Read more.
The COVID-19 global pandemic is caused by SARS-CoV-2, and represents an urgent medical and social issue. Unfortunately, there is still not a single proven effective drug available, and therefore, current therapeutic guidelines recommend supportive care including oxygen administration and treatment with antibiotics. Recently, patients have been also treated with off-label therapies which comprise antiretrovirals, anti-inflammatory compounds, antiparasitic agents and plasma from convalescent patients, all with controversial results. The ubiquitin–proteasome system (UPS) is important for the maintenance of cellular homeostasis, and plays a pivotal role in viral replication processes. In this review, we discuss several aspects of the UPS and the effects of its inhibition with particular regard to the life cycle of the coronaviruses (CoVs). In fact, proteasome inhibition by various chemical compounds, such as MG132, epoxomycin and bortezomib, may reduce the virus entry into the eucariotic cell, the synthesis of RNA, and the subsequent protein expression necessary for CoVs. Importantly, since UPS inhibitors reduce the cytokine storm associated with various inflammatory conditions, it is reasonable to assume that they might be repurposed for SARS-CoV-2, thus providing an additional tool to counteract both virus replication as well as its most deleterious consequences triggered by abnormal immunological response. Full article
(This article belongs to the Special Issue Stress, Immunity, and Tissue Microenvironment)
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