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Cells
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Role of Extracellular Vesicles in Inflammatory Diseases
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Role of Extracellular Vesicles in Inflammatory Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 9448

Special Issue Editors

Dr. Lahiru Gangoda

E-Mail Website
Guest Editor
1. Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia
2. Opthalmology, Department of Surgery, University of Melbourne, Melbourne, VIC, Australia
Interests: cancer; inflammation; cell death; extracellular vesicles
Dr. Ishara Atukorala

E-Mail Website
Guest Editor
1. Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, VIC, Australia
2. Mercy Perinatal, Mercy Hospital for Women, Heidelberg, VIC, Australia
3. Northern Center for Health Education and Research, Epping, VIC, Australia
Interests: reproductive biology; extracellular vesicles; perinatal infections

Special Issue Information

Dear Colleagues,

Over the last two decades, significant progress has been made toward understanding the generation and biological role of cell-derived extracellular vesicles (EVs). EVs are membrane-bound structures that are generated by an evolutionarily conserved process. They are secreted by nearly all cell types and present in all body fluids. EVs are potentially vital contributors to inflammation, which carry autoantigens, danger signals, cytokines, lipid mediators and tissue-degrading enzymes.  Sufficient evidence now exists to indicate that inflammatory diseases could be treated by targeting EV release. Furthermore, EVs evidently have critical roles in the initiation, progression and regulation of inflammatory diseases. This Special Issue aims to address the functions of EVs during inflammation and their potential as biomarkers, drug delivery vehicles and targets in inflammatory disorders.

Dr. Lahiru Gangoda
Dr. Ishara Atukorala
Guest Editors

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Keywords

  • extracellular vesicles (EVs)
  • inflammation
  • biomarkers
  • inflammatory diseases
  • cytokines

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Published Papers (4 papers)

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Research

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14 pages, 2007 KiB  
Article
The Systemic Effect of Ischemia Training and Its Impact on Bone Marrow-Derived Monocytes
by Gustavo Falero-Diaz, Catarina de A. Barboza, Katherine Kaiser, Keri A. Tallman, Christopher Montoya, Shailendra B. Patel, Joshua D. Hutcheson and Roberta M. Lassance-Soares
Cells 2024, 13(19), 1602; https://doi.org/10.3390/cells13191602 - 24 Sep 2024
Viewed by 1393
Abstract
Objective: Monocytes are innate immune cells that play a central role in inflammation, an essential component during neovascularization. Our recent publication demonstrated that ischemia training by 24 h unilateral occlusion of the femoral artery (FA) can modify bone marrow-derived monocytes (BM-Mono), allowing them [...] Read more.
Objective: Monocytes are innate immune cells that play a central role in inflammation, an essential component during neovascularization. Our recent publication demonstrated that ischemia training by 24 h unilateral occlusion of the femoral artery (FA) can modify bone marrow-derived monocytes (BM-Mono), allowing them to improve collateral remodeling in a mouse model of hindlimb ischemia. Here, we expand on our previous findings, investigating a potential systemic effect of ischemia training and how this training can impact BM-Mono. Methods and Results: BM-Mono from mice exposed to ischemia training (24 h) or Sham (same surgical procedure without femoral artery occlusion–ischemia training) procedures were used as donors in adoptive transfer experiments where recipients were subjected to hindlimb ischemia. Donor cells were divided corresponding to the limb from which they were isolated (left—limb previously subjected to 24 h ischemia and right—contralateral limb). Recipients who received 24 h ischemic-trained monocytes isolated from either limb had remarkable blood flow recovery compared to recipients with Sham monocytes (monocytes isolated from Sham group—no ischemia training). Since these data suggested a systemic effect of ischemic training, circulating extracellular vesicles (EVs) were investigated as potential players. EVs were isolated from both groups, 24 h-trained and Sham, and the former showed increased expression of histone deacetylase 1 (HDAC1), which is known to downregulate 24-dehydrocholesterol reductase (Dhcr24) gene expression. Since we previously revealed that ischemia training downregulates Dhcr24 in BM-Mono, we incubated EVs from 24 h-trained and Sham groups with wild-type (WT) BM-Mono and demonstrated that WT BM-Mono incubated with 24 h-trained EVs had lower gene expression of Dhcr24 and an HDAC1 inhibitor blunted this effect. Next, we repeated the adoptive transfer experiment using Dhcr24 KO mice as donors of BM-Mono for WT mice subjected to hindlimb ischemia. Recipients who received Dhcr24 KO BM-Mono had greater limb perfusion than those who received WT BM-Mono. Further, we focused on the 24 h-trained monocytes (which previously showed downregulation of Dhcr24 gene expression and higher desmosterol) to test the expression of a few genes downstream of the desmosterol pathway, confirm the Dhcr24 protein level and assess its differentiation in M2-like macrophage phenotype. We found that 24 h-trained BM-Mono had greater expression of key genes in the desmosterol pathway, such as liver X receptors (LXRs) and ATP-binding cassette transporter (ABCA1), and we confirmed low protein expression of Dhcr24. Further, we demonstrated that ischemic-trained BM-Mono polarized towards an anti-inflammatory M2 macrophage phenotype. Finally, we demonstrated that 24 h-trained monocytes adhere less to endothelial cells, and the same pattern was shown by WT BM-Mono treated with Dhcr24 inhibitor. Conclusions: Ischemia training leads to a systemic effect that, at least in part, involves circulating EVs and potential epigenetic modification in BM-Mono. These ischemic-trained BM-Mono demonstrated an anti-inflammatory phenotype towards M2 macrophage differentiation and less ability to adhere to endothelial cells, which is associated with the downregulation of Dhcr24 in those cells. These data together suggest that Dhcr24 might be an important target within monocytes to improve the outcomes of hindlimb ischemia. Full article
(This article belongs to the Special Issue Role of Extracellular Vesicles in Inflammatory Diseases)
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13 pages, 1865 KiB  
Article
Association between Plasma HLA-DR+ Placental Vesicles and Preeclampsia: A Pilot Longitudinal Cohort Study
by Marianna Onori, Rita Franco, Donatella Lucchetti, Silvio Tartaglia, Silvia Buongiorno, Giuliana Beneduce, Fabio Sannino, Silvia Baroni, Andrea Urbani, Antonio Lanzone, Giovanni Scambia, Nicoletta Di Simone and Chiara Tersigni
Cells 2024, 13(2), 196; https://doi.org/10.3390/cells13020196 - 20 Jan 2024
Cited by 1 | Viewed by 2149
Abstract
(1) Background: Preeclampsia (PE) usually presents with hypertension and proteinuria, related to poor placentation. Reduced maternal–fetal immunological tolerance is a possible trigger of inadequate placentation. Aberrant antigen expression of HLA-DR has been observed in the syncytiotrophoblast of PE patients. In this study, we [...] Read more.
(1) Background: Preeclampsia (PE) usually presents with hypertension and proteinuria, related to poor placentation. Reduced maternal–fetal immunological tolerance is a possible trigger of inadequate placentation. Aberrant antigen expression of HLA-DR has been observed in the syncytiotrophoblast of PE patients. In this study, we analyzed plasma levels of Human Leukocyte Antigen (HLA)-DR+ syncytiotrophoblast-derived extracellular vesicles (STEVs) during the three trimesters of pregnancy in relation to PE onset. (2) Methods: Pregnant women underwent venous blood sampling during the three trimesters. STEVs were collected from plasma via ultracentrifugation (120,000 g) and characterized by Western blot, nanotracking analysis and flow cytometry for the expression of Placental Alkaline Phosphatase (PLAP), a placental-derived marker, and HLA-DR. (3) Results: Out of 107 women recruited, 10 developed PE. STEVs were detected in all three trimesters of pregnancy with a zenith in the second trimester. A significant difference was found between the non-PE and PE groups in terms of plasma levels of HLA-DR+ STEVs during all three trimesters of pregnancy. (4) Conclusions: More research is needed to investigate HLA-DR+ as a potential early marker of PE. Full article
(This article belongs to the Special Issue Role of Extracellular Vesicles in Inflammatory Diseases)
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Review

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18 pages, 2055 KiB  
Review
Inflammation and Exosomes in Fabry Disease Pathogenesis
by Bruna Coelho-Ribeiro, Helena G. Silva, Belém Sampaio-Marques, Alexandra G. Fraga, Olga Azevedo, Jorge Pedrosa and Paula Ludovico
Cells 2024, 13(8), 654; https://doi.org/10.3390/cells13080654 - 9 Apr 2024
Cited by 5 | Viewed by 2735
Abstract
Fabry Disease (FD) is one of the most prevalent lysosomal storage disorders, resulting from mutations in the GLA gene located on the X chromosome. This genetic mutation triggers glo-botriaosylceramide (Gb-3) buildup within lysosomes, ultimately impairing cellular functions. Given the role of lysosomes in [...] Read more.
Fabry Disease (FD) is one of the most prevalent lysosomal storage disorders, resulting from mutations in the GLA gene located on the X chromosome. This genetic mutation triggers glo-botriaosylceramide (Gb-3) buildup within lysosomes, ultimately impairing cellular functions. Given the role of lysosomes in immune cell physiology, FD has been suggested to have a profound impact on immunological responses. During the past years, research has been focusing on this topic, and pooled evidence strengthens the hypothesis that Gb-3 accumulation potentiates the production of pro-inflammatory mediators, revealing the existence of an acute inflammatory process in FD that possibly develops to a chronic state due to stimulus persistency. In parallel, extracellular vesicles (EVs) have gained attention due to their function as intercellular communicators. Considering EVs’ capacity to convey cargo from parent to distant cells, they emerge as potential inflammatory intermediaries capable of transporting cytokines and other immunomodulatory molecules. In this review, we revisit the evidence underlying the association between FD and altered immune responses and explore the potential of EVs to function as inflammatory vehicles. Full article
(This article belongs to the Special Issue Role of Extracellular Vesicles in Inflammatory Diseases)
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37 pages, 4962 KiB  
Review
Beyond Macromolecules: Extracellular Vesicles as Regulators of Inflammatory Diseases
by Kaushik Das, Subhojit Paul, Tanmoy Mukherjee, Arnab Ghosh, Anshul Sharma, Prem Shankar, Saurabh Gupta, Shiva Keshava and Deepak Parashar
Cells 2023, 12(15), 1963; https://doi.org/10.3390/cells12151963 - 29 Jul 2023
Cited by 14 | Viewed by 2389
Abstract
Inflammation is the defense mechanism of the immune system against harmful stimuli such as pathogens, toxic compounds, damaged cells, radiation, etc., and is characterized by tissue redness, swelling, heat generation, pain, and loss of tissue functions. Inflammation is essential in the recruitment of [...] Read more.
Inflammation is the defense mechanism of the immune system against harmful stimuli such as pathogens, toxic compounds, damaged cells, radiation, etc., and is characterized by tissue redness, swelling, heat generation, pain, and loss of tissue functions. Inflammation is essential in the recruitment of immune cells at the site of infection, which not only aids in the elimination of the cause, but also initiates the healing process. However, prolonged inflammation often brings about several chronic inflammatory disorders; hence, a balance between the pro- and anti-inflammatory responses is essential in order to eliminate the cause while producing the least damage to the host. A growing body of evidence indicates that extracellular vesicles (EVs) play a major role in cell–cell communication via the transfer of bioactive molecules in the form of proteins, lipids, DNA, RNAs, miRNAs, etc., between the cells. The present review provides a brief classification of the EVs followed by a detailed description of how EVs contribute to the pathogenesis of various inflammation-associated diseases and their implications as a therapeutic measure. The latter part of the review also highlights how EVs act as a bridging entity in blood coagulation disorders and associated inflammation. The findings illustrated in the present review may open a new therapeutic window to target EV-associated inflammatory responses, thereby minimizing the negative outcomes. Full article
(This article belongs to the Special Issue Role of Extracellular Vesicles in Inflammatory Diseases)
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