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Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer

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

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 74377

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Prof. Dr. János G. Filep

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Maisonneuve-Rosemont Hospital, Department of Pathology and Cell Biology, University of Montreal, Montreal, QC H1T 2M4, Canada
Interests: innate immunity; inflammation/resolution of inflammation; acute-phase proteins; leukocyte biology; cardiovascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute inflammation is a protective mechanism to eliminate invading pathogens. It should ideally be localized and self-limited and lead to complete resolution. Inflammation is also an important pathophysiological component of most chronic diseases, including cardiovascular, pulmonary, and immune diseases, diabetes, and cancer. Since the inflammatory response is critical for survival, the current anti-inflammatory therapies have limitations and often do not lead to repair of affected tissues. Hence, there is need for a fresh approach. While the recruitment and functions of innate immune cells have received considerable attention, accumulating data challenge many of our current concepts. Thus, identifying macrophage and neutrophil heterogeneity, characterization of novel mechanisms (for example, NETosis, swarming, reverse migration, transcriptional burst, efferocytosis), and recognition of resolution as an active process with synthesis of specialized pro-resolving mediators shed new light on the roles of leukocyte subsets in acute and chronic inflammatory conditions. Emerging topics include but are not limited to microbiota regulation of leukocyte maturation, neutrophil regulation of adaptive immunity, systemic autoimmune diseases, and cancer. This Special Issue aims to provide an overview of recent advances in these areas, with an emphasis on new avenues for therapeutic interventions.

Prof. János G. Filep
Guest Editor

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Keywords

Neutrophil heterogeneity
Macrophage subsets
Myeloid-derived suppressor cells
Inflammation, adaptive immunity
Cardiovascular diseases
Autoimmune diseases
Cancer

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Related Special Issue

Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer—Series 2 in Cells (4 articles)

Published Papers (12 papers)

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Editorial

Jump to: Research, Review

5 pages, 227 KiB

Open AccessEditorial

Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer

by János G. Filep

Cells 2021, 10(7), 1735; https://doi.org/10.3390/cells10071735 - 9 Jul 2021

Cited by 4 | Viewed by 2217

Abstract

Inflammation is a double-edged sword [...] Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

Research

Jump to: Editorial, Review

14 pages, 8357 KiB

Open AccessArticle

Role of Annexin A1 in NLRP3 Inflammasome Activation in Murine Neutrophils

by José Marcos Sanches, Rebeca D. Correia-Silva, Gustavo H. B. Duarte, Anna Maria A. P. Fernandes, Salvador Sánchez-Vinces, Patrícia O. Carvalho, Sonia M. Oliani, Karina R. Bortoluci, Vanessa Moreira and Cristiane D. Gil

Cells 2021, 10(1), 121; https://doi.org/10.3390/cells10010121 - 11 Jan 2021

Cited by 11 | Viewed by 3853

Abstract

This study evaluated the role of endogenous and exogenous annexin A1 (AnxA1) in the activation of the NLRP3 inflammasome in isolated peritoneal neutrophils. C57BL/6 wild-type (WT) and AnxA1 knockout mice (AnxA1^-/-) received 0.3% carrageenan intraperitoneally and, after 3 h, the peritoneal exudate was collected. WT and AnxA1^-/- neutrophils were then stimulated with lipopolysaccharide, followed by the NLRP3 agonists nigericin or ATP. To determine the exogenous effect of AnxA1, the neutrophils were pretreated with the AnxA1-derived peptide Ac_2-26 followed by the NLRP3 agonists. Ac_2-26 administration reduced NLRP3-derived IL-1β production by WT neutrophils after nigericin and ATP stimulation. However, IL-1β release was impaired in AnxA1^-/- neutrophils stimulated by both agonists, and there was no further impairment in IL-1β release with Ac_2-26 treatment before stimulation. Despite this, ATP- and nigericin-stimulated AnxA1^-/- neutrophils had increased levels of cleaved caspase-1. The lipidomics of supernatants from nigericin-stimulated WT and AnxA1^-/- neutrophils showed potential lipid biomarkers of cell stress and activation, including specific sphingolipids and glycerophospholipids. AnxA1 peptidomimetic treatment also increased the concentration of phosphatidylserines and oxidized phosphocholines, which are lipid biomarkers related to the inflammatory resolution pathway. Together, our results indicate that exogenous AnxA1 negatively regulates NLRP3-derived IL-1β production by neutrophils, while endogenous AnxA1 is required for the activation of the NLRP3 machinery. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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23 pages, 3298 KiB

Open AccessArticle

Infection and Activation of B Cells by Theiler’s Murine Encephalomyelitis Virus (TMEV) Leads to Autoantibody Production in an Infectious Model of Multiple Sclerosis

by Young-Hee Jin, Charles X. Kim, Jocelin Huang and Byung S. Kim

Cells 2020, 9(8), 1787; https://doi.org/10.3390/cells9081787 - 27 Jul 2020

Cited by 10 | Viewed by 3601

Abstract

Theiler’s murine encephalomyelitis virus (TMEV) induces immune-mediated inflammatory demyelinating disease in susceptible mice that is similar to human multiple sclerosis (MS). In light of anti-CD20 therapies for MS, the susceptibility of B cells to TMEV infection is particularly important. In our study, direct viral exposure to macrophages and lymphocytes resulted in viral replication and cellular stimulation in the order of DCs, macrophages, B cells, and T cells. Notably, B cells produced viral proteins and expressed elevated levels of CD69, an activation marker. Similarly, the expression of major histocompatibility complex class II and costimulatory molecules in B cells was upregulated. Moreover, TMEV-infected B cells showed elevated levels of antigen-presenting function and antibody production. TMEV infection appeared to polyclonally activate B cells to produce autoantibodies and further T cell stimulation. Thus, the viral infection might potentially affect the outcome of autoimmune diseases, and/or the development of other chronic infections, including the protection and/or pathogenesis of TMEV-induced demyelinating disease. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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21 pages, 6259 KiB

Open AccessArticle

RELMα Is Induced in Airway Epithelial Cells by Oncostatin M without Requirement of STAT6 or IL-6 in Mouse Lungs In Vivo

by Lilian Ho, Ashley Yip, Francis Lao, Fernando Botelho and Carl D. Richards

Cells 2020, 9(6), 1338; https://doi.org/10.3390/cells9061338 - 27 May 2020

Cited by 8 | Viewed by 4418

Abstract

Resistin-like molecule alpha (RELMα) and YM-1 are secreted proteins implicated in murine models of alternatively activated macrophage (AA/M2) accumulation and Th2-skewed inflammation. Since the gp130 cytokine Oncostatin M (OSM) induces a Th2-like cytokine and AA/M2 skewed inflammation in mouse lung, we here investigated regulation of RELMα and YM-1. Transient pulmonary overexpression of OSM by Adenovirus vector (AdOSM) markedly induced RELMα and YM-1 protein expression in total lung. In situ hybridization showed that RELMα mRNA was highly induced in airway epithelial cells (AEC) and was co-expressed with CD68 mRNA in some but not all CD68+ cells in parenchyma. IL-6 overexpression (a comparator gp130 cytokine) induced RELMα, but at significantly lower levels. IL-6 (assessing IL-6^−/− mice) was not required, nor was STAT6 (IL-4/13 canonical signalling) for AdOSM-induction of RELMα in AEC. AEC responded directly to OSM in vitro as assessed by pSTAT3 activation. RELMα-deficient mice showed similar inflammatory cell infiltration and cytokine responses to wt in response to AdOSM, but showed less accumulation of CD206+ AA/M2 macrophages, reduced induction of extracellular matrix gene mRNAs for COL1A1, COL3A1, MMP13, and TIMP1, and reduced parenchymal alpha smooth muscle actin. Thus, RELMα is regulated by OSM in AEC and contributes to extracellular matrix remodelling in mouse lung. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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20 pages, 2856 KiB

Open AccessEditor’s ChoiceArticle

Lung Tumor Cell-Derived Exosomes Promote M2 Macrophage Polarization

by Alexandra Pritchard, Sultan Tousif, Yong Wang, Kenneth Hough, Saad Khan, John Strenkowski, Balu K. Chacko, Victor M. Darley-Usmar and Jessy S. Deshane

Cells 2020, 9(5), 1303; https://doi.org/10.3390/cells9051303 - 24 May 2020

Cited by 138 | Viewed by 10768

Abstract

Cellular cross-talk within the tumor microenvironment (TME) by exosomes is known to promote tumor progression. Tumor promoting macrophages with an M2 phenotype are suppressors of anti-tumor immunity. However, the impact of tumor-derived exosomes in modulating macrophage polarization in the lung TME is largely unknown. Herein, we investigated if lung tumor-derived exosomes alter transcriptional and bioenergetic signatures of M0 macrophages and polarize them to an M2 phenotype. The concentration of exosomes produced by p53 null H358 lung tumor cells was significantly reduced compared to A549 (p53 wild-type) lung tumor cells, consistent with p53-mediated regulation of exosome production. In co-culture studies, M0 macrophages internalized tumor-derived exosomes, and differentiated into M2 phenotype. Importantly, we demonstrate that tumor-derived exosomes enhance the oxygen consumption rate of macrophages, altering their bioenergetic state consistent with that of M2 macrophages. In vitro co-cultures of M0 macrophages with H358 exosomes demonstrated that exosome-induced M2 polarization may be p53 independent. Murine bone marrow cells and bone marrow-derived myeloid-derived suppressor cells (MDSCs) co-cultured with lewis lung carcinoma (LLC)-derived exosomes differentiated to M2 macrophages. Collectively, these studies provide evidence for a novel role for lung tumor-exosomes in M2 macrophage polarization, which then offers new therapeutic targets for immunotherapy of lung cancer. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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Review

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21 pages, 1510 KiB

Open AccessFeature PaperReview

Cardiac Dysfunction in Rheumatoid Arthritis: The Role of Inflammation

by Jianmin Chen, Lucy V. Norling and Dianne Cooper

Cells 2021, 10(4), 881; https://doi.org/10.3390/cells10040881 - 13 Apr 2021

Cited by 38 | Viewed by 8161

Abstract

Rheumatoid arthritis is a chronic, systemic inflammatory disease that carries an increased risk of mortality due to cardiovascular disease. The link between inflammation and atherosclerotic disease is clear; however, recent evidence suggests that inflammation may also play a role in the development of nonischemic heart disease in rheumatoid arthritis (RA) patients. We consider here the link between inflammation and cardiovascular disease in the RA community with a focus on heart failure with preserved ejection fraction. The effect of current anti-inflammatory therapeutics, used to treat RA patients, on cardiovascular disease are discussed as well as whether targeting resolution of inflammation might offer an alternative strategy for tempering inflammation and subsequent inflammation-driven comorbidities in RA. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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17 pages, 1163 KiB

Open AccessReview

Epithelial Cells and Inflammation in Pulmonary Wound Repair

by Amanda Croasdell Lucchini, Naomi N. Gachanja, Adriano G. Rossi, David A. Dorward and Christopher D. Lucas

Cells 2021, 10(2), 339; https://doi.org/10.3390/cells10020339 - 5 Feb 2021

Cited by 39 | Viewed by 7065

Abstract

Respiratory diseases are frequently characterised by epithelial injury, airway inflammation, defective tissue repair, and airway remodelling. This may occur in a subacute or chronic context, such as asthma and chronic obstructive pulmonary disease, or occur acutely as in pathogen challenge and acute respiratory distress syndrome (ARDS). Despite the frequent challenge of lung homeostasis, not all pulmonary insults lead to disease. Traditionally thought of as a quiescent organ, emerging evidence highlights that the lung has significant capacity to respond to injury by repairing and replacing damaged cells. This occurs with the appropriate and timely resolution of inflammation and concurrent initiation of tissue repair programmes. Airway epithelial cells are key effectors in lung homeostasis and host defence; continual exposure to pathogens, toxins, and particulate matter challenge homeostasis, requiring robust defence and repair mechanisms. As such, the epithelium is critically involved in the return to homeostasis, orchestrating the resolution of inflammation and initiating tissue repair. This review examines the pivotal role of pulmonary airway epithelial cells in initiating and moderating tissue repair and restitution. We discuss emerging evidence of the interactions between airway epithelial cells and candidate stem or progenitor cells to initiate tissue repair as well as with cells of the innate and adaptive immune systems in driving successful tissue regeneration. Understanding the mechanisms of intercellular communication is rapidly increasing, and a major focus of this review includes the various mediators involved, including growth factors, extracellular vesicles, soluble lipid mediators, cytokines, and chemokines. Understanding these areas will ultimately identify potential cells, mediators, and interactions for therapeutic targeting. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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27 pages, 1636 KiB

Open AccessFeature PaperReview

The Functional Heterogeneity of Neutrophil-Derived Extracellular Vesicles Reflects the Status of the Parent Cell

by Ferenc Kolonics, Viktória Szeifert, Csaba I. Timár, Erzsébet Ligeti and Ákos M. Lőrincz

Cells 2020, 9(12), 2718; https://doi.org/10.3390/cells9122718 - 18 Dec 2020

Cited by 51 | Viewed by 5279

Abstract

Similar to other cell types, neutrophilic granulocytes also release extracellular vesicles (EVs), mainly medium-sized microvesicles/microparticles. According to published data, authors have reached a consensus on the physical parameters (size, density) and chemical composition (surface proteins, proteomics) of neutrophil-derived EVs. In contrast, there is large diversity and even controversy in the reported functional properties. Part of the discrepancy may be ascribed to differences in the viability of the starting cells, in eliciting factors, in separation techniques and in storage conditions. However, the most recent data from our laboratory prove that the same population of neutrophils is able to generate EVs with different functional properties, transmitting pro-inflammatory or anti-inflammatory effects on neighboring cells. Previously we have shown that Mac-1 integrin is a key factor that switches anti-inflammatory EV generation into pro-inflammatory and antibacterial EV production. This paper reviews current knowledge on the functional alterations initiated by neutrophil-derived EVs, listing their effects according to the triggering agents and target cells. We summarize the presence of neutrophil-derived EVs in pathological processes and their perspectives in diagnostics and therapy. Finally, the functional heterogeneity of differently triggered EVs indicates that neutrophils are capable of producing a broad spectrum of EVs, depending on the environmental conditions prevailing at the time of EV genesis. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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18 pages, 1144 KiB

Open AccessReview

Leukocytes, Systemic Inflammation and Immunopathology in Acute-on-Chronic Liver Failure

by Mireia Casulleras, Ingrid W. Zhang, Cristina López-Vicario and Joan Clària

Cells 2020, 9(12), 2632; https://doi.org/10.3390/cells9122632 - 8 Dec 2020

Cited by 82 | Viewed by 7450

Abstract

Acute-on-chronic liver failure (ACLF) is a complex syndrome that develops in patients with cirrhosis and is characterized by acute decompensation, organ failure(s) and high short-term mortality. ACLF frequently occurs in close temporal relationship to a precipitating event, such as acute alcoholic, drug-induced or viral hepatitis or bacterial infection and, in cases without precipitating events, probably related to intestinal translocation of bacterial products. Dysbalanced immune function is central to its pathogenesis and outcome with an initial excessive systemic inflammatory response that drives organ failure and mortality. This hyperinflammatory state ultimately impairs the host defensive mechanisms of immune cells, rendering ACLF patients immunocompromised and more vulnerable to secondary infections, and therefore to higher organ dysfunction and mortality. In this review, we describe the prevailing characteristics of the hyperinflammatory state in patients with acutely decompensated cirrhosis developing ACLF, with special emphasis on cells of the innate immune system (i.e., monocytes and neutrophils), their triggers (pathogen- and damage-associated molecular patterns [PAMPs and DAMPs]), their effector molecules (cytokines, chemokines, growth factors and bioactive lipid mediators) and the consequences on tissue immunopathology. In addition, this review includes a chapter discussing new emerging therapies based on the modulation of leukocyte function by the administration of pleiotropic proteins such as albumin, Toll-like receptor 4 antagonists, interleukin-22 or stem cell therapy. Finally, the importance of finding an appropriate intervention that reduces inflammation without inducing immunosuppression is highlighted as one of the main therapeutic challenges in cirrhosis. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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20 pages, 1576 KiB

Open AccessReview

Gene Expression Comparison between Sézary Syndrome and Lymphocytic-Variant Hypereosinophilic Syndrome Refines Biomarkers for Sézary Syndrome

by Andrea Moerman-Herzog, Syed J. Mehdi and Henry K. Wong

Cells 2020, 9(9), 1992; https://doi.org/10.3390/cells9091992 - 29 Aug 2020

Cited by 8 | Viewed by 3560

Abstract

Sézary syndrome (SS), an aggressive cutaneous T-cell lymphoma (CTCL) with poor prognosis, is characterized by the clinical hallmarks of circulating malignant T cells, erythroderma and lymphadenopathy. However, highly variable clinical skin manifestations and similarities with benign mimickers can lead to significant diagnostic delay and inappropriate therapy that can lead to disease progression and mortality. SS has been the focus of numerous transcriptomic-profiling studies to identify sensitive and specific diagnostic and prognostic biomarkers. Benign inflammatory disease controls (e.g., psoriasis, atopic dermatitis) have served to identify chronic inflammatory phenotypes in gene expression profiles, but provide limited insight into the lymphoproliferative and oncogenic roles of abnormal gene expression in SS. This perspective was recently clarified by a transcriptome meta-analysis comparing SS and lymphocytic-variant hypereosinophilic syndrome, a benign yet often clonal T-cell lymphoproliferation, with clinical features similar to SS. Here we review the rationale for selecting lymphocytic-variant hypereosinophilic syndrome (L-HES) as a disease control for SS, and discuss differentially expressed genes that may distinguish benign from malignant lymphoproliferative phenotypes, including additional context from prior gene expression studies to improve understanding of genes important in SS. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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13 pages, 2163 KiB

Open AccessReview

The NLRP3 Inflammasome Role in the Pathogenesis of Pregnancy Induced Hypertension and Preeclampsia

by Maciej W. Socha, Bartosz Malinowski, Oskar Puk, Mariusz Dubiel and Michał Wiciński

Cells 2020, 9(7), 1642; https://doi.org/10.3390/cells9071642 - 8 Jul 2020

Cited by 44 | Viewed by 9043

Abstract

Pregnancy-induced hypertension and preeclampsia are associated with significant maternal and fetal mortality. A better understanding of these diseases, delineation of molecular pathomechanism, and efficient treatment development are some of the most urgent tasks in obstetrics and gynecology. Recent findings indicate the crucial role of inflammation in the development of hypertension and preeclampsia. Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1β, IL-18, and gasdermin D. Production of these proinflammatory chemokines is the beginning of a local and general inflammation, which results in sympathetic outflow, angiotensin II production, proteinuria, hemolysis, liver damage, immunothrombosis, and coagulopathy. The NLRP3 inflammasome is a critical complex in the mediation of the inflammatory response, which makes it crucial for the development of pregnancy-induced hypertension and preeclampsia, as well as its complications, such as placental abruption and HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Herein, the presented article delineates molecular mechanisms of these processes, indicating directions of future advance. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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19 pages, 292 KiB

Open AccessReview

Macrophage Modification Strategies for Efficient Cell Therapy

by Anastasiya S. Poltavets, Polina A. Vishnyakova, Andrey V. Elchaninov, Gennady T. Sukhikh and Timur Kh. Fatkhudinov

Cells 2020, 9(6), 1535; https://doi.org/10.3390/cells9061535 - 24 Jun 2020

Cited by 80 | Viewed by 7671

Abstract

Macrophages, important cells of innate immunity, are known for their phagocytic activity, capability for antigen presentation, and flexible phenotypes. Macrophages are found in all tissues and therefore represent an attractive therapeutic target for the treatment of diseases of various etiology. Genetic programming of macrophages is an important issue of modern molecular and cellular medicine. The controllable activation of macrophages towards desirable phenotypes in vivo and in vitro will provide effective treatments for a number of inflammatory and proliferative diseases. This review is focused on the methods for specific alteration of gene expression in macrophages, including the controllable promotion of the desired M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes in certain pathologies or model systems. Here we review the strategies of target selection, the methods of vector delivery, and the gene editing approaches used for modification of macrophages. Full article

(This article belongs to the Special Issue Leukocytes in Inflammation, Resolution of Inflammation, Autoimmune Diseases and Cancer)

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