Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Macrophages, Immunity and Inflammation in Health and Disease

Special Issue Editors
Special Issue Information
Keywords
Published Papers

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 March 2023) | Viewed by 33090

Share This Special Issue

Special Issue Editors

Prof. Dr. Alexander N. Orekhov

E-Mail Website
Guest Editor

1. Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, Russia
2. Laboratory of Infection Pathology and Molecular Microecology, Institute of Human Morphology, 3 Tsyurupa Street, 117418 Moscow, Russia
Interests: atherosclerosis; mitophagy; atherogenicity; autoantibodies; inflammation; innate immunity; cell test; macrophage; membrane transport; modified low density lipoprotein; monocyte; transcriptome; trans-sialydase; enzymatic test; cytokine; epigenetics
Special Issues, Collections and Topics in MDPI journals

Dr. Evgeny E. Bezsonov

E-Mail Website
Guest Editor

1. Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
2. Laboratory of Cellular and Molecular Pathology of Cardiovascular System, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution “Petrovsky National Research Center of Surgery”, 117418 Moscow, Russia
3. Department of Biology and General Genetics, I.M. Sechenov First Moscow State Medical University (Sechenov University), 105043 Moscow, Russia
Interests: atherosclerosis; mitophagy; atherogenicity; atherosclerosis; autoantibodies; inflammation; innate immunity; amyloid
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In this Special Issue, we aim to collect the most recent publications on the mechanisms that macrophages use to regulate homeostasis and their involvement in the pathogenesis of non-infectious diseases. We also welcome research describing novel macrophage markers that reflect their functional state or are involved in macrophage tolerance and training, as well as the interaction of macrophages with resident microbiomes. Having first been described more than 100 years ago, macrophages are still the focus of biomedical research. For about 50 years, they were considered solely part of the defense against pathogens intruding an organism; however, unravelling the mechanisms of inflammatory reaction regulation made it clear that macrophages not only possess effector functions but also act as important regulators of inflammation. A new boost was given to macrophage research in the last decade of the 20th century with the essential study conducted in the lab of Siamon Gordon, which demonstrated alternative macrophage activation. This was a literal milestone in understanding macrophage function. Since that publication, a variety of macrophage markers and functional peculiarities have been described, and it has become clear that in a healthy organism, macrophages actively contribute to homeostasis and regulate processes of tolerance. Another intriguing subject is a complex interaction of tissue macrophages with resident microbiomes. This phenomenon contributes to the normal functioning of the gastrointestinal tract but also plays an important role in other organs. Apart from infectious diseases, it has been demonstrated that macrophages are actively involved in the pathogenesis of socially important non-infectious diseases, such as atherosclerosis, cancer, and diabetes. These findings have, as expected, led to the identification of macrophages as potential and highly attractive therapeutic targets. The adequate resolution of inflammation and normal lipid metabolism are vital for maintaining a healthy body state. It is well-known that chronic inflammation plays an important role in cancer development and the lipid metabolism of metabolic diseases. Thus, this is very important to study these processes, their interaction and their interconnection for the successful diagnosis and treatment of these diseases. In recent years, transcriptomic and bioinformatics analysis have come to the fore as ways to reveal the role of specific genes and signaling pathways in the processes of inflammation and lipid metabolism leading to the development of metabolic diseases. First results of such studies have already demonstrated that both inflammation and lipid metabolism are tightly connected via their molecular pathways. Thus, future meticulous molecular studies of intracellular processes with a bioinformatic approach may give novel insights into the role of inflammation and lipid metabolism in related diseases. Anti-inflammatory therapy with a monoclonal antibody that targets IL-1b (the CANTOS study) possesses significant cardiovascular benefits without affecting lipid levels. These findings have forced us to seriously turn towards anti-inflammatory therapy at the immune level. Current knowledge links lipid-induced activation of the innate and adaptive immunity in the chronic inflammation that explains many mechanisms of atherogenesis, including the role of immune cells, such as macrophages, dendritic cells, and a variety of effector molecules, including cytokines. In recent years, great advances in genetic studies and the accumulating pool of available data have made possible the discovery of molecular mechanisms of a number of chronic human pathologies, investigation of genetic predispositions to various disorders, and identification of numerous potential therapeutic targets. This progress in turn has been followed by a number of preclinical and clinical trials that collect important data on the safety and efficacy of new drugs. Research articles provide numerous examples of successful development and the application of drugs and gene therapies of cardiovascular diseases, cancer, and other human pathologies. Moreover, a significant amount of data is coming from clinical applications and molecular studies of traditional medicines.

Prof. Dr. Alexander N. Orekhov
Dr. Evgeny E. Bezsonov
Guest 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.

Keywords

arterial hypertension
atherogenesis
atherogenic antigens
atherosclerosis
cancer
cardiovascular disease
chronic inflammation
coronary heart disease
dendritic cells
diabetes mellitus
genetic markers
HDL
homeostasis
inflammation
innate and adaptive immunity
LDL
lipid metabolism
lipoprotein metabolism
macrophage training and tolerance
metabolic syndrome
microbiome
mitochondria
neurodegenerative diseases
non-infectious diseases
stroke
tumor-associated macrophages

Published Papers (11 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

23 pages, 4274 KiB

Open AccessArticle

Less Severe Lipopolysaccharide-Induced Inflammation in Conditional mgmt-Deleted Mice with LysM-Cre System: The Loss of DNA Repair in Macrophages

by Wilasinee Saisorn, Pornpimol Phuengmaung, Jiraphorn Issara-Amphorn, Jiradej Makjaroen, Peerapat Visitchanakun, Kritsanawan Sae-khow, Atsadang Boonmee, Salisa Benjaskulluecha, Aleksandra Nita-Lazar, Tanapat Palaga and Asada Leelahavanichkul

Int. J. Mol. Sci. 2023, 24(12), 10139; https://doi.org/10.3390/ijms241210139 - 14 Jun 2023

Cited by 1 | Viewed by 1656

Abstract

Despite the known influence of DNA methylation from lipopolysaccharide (LPS) activation, data on the O6-methylguanine-DNA methyltransferase (MGMT, a DNA suicide repair enzyme) in macrophages is still lacking. The transcriptomic profiling of epigenetic enzymes from wild-type macrophages after single and double LPS stimulation, representing acute inflammation and LPS tolerance, respectively, was performed. Small interfering RNA (siRNA) silencing of mgmt in the macrophage cell line (RAW264.7) and mgmt null (mgmt^flox/flox; LysM-Cre^cre/−) macrophages demonstrated lower secretion of TNF-α and IL-6 and lower expression of pro-inflammatory genes (iNOS and IL-1β) compared with the control. Macrophage injury after a single LPS dose and LPS tolerance was demonstrated by reduced cell viability and increased oxidative stress (dihydroethidium) compared with the activated macrophages from littermate control mice (mgmt^flox/flox; LysM-Cre^−/−). Additionally, a single LPS dose and LPS tolerance also caused mitochondrial toxicity, as indicated by reduced maximal respiratory capacity (extracellular flux analysis) in the macrophages of both mgmt null and control mice. However, LPS upregulated mgmt only in LPS-tolerant macrophages but not after the single LPS stimulation. In mice, the mgmt null group demonstrated lower serum TNF-α, IL-6, and IL-10 than control mice after either single or double LPS stimulation. Suppressed cytokine production resulting from an absence of mgmt in macrophages caused less severe LPS-induced inflammation but might worsen LPS tolerance. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

13 pages, 3069 KiB

Open AccessArticle

Oral Cladribine Impairs Intermediate, but Not Conventional, Monocyte Transmigration in Multiple Sclerosis Patients across a Model Blood-Brain Barrier

by Linda Y. Lin, Pierre Juillard, Simon Hawke, Felix Marsh-Wakefield and Georges E. Grau

Int. J. Mol. Sci. 2023, 24(7), 6487; https://doi.org/10.3390/ijms24076487 - 30 Mar 2023

Cited by 1 | Viewed by 1965

Abstract

Multiple sclerosis (MS) is a disease in which the immune system damages components of the central nervous system (CNS), leading to the destruction of myelin and the formation of demyelinating plaques. This often occurs in episodic “attacks” precipitated by the transmigration of leukocytes across the blood-brain barrier (BBB), and repeated episodes of demyelination lead to substantial losses of axons within and removed from plaques, ultimately leading to progressive neurological dysfunction. Within leukocyte populations, macrophages and T and B lymphocytes are the predominant effectors. Among current immunotherapies, oral cladribine’s impact on lymphocytes is well characterised, but little is known about its impact on other leukocytes such as monocytes and dendritic cells (DCs). The aim of this study was to determine the transmigratory ability of monocyte and DC subsets in healthy subjects and untreated and cladribine-treated relapse-remitting MS (RRMS) patients using a well-characterised model of the BBB. Peripheral blood mononuclear cells from subjects were added to an in vitro transmigration assay to assess cell migration. Our findings show that while prior treatment with oral cladribine inhibits the migration of intermediate monocytes, it has no impact on the transmigration of DC subsets. Overall, our data indicate a previously unrecognised role of cladribine on intermediate monocytes, known to accumulate in the brain active MS lesions. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

22 pages, 21487 KiB

Open AccessArticle

Molecular Profiling of Inflammatory Processes in a Mouse Model of IC/BPS: From the Complete Transcriptome to Major Sex-Related Histological Features of the Urinary Bladder

by Dominika Peskar, Tadeja Kuret, Katja Lakota and Andreja Erman

Int. J. Mol. Sci. 2023, 24(6), 5758; https://doi.org/10.3390/ijms24065758 - 17 Mar 2023

Cited by 1 | Viewed by 1752

Abstract

Animal models are invaluable in the research of the pathophysiology of interstitial cystitis/bladder pain syndrome (IC/BPS), a chronic aseptic urinary bladder disease of unknown etiology that primarily affects women. Here, a mouse model of IC/BPS was induced with multiple low-dose cyclophosphamide (CYP) applications and thoroughly characterized by RNA sequencing, qPCR, Western blot, and immunolabeling to elucidate key inflammatory processes and sex-dependent differences in the bladder inflammatory response. CYP treatment resulted in the upregulation of inflammatory transcripts such as Ccl8, Eda2r, and Vegfd, which are predominantly involved in innate immunity pathways, recapitulating the crucial findings in the bladder transcriptome of IC/BPS patients. The JAK/STAT signaling pathway was analyzed in detail, and the JAK3/STAT3 interaction was found to be most activated in cells of the bladder urothelium and lamina propria. Sex-based data analysis revealed that cell proliferation was more pronounced in male bladders, while innate immunity and tissue remodeling processes were the most distinctive responses of female bladders to CYP treatment. These processes were also reflected in prominent histological changes in the bladder. The study provides an invaluable reference dataset for preclinical research on IC/BPS and an insight into the sex-specific mechanisms involved in the development of IC/BPS pathology, which may explain the more frequent occurrence of this disease in women. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

22 pages, 4538 KiB

Open AccessArticle

Bidirectional Regulation of Sodium Acetate on Macrophage Activity and Its Role in Lipid Metabolism of Hepatocytes

by Weiwei Li, Mingjuan Deng, Jiahui Gong, Yichao Hou and Liang Zhao

Int. J. Mol. Sci. 2023, 24(6), 5536; https://doi.org/10.3390/ijms24065536 - 14 Mar 2023

Cited by 4 | Viewed by 2098

Abstract

Short-chain fatty acids (SCFAs) are important metabolites of the intestinal flora that are closely related to the development of non-alcoholic fatty liver disease (NAFLD). Moreover, studies have shown that macrophages have an important role in the progression of NAFLD and that a dose effect of sodium acetate (NaA) on the regulation of macrophage activity alleviates NAFLD; however, the exact mechanism of action remains unclear. This study aimed to assess the effect and mechanism of NaA on regulating the activity of macrophages. RAW264.7 and Kupffer cells cell lines were treated with LPS and different concentrations of NaA (0.01, 0.05, 0.1, 0.5, 1, 1.5, 2, and 5 mM). Low doses of NaA (0.1 mM, NaA-L) significantly increased the expression of inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin 1 beta (IL-1β); it also increased the phosphorylation of inflammatory proteins nuclear factor-κB p65 (NF-κB p65) and c-Jun (p < 0.05), and the M1 polarization ratio of RAW264.7 or Kupffer cells. Contrary, a high concentration of NaA (2 mM, NaA-H) reduced the inflammatory responses of macrophages. Mechanistically, high doses of NaA increased intracellular acetate concentration in macrophages, while a low dose had the opposite effect, consisting of the trend of changes in regulated macrophage activity. Besides, GPR43 and/or HDACs were not involved in the regulation of macrophage activity by NaA. NaA significantly increased total intracellular cholesterol (TC), triglycerides (TG), and lipid synthesis gene expression levels in macrophages and hepatocytes at either high or low concentrations. Furthermore, NaA regulated the intracellular AMP/ATP ratio and AMPK activity, achieving a bidirectional regulation of macrophage activity, in which the PPARγ/UCP2/AMPK/iNOS/IκBα/NF-κB signaling pathway has an important role. In addition, NaA can regulate lipid accumulation in hepatocytes by NaA-driven macrophage factors through the above-mentioned mechanism. The results revealed that the mode of NaA bi-directionally regulating the macrophages further affects hepatocyte lipid accumulation. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

20 pages, 2804 KiB

Open AccessArticle

The Regulatory Roles of Ezh2 in Response to Lipopolysaccharide (LPS) in Macrophages and Mice with Conditional Ezh2 Deletion with LysM-Cre System

by Areerat Kunanopparat, Asada Leelahavanichkul, Peerapat Visitchanakun, Patipark Kueanjinda, Pornpimol Phuengmaung, Kritsanawan Sae-khow, Atsadang Boonmee, Salisa Benjaskulluecha, Tanapat Palaga and Nattiya Hirankarn

Int. J. Mol. Sci. 2023, 24(6), 5363; https://doi.org/10.3390/ijms24065363 - 10 Mar 2023

Cited by 6 | Viewed by 1744

Abstract

The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. Transcriptomic analysis on LPS-activated wild-type macrophages demonstrated an alteration of several epigenetic enzymes. Although the Ezh2-silencing macrophages (RAW264.7), using small interfering RNA (siRNA), indicated a non-different response to the control cells after a single LPS stimulation, the Ezh2-reducing cells demonstrated a less severe LPS tolerance, after two LPS stimulations, as determined by the higher supernatant TNF-α. With a single LPS stimulation, Ezh2 null (Ezh2^flox/flox; LysM-Cre^cre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2^fl/fl; LysM-Cre^−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. On the other hand, there were similar serum cytokines after LPS tolerance and the non-reduction of serum cytokines after the second dose of LPS, indicating less severe LPS tolerance in Ezh2 null mice compared with control mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

13 pages, 3147 KiB

Open AccessArticle

Macrophage-Specific Coxsackievirus and Adenovirus Receptor Deletion Enhances Macrophage M1 Polarity in CVB3-Induced Myocarditis

by Ha-Hyeon Shin, Eun-Seok Jeon and Byung-Kwan Lim

Int. J. Mol. Sci. 2023, 24(6), 5309; https://doi.org/10.3390/ijms24065309 - 10 Mar 2023

Cited by 2 | Viewed by 1948

Abstract

The coxsackievirus and adenovirus receptor (CAR) is very well known as an epithelial tight junction and cardiac intercalated disc protein; it mediates attachment and infection via the coxsackievirus B3 (CVB3) and type 5 adenovirus. Macrophages play important roles in early immunity during viral infections. However, the role of CAR in macrophages is not well studied in relation to CVB3 infection. In this study, the function of CAR was observed in the Raw264.7 mouse macrophage cell line. CAR expression was stimulated by treatment with lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α). In thioglycollate-induced peritonitis, the peritoneal macrophage was activated and CAR expression was increased. The macrophage-specific CAR conditional knockout mice (KO) were generated from lysozyme Cre mice. The expression of inflammatory cytokine (IL-1β and TNF-α) was attenuated in the KO mice’s peritoneal macrophage after LPS treatment. In addition, the virus was not replicated in CAR-deleted macrophages. The organ virus replication was not significantly different in both wild-type (WT) and KO mice at days three and seven post-infection (p.i). However, the inflammatory M1 polarity genes (IL-1β, IL-6, TNF-α and MCP-1) were significantly increased, with increased rates of myocarditis in the heart of KO mice compared to those of WT mice. In contrast, type1 interferon (IFN-α and β) was significantly decreased in the heart of KO mice. Serum chemokine CXCL-11 was increased in the KO mice at day three p.i. compared to the WT mice. The attenuation of IFN-α and β in macrophage CAR deletion induced higher levels of CXCL-11 and more increased CD4 and CD8 T cells in KO mice hearts compared to those of WT mice at day seven p.i. These results demonstrate that macrophage-specific CAR deletion increased the macrophage M1 polarity and myocarditis in CVB3 infection. In addition, chemokine CXCL-11 expression was increased, and stimulated CD4 and CD8 T cell activity. Macrophage CAR may be important for the regulation of innate-immunity-induced local inflammation in CVB3 infection. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

16 pages, 2844 KiB

Open AccessArticle

IFNβ-Induced CXCL10 Chemokine Expression Is Regulated by Pellino3 Ligase in Monocytes and Macrophages

by Edyta Makuch, Izabella Jasyk, Anna Kula, Tomasz Lipiński and Jakub Siednienko

Int. J. Mol. Sci. 2022, 23(23), 14915; https://doi.org/10.3390/ijms232314915 - 29 Nov 2022

Cited by 2 | Viewed by 4066

Abstract

IFN-I is the key regulatory component activating and modulating the response of innate and adaptive immune system to bacterial as well as viral pathogens. IFN-I promotes the expression of IFN-induced genes (ISG) and, consequently, the production of chemokines, e.g., CXCL10. Those chemokines control migration and localization of immune cells in tissues, and, thus, are critical to the function of the innate immune system during infection. Consequently, the regulation of IFN-I signaling is essential for the proper induction of an immune response. Our previous study has shown that E3 ubiquitin ligase Pellino3 positively regulates IFNβ expression and secretion. Herein, we examined the role of Pellino3 ligase in regulating CXCL10 expression in response to IFNβ stimulation. Our experiments were carried out on murine macrophage cell line (BMDM) and human monocytes cell line (THP-1) using IFNβ as a IFNAR ligand. We demonstrate that Pellino3 is important for IFNβ-induced phosphorylation and nuclear translocation of STAT1/STAT2/IRF9 complex which interacts with CXCL10 promoter and enhances its expression. In this study, we characterize a novel molecular mechanism allowing Pellino3-dependent modulation of the IFNβ-induced response in BMDM and THP-1 cell lines. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

Review

Jump to: Research

13 pages, 277 KiB

Open AccessReview

The Role of Macrophages in Atherosclerosis: Pathophysiologic Mechanisms and Treatment Considerations

by Panagiotis Theofilis, Evangelos Oikonomou, Konstantinos Tsioufis and Dimitris Tousoulis

Int. J. Mol. Sci. 2023, 24(11), 9568; https://doi.org/10.3390/ijms24119568 - 31 May 2023

Cited by 9 | Viewed by 2286

Abstract

Atherosclerotic diseases are a leading cause of morbidity and mortality worldwide, despite the recent diagnostic and therapeutic advances. A thorough understanding of the pathophysiologic mechanisms is thus essential to improve the care of affected individuals. Macrophages are crucial mediators of the atherosclerotic cascade, but their role has not been fully elucidated. The two main subtypes, tissue-resident and monocyte-derived macrophages, have distinct functions that contribute to atherosclerosis development or regression. Since polarization of macrophages to an M2 phenotype and induction of macrophage autophagy have been demonstrated to be atheroprotective, targeting these pathways could represent an appealing approach. Interestingly, macrophage receptors could act as drug targets, as seen in recent experimental studies. Last but not least, macrophage-membrane-coated carriers have been investigated with encouraging results. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

16 pages, 1854 KiB

Open AccessReview

The Pharmacological Efficacy of Baicalin in Inflammatory Diseases

by Yongqiang Wen, Yazhou Wang, Chenxu Zhao, Baoyu Zhao and Jianguo Wang

Int. J. Mol. Sci. 2023, 24(11), 9317; https://doi.org/10.3390/ijms24119317 - 26 May 2023

Cited by 13 | Viewed by 3889

Abstract

Baicalin is one of the most abundant flavonoids found in the dried roots of Scutellaria baicalensis Georgi (SBG) belonging to the genus Scutellaria. While baicalin is demonstrated to have anti-inflammatory, antiviral, antitumor, antibacterial, anticonvulsant, antioxidant, hepatoprotective, and neuroprotective effects, its low hydrophilicity and lipophilicity limit the bioavailability and pharmacological functions. Therefore, an in-depth study of baicalin’s bioavailability and pharmacokinetics contributes to laying the theoretical foundation for applied research in disease treatment. In this view, the physicochemical properties and anti-inflammatory activity of baicalin are summarized in terms of bioavailability, drug interaction, and inflammatory conditions. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

32 pages, 3576 KiB

Open AccessReview

Tumor-Associated Macrophage Subsets: Shaping Polarization and Targeting

by Qindong Zhang and Mouldy Sioud

Int. J. Mol. Sci. 2023, 24(8), 7493; https://doi.org/10.3390/ijms24087493 - 19 Apr 2023

Cited by 35 | Viewed by 8018

Abstract

The tumor microenvironment (TME) is a critical regulator of tumor growth, progression, and metastasis. Among the innate immune cells recruited to the tumor site, macrophages are the most abundant cell population and are present at all stages of tumor progression. They undergo M1/M2 polarization in response to signals derived from TME. M1 macrophages suppress tumor growth, while their M2 counterparts exert pro-tumoral effects by promoting tumor growth, angiogenesis, metastasis, and resistance to current therapies. Several subsets of the M2 phenotype have been observed, often denoted as M2a, M2b, M2c, and M2d. These are induced by different stimuli and differ in phenotypes as well as functions. In this review, we discuss the key features of each M2 subset, their implications in cancers, and highlight the strategies that are being developed to harness TAMs for cancer treatment. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Figure 1

12 pages, 2006 KiB

Open AccessReview

Role of Sulfur Compounds in Garlic as Potential Therapeutic Option for Inflammation and Oxidative Stress in Asthma

by José L. Sánchez-Gloria, Karla M. Rada, Juan G. Juárez-Rojas, Laura G. Sánchez-Lozada, Ivan Rubio-Gayosso, Fausto Sánchez-Muñoz and Horacio Osorio-Alonso

Int. J. Mol. Sci. 2022, 23(24), 15599; https://doi.org/10.3390/ijms232415599 - 9 Dec 2022

Cited by 6 | Viewed by 2638

Abstract

Asthma is a chronic inflammatory disease in the airways with a multifactorial origin but with inflammation and oxidative stress as related pathogenic mechanisms. Garlic (Allium sativum) is a nutraceutical with different biological properties due to sulfur-containing natural compounds. Studies have shown that several compounds in garlic may have beneficial effects on cardiovascular diseases, including those related to the lungs. Therefore, it is possible to take advantage of the compounds from garlic as nutraceuticals for treating lung diseases. The objective of this article is to review the biological properties of the sulfur compounds present in garlic for the treatment of asthma, as well as the cellular mechanisms involved. Here, we discuss the potential therapeutic effects of garlic compounds in the modulation of inflammation and oxidative stress, as well as its antibiotic and antiviral activities for identifying and testing potential treatment options for asthma management. Full article

(This article belongs to the Special Issue Macrophages, Immunity and Inflammation in Health and Disease)

► Show Figures

Journal Menu

Journal Browser

Macrophages, Immunity and Inflammation in Health and Disease

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Published Papers (11 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI