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Macrophages in Human Diseases and Their Treatment
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Macrophages in Human Diseases and Their Treatment

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: 20 June 2025 | Viewed by 7279

Special Issue Editor

Dr. Mirjana Jerkic

E-Mail Website
Guest Editor
The Keenan Research Centre for Biomedical Science of St. Michael’s Hospital, Unity Health Toronto, University of Toronto, Toronto, ON M5B 1T8, Canada
Interests: stem cells (and MSCs, in particular); mitochondria; macrophages; brain and lung injury; sepsis; ischemia-reperfusion; TGFβ pathways; translational research and clinical studies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a Special Issue, “Macrophages in Human Diseases and Their Treatment”. Macrophages (Mφs) have a fundamental role in the regulation of tissue homeostasis and inflammation. They are critically involved in processes that could lead to disease progression or its resolution. Modulation of Mφ functions and their plasticity could be used as a direct target for injury prevention, treatment and reparatory responses, both in acute and chronic disorders.

The main scope of this issue is to highlight the current state of knowledge surrounding molecular mechanisms by which Mφs function in health and disease, modulate other cells, interact with the environment, cause tissue damage or orchestrate tissue repair.

We are welcoming original research and recent review papers. Generally, pure clinical research or model studies, survey studies and correlation research are out of the scope of IJMS. However, clinical or model submissions with biomolecular experiments are welcome here.

This Special Issue is supervised by Dr. Mirjana Jerkic and assisted by our Topical Advisory Panel Member Dr. Razieh Rabani (University of Toronto) and Dr. Esmaeel Ghasemi-Gojani (University of Lethbridge).

Dr. Mirjana Jerkić
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. 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

  • macrophages
  • organ dysfunction
  • human diseases
  • involvement of macrophages in treatment options

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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20 pages, 16668 KiB  
Article
Inflammatory Responses to Zn/Cu-Containing Welding Fume in Human Alveolar Epithelial and Macrophage Cell Lines, with MIP-1β/CCL4 as a Much More Sensitive Macrophage Activation Marker than IL-8 and TNF-α
by Jan Steffens, Katharina Kuth, Thomas Kraus, Wolfgang Dott, Sabrina Michael and Ralf Baumann
Int. J. Mol. Sci. 2025, 26(8), 3843; https://doi.org/10.3390/ijms26083843 - 18 Apr 2025
Viewed by 187
Abstract
Zinc (Zn)- and copper (Cu)-containing welding fumes elevate inflammatory markers (CRP, TNF-α, IL-6, IL-8) in healthy individuals and welders. Zn- and Cu-containing nanoparticles are toxic to human macrophages. Therefore, ZnO exposure limits are under discussion. In this study, the effects of Zn/Cu-containing welding [...] Read more.
Zinc (Zn)- and copper (Cu)-containing welding fumes elevate inflammatory markers (CRP, TNF-α, IL-6, IL-8) in healthy individuals and welders. Zn- and Cu-containing nanoparticles are toxic to human macrophages. Therefore, ZnO exposure limits are under discussion. In this study, the effects of Zn/Cu-containing welding fume suspensions on A549 alveolar epithelial cells (exposure concentrations: 0.01/0.1/1/10/100 µg/mL) and THP-1 macrophages (additionally 0.001 µg/mL) were investigated over a period of 48 h. Effects on apoptosis, cytotoxicity, genotoxicity, superoxide dismutase (SOD) activity, and cytokine levels (IL-6, IL-8, MIP-1β/CCL4, TNF-α) were evaluated. Welding fume exposure increased SOD activity, and it increased Annexin-V binding and cytotoxicity effects starting at 10 µg/mL in A549 cells and particularly in THP-1 macrophages. A549 cells showed increased IL-6 at 10 and 100 µg/mL, and significant IL-8 release occurred at 10 µg/mL for A549 and 0.1 µg/mL for macrophages. Exposed macrophages released TNF-α at 1 µg/mL after 24 and 48 h and MIP-1β/CCL4 at 0.01 µg/mL after 6 h and at 0.001 µg/mL after 48 h. No genotoxic effects were detected. MIP-1β/CCL4 is a sensitive new biomarker for human macrophages exposed to Zn/Cu-containing welding fumes. The findings suggest that Zn/Cu particles affect lung cells already at doses below current occupational thresholds. Full article
(This article belongs to the Special Issue Macrophages in Human Diseases and Their Treatment)
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18 pages, 4739 KiB  
Article
Pharmacological Inhibition of MMP-12 Exerts Protective Effects on Angiotensin II-Induced Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Mice
by Karina Di Gregoli, Georgia Atkinson, Helen Williams, Sarah J. George and Jason L. Johnson
Int. J. Mol. Sci. 2024, 25(11), 5809; https://doi.org/10.3390/ijms25115809 - 27 May 2024
Cited by 3 | Viewed by 2206
Abstract
Human abdominal aortic aneurysms (AAAs) are characterized by increased activity of matrix metalloproteinases (MMP), including MMP-12, alongside macrophage accumulation and elastin degradation, in conjunction with superimposed atherosclerosis. Previous genetic ablation studies have proposed contradictory roles for MMP-12 in AAA development. In this study, [...] Read more.
Human abdominal aortic aneurysms (AAAs) are characterized by increased activity of matrix metalloproteinases (MMP), including MMP-12, alongside macrophage accumulation and elastin degradation, in conjunction with superimposed atherosclerosis. Previous genetic ablation studies have proposed contradictory roles for MMP-12 in AAA development. In this study, we aimed to elucidate if pharmacological inhibition of MMP-12 activity with a phosphinic peptide inhibitor protects from AAA formation and progression in angiotensin (Ang) II-infused Apoe−/− mice. Complimentary studies were conducted in a human ex vivo model of early aneurysm development. Administration of an MMP-12 inhibitor (RXP470.1) protected hypercholesterolemia Apoe−/− mice from Ang II-induced AAA formation and rupture-related death, associated with diminished medial thinning and elastin fragmentation alongside increased collagen deposition. Proteomic analyses confirmed a beneficial effect of MMP-12 inhibition on extracellular matrix remodeling proteins combined with inflammatory pathways. Furthermore, RXP470.1 treatment of mice with pre-existing AAAs exerted beneficial effects as observed through suppressed aortic dilation and rupture, medial thinning, and elastin destruction. Our findings indicate that pharmacological inhibition of MMP-12 activity retards AAA progression and improves survival in mice providing proof-of-concept evidence to motivate translational work for MMP-12 inhibitor therapy in humans. Full article
(This article belongs to the Special Issue Macrophages in Human Diseases and Their Treatment)
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Review

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40 pages, 2588 KiB  
Review
Targeting Macrophage Polarization for Reinstating Homeostasis following Tissue Damage
by Qiran Du, Anna Dickinson, Pruthvi Nakuleswaran, Susan Maghami, Savindu Alagoda, Andrew L. Hook and Amir M. Ghaemmaghami
Int. J. Mol. Sci. 2024, 25(13), 7278; https://doi.org/10.3390/ijms25137278 - 2 Jul 2024
Cited by 8 | Viewed by 3673
Abstract
Tissue regeneration and remodeling involve many complex stages. Macrophages are critical in maintaining micro-environmental homeostasis by regulating inflammation and orchestrating wound healing. They display high plasticity in response to various stimuli, showing a spectrum of functional phenotypes that vary from M1 (pro-inflammatory) to [...] Read more.
Tissue regeneration and remodeling involve many complex stages. Macrophages are critical in maintaining micro-environmental homeostasis by regulating inflammation and orchestrating wound healing. They display high plasticity in response to various stimuli, showing a spectrum of functional phenotypes that vary from M1 (pro-inflammatory) to M2 (anti-inflammatory) macrophages. While transient inflammation is an essential trigger for tissue healing following an injury, sustained inflammation (e.g., in foreign body response to implants, diabetes or inflammatory diseases) can hinder tissue healing and cause tissue damage. Modulating macrophage polarization has emerged as an effective strategy for enhancing immune-mediated tissue regeneration and promoting better integration of implantable materials in the host. This article provides an overview of macrophages’ functional properties followed by discussing different strategies for modulating macrophage polarization. Advances in the use of synthetic and natural biomaterials to fabricate immune-modulatory materials are highlighted. This reveals that the development and clinical application of more effective immunomodulatory systems targeting macrophage polarization under pathological conditions will be driven by a detailed understanding of the factors that regulate macrophage polarization and biological function in order to optimize existing methods and generate novel strategies to control cell phenotype. Full article
(This article belongs to the Special Issue Macrophages in Human Diseases and Their Treatment)
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