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Macrophage Polarization: Learning to Manage It 4.0
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Macrophage Polarization: Learning to Manage It 4.0

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 May 2025 | Viewed by 2262

Special Issue Editor

Dr. Nadia Lampiasi

E-Mail Website
Guest Editor
National Research Council, Institute for Research and BioMedical Innovation “IRIB”, Via U. La Malfa, 153, 90146 Palermo, Italy
Interests: inflammation and innate immunity; macrophages polarization; osteoimmunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Macrophages are crucial components of innate immunity. They possess high plasticity and the ability to differentiate in response to numerous stimuli. The physiological and/or pathological conditions characterize the environment in which the macrophages reside and determine their heterogeneity. There is a plethora of different specialized functional phenotypes, among which inflammatory (M1) and reparative (M2) subtypes are proposed, which are almost exactly opposite to each other. Two key cytokines, IFN-γ and TNF-α, are responsible for M1, or classical activation, while the alternate M2 activation is mediated mainly by IL-4 and IL-13. Interestingly, microRNAs and some immunomodulators are critical regulators of macrophage polarization. The link with many human diseases and infections, including cancer, autoimmunity and periodontitis, is to be found in the dysregulation of macrophage plasticity. Furthermore, recent studies on naturally occurring compounds emphasize their regulatory effects on macrophage polarization, suggesting that some of them could be promising for the treatment of sensitive diseases.

This Special Issue aims to cover all areas of molecular research, but is not limited to this, as it may include clinical studies with biomolecular experiments.

Dr. Nadia Lampiasi
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
  • macrophage plasticity
  • macrophage polarization
  • innate immunity
  • IFN-γ
  • TNF-α
  • immunomodulators
  • diseases
  • homeostasis
  • inflammation
  • cancer

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Published Papers (2 papers)

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18 pages, 4213 KiB  
Article
Combining antimiR-25 and cGAMP Nanocomplexes Enhances Immune Responses via M2 Macrophage Reprogramming
by Marija Petrovic, Oliwia B. Majchrzak, Rihana Amreen Mohamed Hachime Marecar, Annick C. Laingoniaina, Paul R. Walker, Gerrit Borchard, Olivier Jordan and Stoyan Tankov
Int. J. Mol. Sci. 2024, 25(23), 12787; https://doi.org/10.3390/ijms252312787 - 28 Nov 2024
Viewed by 339
Abstract
Glioblastoma (GBM) is an aggressive brain cancer with a highly immunosuppressive tumor microenvironment (TME), invariably infiltrated by tumor-associated macrophages (TAMs). These TAMs resemble M2 macrophages, which promote tumor growth and suppress immune responses. GBM cells secrete extracellular vesicles (EVs) containing microRNA-25, which inhibits [...] Read more.
Glioblastoma (GBM) is an aggressive brain cancer with a highly immunosuppressive tumor microenvironment (TME), invariably infiltrated by tumor-associated macrophages (TAMs). These TAMs resemble M2 macrophages, which promote tumor growth and suppress immune responses. GBM cells secrete extracellular vesicles (EVs) containing microRNA-25, which inhibits the cGAS-STING pathway and prevents TAMs from adopting a pro-inflammatory M1 phenotype. This study characterizes antimiR-25/cGAMP nanocomplexes (NCs) for potential therapeutic applications. A particle size analysis revealed a significant reduction upon complexation with antimiR-25, resulting in smaller, more stable nanoparticles. Stability tests across pH levels (4–6) and temperatures (25–37 °C) demonstrated their resilience in various biological environments. Biological assays showed that antimiR-25 NCs interacted strongly with transferrin (Tf), suggesting potential for blood–brain barrier passage. The use of cGAMP NCs activated the cGAS-STING pathway in macrophages, leading to increased type I IFN (IFN-β) production and promoting a shift from the M2 to M1 phenotype. The combined use of cGAMP and antimiR-25 NCs also increased the expression of markers involved in M1 polarization. These findings offer insights into optimizing antimiR-25/cGAMP NCs for enhancing immune responses in GBM. Full article
(This article belongs to the Special Issue Macrophage Polarization: Learning to Manage It 4.0)
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Review

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13 pages, 976 KiB  
Review
Regenerative Inflammation: The Mechanism Explained from the Perspective of Buffy-Coat Protagonism and Macrophage Polarization
by Rubens Andrade Martins, Fábio Ramos Costa, Luyddy Pires, Márcia Santos, Gabriel Silva Santos, João Vitor Lana, Bruno Ramos Costa, Napoliane Santos, Alex Pontes de Macedo, André Kruel and José Fábio Lana
Int. J. Mol. Sci. 2024, 25(20), 11329; https://doi.org/10.3390/ijms252011329 - 21 Oct 2024
Viewed by 1338
Abstract
The buffy-coat, a layer of leukocytes and platelets obtained from peripheral blood centrifugation, plays a crucial role in tissue regeneration and the modulation of inflammatory responses. This article explores the mechanisms of regenerative inflammation, highlighting the critical role of the buffy-coat in influencing [...] Read more.
The buffy-coat, a layer of leukocytes and platelets obtained from peripheral blood centrifugation, plays a crucial role in tissue regeneration and the modulation of inflammatory responses. This article explores the mechanisms of regenerative inflammation, highlighting the critical role of the buffy-coat in influencing macrophage polarization and its therapeutic potential. Macrophage polarization into M1 and M2 subtypes is pivotal in balancing inflammation and tissue repair, with M1 macrophages driving pro-inflammatory responses and M2 macrophages promoting tissue healing and regeneration. The buffy-coat’s rich composition of progenitor cells, cytokines, and growth factors—such as interleukin-10, transforming growth factor-β, and monocyte colony-stimulating factor—supports the transition from M1 to M2 macrophages, enhancing tissue repair and the resolution of inflammation. This dynamic interaction between buffy-coat components and macrophages opens new avenues for therapeutic strategies aimed at improving tissue regeneration and managing inflammatory conditions, particularly in musculoskeletal diseases such as osteoarthritis. Furthermore, the use of buffy-coat-derived therapies in conjunction with other regenerative modalities, such as platelet-rich plasma, holds promise for more effective clinical outcomes. Full article
(This article belongs to the Special Issue Macrophage Polarization: Learning to Manage It 4.0)
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