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The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders

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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: 10 July 2024 | Viewed by 2620

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Special Issue Editors

Special Issue Information

Dear Colleagues,

Chronic inflammation, which is characterized by a long persistent inflammatory response, is linked to a variety of diseases, including cancer, fibrosis, organ dysfunction, Alzheimer's disease, cardiovascular disease, and obesity. Neutrophils and macrophages are the two main cellular players that can control chronic inflammation in a variety of tissues. Therefore, it is essential to comprehend how neutrophils and macrophages act in chronic inflammation-mediated diseases.

In vitro, in vivo or translational knowledge of neutrophils and macrophages, including, but not limited to, trafficking, recruitment, tissue microenvironment, chemokines, cellular crosstalk, and subtypes, will help us to develop better therapeutic approaches.

This Special Issue aims to publish manuscripts addressing the role of neutrophils and macrophages in the onset and persistence of chronic inflammation. Therefore, we cordially invite researchers to submit both original research and reviews related to the aforementioned areas.

Dr. Pei-Hui Lin
Dr. Kumaraswami Konda
Guest Editors

Manuscript Submission Information

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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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

chronic inflammation
neutrophils
macrophages
Alzheimer’s disease
aging
cardiovascular diseases
obesity
cancer, fibrosis, tissue injury and repair

Published Papers (2 papers)

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Research

12 pages, 1426 KiB

Open AccessArticle

Granular Insights: Neutrophil Predominance and Elastase Release in Severe Asthma Exacerbations in a Pediatric Cohort

by Kirstin Henley, Erin Tresselt, Jessica S. Hook, Parth A. Patel, Michelle A. Gill and Jessica G. Moreland

Cells 2024, 13(6), 533; https://doi.org/10.3390/cells13060533 - 18 Mar 2024

Viewed by 732

Abstract

The chronic inflammatory component of asthma is propagated by granulocytes, including neutrophils and eosinophils, in the peripheral circulation and airway. Previous studies have suggested that these cells have an altered expression of adhesion-related molecules and a propensity for the release of granule contents that may contribute to tissue damage and enhance inflammatory complications in patients with status asthmaticus. The goal of this prospective cohort study at a tertiary care pediatric hospital with a large population of asthma patients was to assess the role of granulocyte-based inflammation in the development of asthma exacerbation. Subjects were enrolled from two patient populations: those with mild-to-moderate asthma exacerbations seen in the emergency department and those with severe asthma admitted to the intensive care unit (PICU). Clinical data were collected, and blood was drawn. Granulocytes were immediately purified, and the phenotype was assessed, including the expression of cell surface markers, elastase release, and cytokine production. Severe asthmatics admitted to the PICU displayed a significantly higher total neutrophil count when compared with healthy donors. Moreover, little to no eosinophils were found in granulocyte preparations from severe asthmatics. Circulating neutrophils from severe asthmatics admitted to the PICU displayed significantly increased elastase release ex vivo when compared with the PMN from healthy donors. These data suggest that the neutrophil-based activation and release of inflammatory products displayed by severe asthmatics may contribute to the propagation of asthma exacerbations. Full article

(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)

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15 pages, 3367 KiB

Open AccessArticle

Anti-Inflammatory Neutrophils Reprogram Macrophages toward a Pro-Healing Phenotype with Increased Efferocytosis Capacity

by Andreea Cristina Mihaila, Letitia Ciortan, Monica Madalina Tucureanu, Maya Simionescu and Elena Butoi

Cells 2024, 13(3), 208; https://doi.org/10.3390/cells13030208 - 23 Jan 2024

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Abstract

Following myocardial infarction (MI), blood neutrophils quickly and extensively infiltrate the heart, where they are temporally polarized into pro-inflammatory (N1) and anti-inflammatory (N2) subpopulations. Neutrophil transmigration is rapidly followed by the accrual of macrophages (MACs), which are believed to undergo local phenotypic transformations from pro-inflammatory to pro-healing MACs that mediate inflammation resolution. We hypothesized that N2 neutrophils can reprogram MACs toward a healing phenotype with increased efferocytosis capacity. To examine this, human neutrophils isolated from healthy subjects were polarized in N1 and N2 neutrophils, and their secretome was added to human MACs derived from THP monocytes. The impact of neutrophil factors on macrophages was investigated using qPCR, ELISA, Western blot, immunofluorescence, or an efferocytosis assay. The results show that the MACs exposed to N2 neutrophil secretome exhibited (i) increased expression of the anti-inflammatory molecules CD206, TGF-β, and IL-10 and the nuclear factors associated with reparatory macrophages (PPARγ, Nur77, and KLF4); (ii) enhanced expression of efferocytosis receptors (MerTK, CD36, CX3CR1, and integrins αv/β5) and of the bridge molecules Mfage8 and Gas6; and (iii) enhanced efferocytosis. In conclusion, factors released by N2 neutrophils induce a pro-healing phenotype of MACs by upregulating anti-inflammatory molecules and efferocytosis receptors and ensuing the efferocytosis capacity. The data suggest that molecular therapy to foster N2 polarization, which boosts macrophages’ pro-healing phenotype, could be a promising strategy to speed up inflammation resolution and tissue repair. Full article

(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)

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