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

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 3211

Special Issue Editors


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Guest Editor
Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA
Interests: tissue injury; repair; inflammation; kidney; wound healing; signaling
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Guest Editor
National Institute on Aging, NIA/NIH, Baltimore, MD, USA
Interests: aging; Alzheimer’s disease; inflammation; immunology; macrophages; neutrophils

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

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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  
Article
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
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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 [...] Read more.
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
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15 pages, 3367 KiB  
Article
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
Cited by 1 | Viewed by 1624
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 [...] Read more.
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
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