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Cells
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The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders
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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 May 2025 | Viewed by 9761

Special Issue Editors

Dr. Pei-Hui Lin

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Dr. Kumaraswami Konda

E-Mail
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

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. 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

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Published Papers (5 papers)

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Research

15 pages, 10679 KiB  
Article
Bovine Meat and Milk Factor (BMMF) Protein Is Expressed in Macrophages Spread Widely over the Mucosa of Colorectal Cancer Patients
by Sumen Siqin, Ekaterina Nikitina, Mohammad Rahbari, Claudia Ernst, Damir Krunic, Emrullah Birgin, Claudia Tessmer, Ilse Hofmann, Nuh Rahbari and Timo Bund
Cells 2025, 14(6), 455; https://doi.org/10.3390/cells14060455 - 19 Mar 2025
Viewed by 94
Abstract
Red meat consumption is considered a risk factor for colorectal cancer (CRC) development and stimulated isolation of plasmid-like DNA molecules from bovine serum and milk, termed bovine meat and milk factors (BMMFs). BMMFs encode a conserved replication protein (Rep). Increased populations of Rep-expressing [...] Read more.
Red meat consumption is considered a risk factor for colorectal cancer (CRC) development and stimulated isolation of plasmid-like DNA molecules from bovine serum and milk, termed bovine meat and milk factors (BMMFs). BMMFs encode a conserved replication protein (Rep). Increased populations of Rep-expressing macrophages have been identified in the peritumor of CRC patients and pre-cancerous tissues when compared to the tissues of healthy individuals. This supports the concept that BMMFs increase cancer risk by indirect carcinogenesis, upon induction of chronic inflammation. However, the spread of Rep+ immune cells in tissues at greater distances from primary tumors has not yet been assessed. Here, we immunohistologically analyzed the presence of Rep+ immune cells in sets of tumor, peritumor and, additionally, distant tissues of CRC patients (n = 13). We identified consistently high numbers of BMMF-positive macrophages in mucosal tissues at distances of as much as 25 cm away from the primary tumors, at levels comparable to peritumors and associated with M2-like macrophage polarization. The broad distribution of BMMFs suggests that BMMF+ macrophages might already exist at stages of pre-cancerous dysplasia or before. Quantification of BMMF tissue expression during colonoscopy might help to preventively stratify individuals at risk of developing polyps/CRC and recommend them for enhanced surveillance and/or changes in dietary lifestyle. Full article
(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)
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13 pages, 4449 KiB  
Article
Berberine Inhibits the Inflammatory Response Induced by Staphylococcus aureus Isolated from Atopic Eczema Patients via the TNF-α/Inflammation/RAGE Pathways
by Anish R. Maskey, Daniel Kopulos, Matthew Kwan, Niradiz Reyes, Christian Figueroa, Xian Mo, Nang Yang, Raj Tiwari, Jan Geliebter and Xiu-Min Li
Cells 2024, 13(19), 1639; https://doi.org/10.3390/cells13191639 - 1 Oct 2024
Cited by 1 | Viewed by 1652
Abstract
Atopic eczema patients exhibit high levels of Staphylococcus aureus (S. aureus) skin colonization. S. aureus can stimulate macrophages and the expression of proinflammatory cytokines. Berberine (BBR), an alkaloid, attenuates S. aureus toxin production. This study investigated if BBR suppressed bacterial growth [...] Read more.
Atopic eczema patients exhibit high levels of Staphylococcus aureus (S. aureus) skin colonization. S. aureus can stimulate macrophages and the expression of proinflammatory cytokines. Berberine (BBR), an alkaloid, attenuates S. aureus toxin production. This study investigated if BBR suppressed bacterial growth and inflammatory response induced by eczema-patient-derived S. aureus using murine macrophage (RAW 264.7) and human monocyte cell lines (U937). RAW 264.7 and U937 were treated with BBR at different concentrations and stimulated with heat-killed S. aureus (ATCC #33591) or S. aureus derived from severe eczema patients (EC01–EC10), who were undergoing topical steroid withdrawal, for 24 h. TNF-α protein levels were determined by ELISA, gene expression by qRT-PCR, cell cytotoxicity by trypan blue excursion, and reactive oxygen species (ROS) levels by fluorometric assay. BBR showed a bacteriostatic effect in S. aureus (ATCC strain #33591 and clinical isolates (EC01–EC10) and suppressed TNF-α production in RAW 264.7 and U937 cells exposed to heat-killed S. aureus (ATCC and clinical isolates) dose-dependently without any cell cytotoxicity. BBR (20 µg/mL) suppressed >90% of TNF-α production (p < 0.001), downregulated genes involved in inflammatory pathways, and inhibited S. aureus ROS production in U937 and RAW 264.7 cells (p < 0.01). BBR suppresses S. aureus-induced inflammation via inhibition of TNF-α release, ROS production, and expression of key genes involved in the inflammatory pathway. Full article
(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)
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13 pages, 1705 KiB  
Article
Signalling Pathways of Inflammation and Cancer in Human Mononuclear Cells: Effect of Nanoparticle Air Pollutants
by Agata Niechoda, Maciej Roslan, Katarzyna Milewska, Piotr Szoka, Katarzyna Maciorowska and Adam Holownia
Cells 2024, 13(16), 1367; https://doi.org/10.3390/cells13161367 - 17 Aug 2024
Viewed by 1309
Abstract
Fine inhalable particulate matter (PM) triggers an inflammatory response in the airways and activates mononuclear cells, mediators of tissue homeostasis, and tumour-promoting inflammation. We have assessed ex vivo responses of human monocytes and monocyte-derived macrophages to standardised air pollutants: carbon black, urban dust, [...] Read more.
Fine inhalable particulate matter (PM) triggers an inflammatory response in the airways and activates mononuclear cells, mediators of tissue homeostasis, and tumour-promoting inflammation. We have assessed ex vivo responses of human monocytes and monocyte-derived macrophages to standardised air pollutants: carbon black, urban dust, and nanoparticulate carbon black, focusing on their pro-inflammatory and DNA-damaging properties. None of the PM (100 μg/mL/24 h) was significantly toxic to the cells, aside from inducing oxidative stress, fractional DNA damage, and inhibiting phagocytosis. TNFα was only slightly increased. PM nanoparticles increase the expression and activate DNA-damage–related histone H2A.X as well as pro-inflammatory NF-κB. We have shown that the urban dust stimulates the pathway of DNA damage/repair via the selective post-translational phosphorylation of H2A.X while nanoparticulate carbon black increases inflammation via activation of NF-κB. Moreover, the inflammatory response to lipopolysaccharide was significantly stronger in macrophages pre-exposed to urban dust or nanoparticulate carbon black. Our data show that airborne nanoparticles induce PM-specific, epigenetic alterations in the subsets of cultured mononuclear cells, which may be quantified using binary fluorescence scatterplots. Such changes intercede with inflammatory signalling and highlight important molecular and cell-specific epigenetic mechanisms of tumour-promoting inflammation. Full article
(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)
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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
Viewed by 1635
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
(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  
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 8 | Viewed by 3703
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
(This article belongs to the Special Issue The Role of Macrophages and Neutrophils in Chronic Inflammation-Related Disorders)
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