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Myeloid Cells in Intestinal Inflammation, Infection, and Wound Healing
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Myeloid Cells in Intestinal Inflammation, Infection, and Wound Healing

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Laboratory Medicine".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 1937

Special Issue Editors

Dr. Felix Becker

E-Mail Website
Guest Editor
Department of General, Visceral and Transplant Surgery, University Hospital Münster, 48149 Münster, Germany
Interests: solid organ transplantation; machine perfusion; innate immune cells; macrophages; resolution of inflammation; ischemia reperfusion injury
Special Issues, Collections and Topics in MDPI journals
Dr. Alexander Bungert

E-Mail Website
Guest Editor Assistant
Department of General, Visceral and Transplant Surgery, University Hospital Münster, 48149 Münster, Germany
Interests: macrophages; intestinal wound healing; IBD; colorectal surgery; monocytes

Special Issue Information

Dear Colleagues,

Gastrointestinal disorders remain a global health problem with an increasing incidence around the world.

Myeloid cells are versatile immune cells that have been shown to be paramount for intestinal homeostasis. In addition, these cells are a primary component of the innate immune and critically involved in the complex mucosal immune system, making them instrumental in orchestrating the hosts’ defense against injury. A growing body of evidence has now established a unique functional plasticity of myeloid cells. In line with this, recent research has linked myeloid cells to key pathways involved in the initiation and resolution of intestinal inflammation.

In this Special Issue of the Journal of Clinical Medicine, we will focus on the critical role of monocytes, neutrophils, macrophages, and dendritic cells in orchestrating the physiological and pathological mucosal repair and healing response of damaged tissues during intestinal inflammation, infection, and wound healing.

We welcome submissions covering the entire clinical field of gastrointestinal disorders (especially inflammatory bowel disease, celiac disease, infectious diseases), as well as cutting-edge experimental preclinical work. We would like to invite researchers to submit high-quality original clinical (observational, retrospective, and prospective studies) as well as basic research, meta-analyses, and state-of-the-art reviews.

We look forward to receiving your submissions.

Dr. Felix Becker
Guest Editor
Dr. Alexander Bungert
Guest Editor Assistant

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. Journal of Clinical Medicine 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 2600 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

  • monocytes
  • macrophages
  • dendritic cells
  • neutrophils
  • intestinal inflammation
  • infection
  • mucosal wound healing

Published Papers (1 paper)

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Research

15 pages, 2090 KiB  
Article
The Influence of Apremilast-Induced Macrophage Polarization on Intestinal Wound Healing
by Annika Mohr, Manuela Besser, Sonja Broichhausen, Maximiliane Winter, Alexander D. Bungert, Benjamin Strücker, Mazen A. Juratli, Andreas Pascher and Felix Becker
J. Clin. Med. 2023, 12(10), 3359; https://doi.org/10.3390/jcm12103359 - 9 May 2023
Viewed by 1646
Abstract
There is compelling evidence suggesting a pivotal role played by macrophages in orchestrating intestinal wound healing. Since macrophages display significant plasticity and heterogeneity, exhibiting an either classically activated (M1-like) or alternatively activated (M2-like) phenotype, they can aggravate or attenuate intestinal wound healing. Growing [...] Read more.
There is compelling evidence suggesting a pivotal role played by macrophages in orchestrating intestinal wound healing. Since macrophages display significant plasticity and heterogeneity, exhibiting an either classically activated (M1-like) or alternatively activated (M2-like) phenotype, they can aggravate or attenuate intestinal wound healing. Growing evidence also demonstrates a causal link between impaired mucosal healing in inflammatory bowel disease (IBD) and defects in the polarization of pro-resolving macrophages. By targeting the switch from M1 to M2 macrophages, the phosphodiesterase-4 inhibitor Apremilast has gained recent attention as a potential IBD drug. However, there is a gap in our current knowledge regarding the impact of Apremilast-induced macrophages’ polarization on intestinal wound healing. The THP-1 cells were differentiated and polarized into M1 and M2 macrophages, and subsequently treated with Apremilast. Gene expression analysis was performed to characterize macrophage M1 and M2 phenotypes, and to identify possible target genes of Apremilast and the involved pathways. Next, intestinal fibroblast (CCD-18) and epithelial (CaCo-2) cell lines were scratch-wounded and exposed to a conditioned medium of Apremilast-treated macrophages. Apremilast had a clear effect on macrophage polarization, inducing an M1 to M2 phenotype switch, which was associated with NF-κB signaling. In addition, the wound-healing assays revealed an indirect influence of Apremilast on fibroblast migration. Our results support the hypothesis of Apremilast acting through the NF-κB-pathway and provide new insights into the interaction with fibroblast during intestinal wound healing. Full article
(This article belongs to the Special Issue Myeloid Cells in Intestinal Inflammation, Infection, and Wound Healing)
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