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The Research of Macrophages in Inflammation

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: closed (25 August 2021) | Viewed by 3146

Special Issue Editors


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Guest Editor
University of Montana Missoula, Department of Biomedical and Pharmaceutical Sciences, Missoula, MT 59812, USA
Interests: nanoparticles; particulate matter; asbestos; silica; alveolar macrophages; innate immunity; NLRP3 inflammasome; macrophage receptors; lysosomes
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Co-Guest Editor
Center for Environmental Health Sciences, University of Montana, Missoula, MT 59812, USA
Interests: respiratory immunity; fibrosis; inflammation; autoimmune diseases; particle exposures
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Macrophages are involved in both innate and adaptive immune responses to regulate both acute and chronic inflammation. Macrophages have been recognized as key regulators in a variety of disease states. They are plastic and respond to their microenvironments with amazing adaptability and function, with constant interplay between phenotypes. Therefore, based on their key roles in regulating inflammation, it is important to bring together the most current information to identify gaps of knowledge that need to be filled in understanding how their many functions are regulated in order to assist and guide future research toward treating human diseases. We propose that this information is central to being able to develop new therapeutic approaches to treat chronic inflammatory diseases. This Special Issue will include studies that describe macrophage responses to endogenous and exogenous triggers, regulation of phenotypes and responses, their relationship to and involvement in trained immunity, key steps in regulating their functions, their roles in acute and chronic inflammation, and therapeutic approaches to regulate their functions.

Prof. Dr. Andrij Holian
Dr. Christopher Migliaccio
Guest Editors

Manuscript Submission Information

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Published Papers (1 paper)

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Research

53 pages, 44478 KiB  
Article
Transcriptomics Changes in the Peritoneum of Mice with Lipopolysaccharide-Induced Peritonitis
by Shaoguang Liu, Shaotong Zhang, Yulong Sun and Wence Zhou
Int. J. Mol. Sci. 2021, 22(23), 13008; https://doi.org/10.3390/ijms222313008 - 30 Nov 2021
Cited by 5 | Viewed by 2485
Abstract
Peritonitis caused by LPS is a severe clinical challenge, which causes organ damage and death. However, the mechanism of LPS-induced peritonitis has not been fully revealed yet. Here, we investigated the transcriptome profile of the peritoneal tissue of LPS-induced peritonitis in mice. A [...] Read more.
Peritonitis caused by LPS is a severe clinical challenge, which causes organ damage and death. However, the mechanism of LPS-induced peritonitis has not been fully revealed yet. Here, we investigated the transcriptome profile of the peritoneal tissue of LPS-induced peritonitis in mice. A model of LPS-induced peritonitis in mice was established (LPS 10 mg/kg, i.p.), and the influence of TAK 242 (TLR4 inhibitor) on the level of inflammatory cytokines in mouse peritoneal lavage fluid was investigated by using an ELISA test. Next, the peritoneal tissues of the three groups of mice (Control, LPS, and LPS+TAK 242) (n = 6) were isolated and subjected to RNA-seq, followed by a series of bioinformatics analyses, including differentially expressed genes (DEGs), enrichment pathway, protein-protein interaction, and transcription factor pathway. Then, qPCR verified-hub genes that may interact with TAK 242 were obtained. Subsequently, the three-dimensional structure of hub proteins was obtained by using homology modeling and molecular dynamics optimization (300 ns). Finally, the virtual docking between TAK 242 and hub proteins was analyzed. Our results showed that TAK 242 significantly inhibited the production of inflammatory cytokines in the peritoneal lavage fluid of mice with peritonitis, including IL-6, IFN-γ, IL-1β, NO, and TNF-α. Compared with the Control group, LPS treatment induced 4201 DEGs (2442 down-regulated DEGs and 1759 up-regulated DEGs). Compared with the LPS group, 30 DEGs were affected by TAK 242 (8 down-regulated DEGs and 22 up-regulated DEGs). A total of 10 TAK 242-triggered hub genes were obtained, and the possible docking modes between TAK 242 and hub proteins were acquired. Overall, our data demonstrated that a large number of DEGs were affected in LPS-triggered peritonitis mice. Moreover, the TLR4 inhibitor TAK 242 is capable of suppressing the inflammatory response of LPS-induced peritonitis. Our work provides clues for understanding the pathogenesis of LPS-induced peritonitis in mice. Full article
(This article belongs to the Special Issue The Research of Macrophages in Inflammation)
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