Macrophages play an indispensable role in both innate and acquired immunity, while the persistence of activated macrophages can sometimes be harmful to the host, resulting in multi-organ damage. Macrophages develop from monocytes in the circulation. However, little is known about the organ affinity of macrophages in the normal state. Using in vivo imaging with XenoLight DiR®, we observed that macrophages showed strong affinity for the liver, spleen and lung, and weak affinity for the gut and bone marrow, but little or no affinity for the kidney and skin. We also found that administered macrophages were still alive 168 hours after injection. On the other hand, treatment with clodronate liposomes, which are readily taken up by macrophages via phagocytosis, strongly reduced the number of macrophages in the liver, spleen and lung.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7728253 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0242488 | PLOS |
Plast Reconstr Surg
December 2024
Copenhagen University Hospital, Department of Plastic Surgery and Burns Treatment, Rigshospitalet, Copenhagen, Denmark.
Background: Capsular contracture is a frequent and severe complication following breast implant surgery. Although several theories on the pathophysiology exist, the exact molecular mechanisms remain unclear. This study aimed to identify the specific genes, signaling pathways, and immune cells associated with capsular contracture.
View Article and Find Full Text PDFMelanoma Res
February 2025
Department of Public Health, College of Medicine, Taipei Medical University.
Melanoma is an aggressive tumor that is challenging to treat. Talimogene laherparepvec (T-VEC), the first oncolytic virus treatment approved by the US Food and Drug Administration to treat unresectable melanoma, was recently used in recurrent tumors after initial surgery. Our network meta-analysis aimed to compare T-VEC treatment of metastatic melanoma with treatment of granulocyte-macrophage colony-stimulating factor (GM-CSF) and control group.
View Article and Find Full Text PDFJ Interferon Cytokine Res
January 2025
The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
Suppressor of cytokine signaling (SOCS) 1 is a key negative regulator of interferon (IFN), interleukin (IL)12, and IL-2 family cytokine signaling through inhibition of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. To investigate the temporal induction of SOCS1 in response to cytokine in live cells and its selective regulation of signaling pathways, we generated a mouse expressing a Halo-tag-SOCS1 fusion protein (Halo-SOCS1) under control of the endogenous promoter. Homozygous Halo-SOCS1 mice () were viable with minor T cell abnormalities, most likely due to enhanced Halo-SOCS1 expression in thymocytes compared with the untagged protein.
View Article and Find Full Text PDFJ Hist Dent
January 2025
Professor Emeritus Texas A&M University, College of Dentistry, Dallas, Texas, Distinguished Adjunct Professor, Department of Cariology, Saveetha Dental College and Hospitals Saveetha Institute of Medical and Technical Sciences (SIMATS) Saveetha University, Chennai, India.
Historically the physiological or pathological loss of tooth structure in situ was deemed to be due to the 'absorption' of tooth structure due to the removal of the inorganic components of dentin and cementum by osteoclastic (dentinoclastic) cellular activity. This nomenclature and the activity that it represented was considered by almost all dental researchers and clinicians in the 1800s and early 1900s. The shift to the concept of 'resorption' occurred in the first half of the 20th century, with clarity emanating from significant research activity on the pathology of osseous structures, origin of osteoclastic cell types, and the function of periodontal ligament cells.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
January 2025
Department of Ophthalmology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Purpose: Corneal alkali burns are severe ocular injuries characterized by intense inflammation, tissue damage, and vision impairment, with current treatments often insufficient in restoring corneal function and clarity. This study aimed to evaluate the therapeutic effects of recombinant thrombomodulin domain 1 (rTMD1) in the treatment of corneal alkali burns, focusing on its impact on inflammation, tissue repair, fibrosis, and neovascularization.
Methods: A murine model of corneal alkali burn was utilized to investigate the therapeutic potential of rTMD1.
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