In cancer pathogenesis, soluble mediators are responsible for a type of inflammation that favors the progression of tumors. The mechanisms chiefly involve changes in the cellular composition of the tumor tissue stroma and in the functional modulation of myeloid and lymphoid leukocytes. Active immunosuppression, proangiogenesis, changes in leukocyte traffic, extracellular matrix remodeling, and alterations in tumor-antigen presentation are the main mechanisms linked to the inflammation that fosters tumor growth and metastasis. Soluble inflammatory mediators and their receptors are amenable to various types of inhibitors that can be combined with other immunotherapy approaches. The main proinflammatory targets which can be interfered with at present and which are under preclinical and clinical development are IL1β, IL6, the CXCR1/2 chemokine axis, TNFα, VEGF, leukemia inhibitory factor, CCL2, IL35, and prostaglandins. In many instances, the corresponding neutralizing agents are already clinically available and can be repurposed as a result of their use in other areas of medicine such as autoimmune diseases and chronic inflammatory conditions.
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http://dx.doi.org/10.1158/1078-0432.CCR-22-3653 | DOI Listing |
Medicine (Baltimore)
January 2025
Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, China.
While recent studies suggested a potential causal link between type 1 diabetes mellitus (T1DM) but not type 2 diabetes mellitus (T2DM) and idiopathic pulmonary fibrosis (IPF), the involved mechanism remains unclear. Here, using a Mendelian randomization (MR) approach, we verified the causal relationship between the two types of diabetes mellitus and IPF and investigated the possible role of inflammation in the association between diabetes mellitus and IPF. Based on genome-wide association study (GWAS) summary data of T1DM, T2DM, and IPF, the univariable MR, multivariable MR (MVMR), and mediation MR were successively used to analyze the causal relationship.
View Article and Find Full Text PDFPLoS One
January 2025
Transplant Group, La Paz University Hospital Health Research Institute (IdiPAZ), Madrid, Spain.
Background: Intestinal transplantation (ITx) represents the only curative option for patients with irreversible intestinal failure. Nevertheless, its rejection rate surpasses that of other solid organ transplants due to the heightened immunological load of the gut. Regulatory T-cells (Tregs) are key players in the induction and maintenance of peripheral tolerance, suggesting their potential involvement in modulating host vs.
View Article and Find Full Text PDFQJM
January 2025
Peking University Traditional Chinese Medicine Clinical Medical School (Xiyuan), Peking University Health Science Center, Beijing, 100091, China.
Autoimmune gastritis (AIG) is a chronic inflammatory condition characterized by immune-mediated destruction of gastric parietal cells, leading to oxyntic atrophy, achlorhydria, and hypergastrinemia. While AIG was historically linked to gastric adenocarcinoma and type I neuroendocrine tumors (NETs), recent evidence suggests the risk of adenocarcinoma in AIG is lower than previously believed, particularly in Helicobacter pylori (H. pylori)-negative patients.
View Article and Find Full Text PDFInt J Circumpolar Health
December 2025
Department of Chemistry, Carleton University, Ottawa, ON, Canada.
Rates of respiratory tract infections for children living in remote First Nations communities in the Sioux Lookout Zone in Northwestern Ontario are elevated and associated with poor indoor environmental quality including high exposures to endotoxin and serious dampness and mould damage. The studies also revealed a high prevalence of cigarette smoking and most houses have wood stoves, of variable quality. Depending on structure, polycyclic aromatic hydrocarbons (PAH) are carcinogens, immunotoxins and/or inflammatory mediators that are byproducts of the incomplete combustion of organic materials.
View Article and Find Full Text PDFFEBS J
January 2025
INSERM UMR-1100, "Research Center for Respiratory Diseases (CEPR)", Tours, France.
Transplanted organs are inevitably exposed to ischemia-reperfusion (IR) injury, which is known to cause graft dysfunction. Functional and structural changes that follow IR tissue injury are mediated by neutrophils through the production of oxygen-derived free radicals, as well as from degranulation which entails the release of proteases and other pro-inflammatory mediators. Neutrophil serine proteases (NSPs) are believed to be the principal triggers of post-ischemic reperfusion damage.
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