The growth of mildly pathogenic strain E, its virulent revertant EVir, and prototype virulent strain Breinl of Rickettsia prowazekii in peritoneal macrophage cultures of outbread white rats (WR) was evaluated by light microscopy and bioassay in chick embryos (CE). Macrophage cultures infected with strain E were characteristic by limited number of infected cells, poor or moderate accumulation of rickettsiae in individual cells, poor or nil spread of infectious process during first 7 days of infection, and the death of rickettsiae in cultures as determined by the bioassay in CE. Moreover, rickettsiae were not determined in 20.7% of infected macrophage cultures by either microscopic or bioassay methods. In contrast, the growth of virulent strains EVir and Breinl was characteristic by higher proportion of infected cells, considerable accumulation of rickettsiae, and intensive spread of infectious process within 5-7 days post infection (p.i.). However, the intensity of infectious process in macrophage cultures was less expressed with strain EVir than with strain Breinl.
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Background: Targeting glutamine metabolism has emerged as a promising strategy in cancer therapy. However, several barriers, such as anti-tumor efficacy, drug toxicity, and safety, remain to be overcome to achieve clinical utility. Prior preclinical studies had generated encouraging data showing promises of cancer metabolism targeting drugs, although most were performed on immune-deficient murine models.
View Article and Find Full Text PDFWe have previously identified that infection induces a unique form of myeloid training that protects male but not female mice from high fat diet induced disease. Here we demonstrate that ovarian derived hormones account for this sex specific difference. Ovariectomy of females prior to infection permits metabolic reprogramming of the myeloid lineage, with BMDM exhibiting carbon source flexibility for cellular respiration, and mice protected from systemic metabolic disease.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
Shanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation, College of Traditional Chinese Medicine and Food Engineering, Shanxi University of Chinese Medicine, Jinzhong, People's Republic of China.
Background: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease in which macrophages produce cytokines that enhance inflammation and contribute to the destruction of cartilage and bone. Additive Sishen decoction (ASSD) is a widely used traditional Chinese medicine for the treatment of RA; however, its active ingredients and the mechanism of its therapeutic effects remain unclear.
Methods: To predict the ingredients and key targets of ASSD, we constructed "drug-ingredient-target-disease" and protein-protein interaction networks.
Mater Today Bio
February 2025
China Uruguay Bio-Nano Pharmaceutical Joint Laboratory, Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, 308 Ningxia Road, Qingdao, 266071, Shandong, China.
Well-designed artificial scaffolds are urgently needed due to the limited self-repair capacity of bone, which hampers effective regeneration in critical defects. Optimal scaffolds must provide physical guidance to recruit cells and immune regulation to improve the regenerative microenvironment. This study presents a novel scaffold composed of dual-sided centripetal microgrooved poly(D,L-lactide-co-caprolactone) (PLCL) film combined with a dynamic hydrogel containing prednisolone (PLS)-loaded Prussian blue nanoparticles (PB@PLS).
View Article and Find Full Text PDFBone Rep
March 2025
Beijing Institute of Dental Research, Beijing Stomatological Hospital, Capital Medical University, Beijing 100050, China.
Background: Gnathodiaphyseal dysplasia (GDD) is a rare autosomal dominant genetic disease characterized by osteosclerosis of the tubular bones and cemento-osseous lesions of the mandibles. () is the pathogenic gene, however, the specific molecular mechanism of GDD remains unclear. Herein, a knockin ( ) mouse model expressing the human mutation p.
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