thefforest.co.uk

Caseum development is the process of lipid enrichment with necrosis

4.6 (798) · € 16.00 · En Stock

Download scientific diagram | Caseum development is the process of lipid enrichment with necrosis, leading to cause treatment failure. Following the formation of granuloma against Mtb infection, necrotized foamy macrophages that surround the caseous center gradually begin to form the lipid-rich environment of the caseum. Caseum includes high TAG, cholesterol, lactosylceramide, and cholesterol ester. These lipid species are utilized for the replication of Mtb as well as induce a dormancy state that decreases drug efficacy. In the granuloma, Mtb-infected macrophages become lipid-rich foamy macrophages. Moreover, caseous necrosis with the necrotic death of infected foamy macrophages by activated T cells produces interferons and activates adjacent macrophages to lead to caseous necrosis. In addition, TAG-rich foamy macrophages are present in necrotic granulomas, and the presence of these macrophages is associated with a high level of TNF-α in the necrotic core. Take together acceleration of necrotic cell death in caseous foci provides nutrients for replication and confers TB drug tolerance to Mtb, suggesting inhibition of mycobacterial clearance, resulting in treatment failure. Mtb Mycobacterium tuberculosis, TAG triacylglyceride, TNF-α tumor necrosis factor-α from publication: Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism | Lipid species play a critical role in the growth and virulence expression of Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). During Mtb infection, foamy macrophages accumulate lipids in granulomas, providing metabolic adaptation and survival | Mycobacterium Tuberculosis, Lipid Metabolism and Drug Tolerance | ResearchGate, the professional network for scientists.

Frontiers Phenotypic adaptation of Mycobacterium tuberculosis to host-associated stressors that induce persister formation

Inflammatory signaling in human tuberculosis granulomas is spatially organized. - Abstract - Europe PMC

The spectrum of latent tuberculosis: rethinking the biology and intervention strategies

DGAT1 inhibition leads to altered flux through the eicosanoid

PathTracer Comprehensively Identifies Hypoxia-Induced Dormancy Adaptations in Mycobacterium tuberculosis

Frontiers Foam Cell Macrophages in Tuberculosis

Frontiers Proteomic Profiling Reveals the Architecture of Granulomatous Lesions Caused by Tuberculosis and Mycobacterium avium Complex Lung Disease

Caseum development is the process of lipid enrichment with necrosis

Proteomic Profiling Reveals the Architecture of Granulomatous Lesions Caused by Tuberculosis and Mycobacterium avium Complex Lung Disease. - Abstract - Europe PMC

Frontiers Metabolic Programming of Macrophages: Implications in the Pathogenesis of Granulomatous Disease

Accumulation of Plasma-Derived Lipids in the Lipid Core and Necrotic Core of Human Atheroma: Imaging Mass Spectrometry and Histopathological Analyses