Endotoxin tolerance refers to cells' decreased response to repeated exposure to bacterial components like LPS. This mechanism involves downregulating TLR expression, inhibiting signaling pathways, inducing anti-inflammatory mediators, and making epigenetic modifications. It prevents excessive inflammation, a key factor in septic shock, which requires immediate medical intervention due to its life-threatening nature.
Category: Immunology
Ending Inflammation and Restoring Tissue Homeostasis
The resolution of inflammation is essential for preventing chronic inflammation and tissue damage. It involves anti-inflammatory signals, negative feedback mechanisms, deactivation of inflammatory mediators, clearance of immune cells, specialized pro-resolving mediators, tissue repair, and termination of inflammatory stimuli. Dysregulation can lead to chronic inflammatory conditions and tissue damage.
Details Related to the Effector Phase of Inflammation
Inflammation triggers vasodilation and increased permeability through various molecules like prostaglandins, bradykinin, leukotrienes, nitric oxide, cytokines, platelet-activating factor, and histamine. Chemokines attract immune cells like neutrophils and monocytes, which then engage in phagocytosis and release inflammatory mediators like cytokines and chemokines, ultimately contributing to the acute inflammatory response.
Life and Biology 