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Macrophages repair wounds and remodel tissue by producing extracellular matrix and proteases to modify that specific matrix. [1] A myocardial infarction induces tissue remodeling of the heart in a three-phase process: inflammation, proliferation, and maturation. Inflammation is characterized by massive necrosis in the infarcted area ...
Inflammation is a generic response, and therefore is considered a mechanism of innate immunity, whereas adaptive immunity is specific to each pathogen. [2] Inflammation is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out ...
Inflammaging is thought to be caused by a loss of control over systemic inflammation resulting in chronic overstimulation of the innate immune system. Inflammaging is a significant risk factor in mortality and morbidity in aged individuals. [2] [3] [4] Inflammation is essential to protect against viral and bacterial infection, as well as ...
Heat shock proteins are also believed to play a role in the presentation of pieces of proteins (or peptides) on the cell surface to help the immune system recognize diseased cells. [22] The major HSPs involved in the HSR include HSP70, HSP90, and HSP60. [5] Chaperones include the HSP70s and HSP90s while HSP60s are considered to be chaperonins. [17]
In major injuries, the repair mechanisms are unable to restore the skin to its original condition. The repaired region contains an abnormally large number of collagenous fibers, and relatively few blood vessels. Damaged sweat and sebaceous glands, hair follicles, muscle cells, and nerves are seldom repaired.
Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system.It can contribute to the development or progression of certain conditions such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease, autoimmune and neurodegenerative ...
During cysteinyl leukotriene interaction, they can stimulate proinflammatory activities such as endothelial cell adherence and chemokine production by mast cells. As well as mediating inflammation, they induce asthma and other inflammatory disorders, thereby reducing the airflow to the alveoli.
The inflammasome was discovered by the team of Jürg Tschopp, at the University of Lausanne, in 2002. [17] [18] In 2002, it was first reported by Martinon et al. [17] that NLRP1 (NLR family PYD-containing 1) could assemble and oligomerize into a structure in vitro, which activated the caspase-1 cascade, thereby leading to the production of pro-inflammatory cytokines, including IL-1β and IL-18.