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As defined, acute inflammation is an immunovascular response to inflammatory stimuli, which can include infection or trauma. [24] [25] This means acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (more specifically myeloid granulocytes in the acute setting). [24]
Once a DAMP is released from the cell, it promotes a noninfectious inflammatory response by binding to a pattern recognition receptor (PRR). [4] Inflammation is a key aspect of the innate immune response; it is used to help mitigate future damage to the organism by removing harmful invaders from the affected area and start the healing process. [5]
An immune response is a physiological reaction which occurs within an organism in the context of inflammation for the purpose of defending against exogenous factors. These include a wide variety of different toxins, viruses, intra- and extracellular bacteria, protozoa, helminths, and fungi which could cause serious problems to the health of the host organism if not cleared from the body.
Here, the immune system adapts its response during an infection to improve its recognition of the pathogen. This improved response is then retained after the pathogen has been eliminated, in the form of an immunological memory, and allows the adaptive immune system to mount faster and stronger attacks each time this pathogen is encountered. [4] [5]
Type 2 inflammation is a pattern of immune response. Its physiological function is to defend the body against helminths , but a dysregulation of the type 2 inflammatory response has been implicated in the pathophysiology of several diseases.
Inflammatory cytokines play a role in initiating the inflammatory response and to regulate the host defence against pathogens mediating the innate immune response. [4] Some inflammatory cytokines have additional roles such as acting as growth factors. [5] Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain ...
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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.