<unk>  is a complex and systemic issue, likely a result of several factors. Inflammasome Activation Inflammasome Activation and Assembly Release of ROS and pro-inflammatory cytokine secretion in response to inflammasome assembly after DAMP / PAMP binding Over-activation of the inflammasome is one mechanism contributing to<unk> . The inflammasome is a multi-protein complex consisting of a sensor, an adapter, and an effector, that when activated, modulates caspases which cleave cytokines and result in an inflammatory signaling response. Receptors present on the cell surface act as sensors for the detection of damage and pathogens. When activated, this system can go on to elicit pro-inflammatory cytokine secretion and sometimes cell death. Pro-inflammatory cytokines secretion acts as the effector, or the response to such stimuli. Stimuli that can fuel inflammasome assembly includes pathogen associated molecular patterns (PAMPS), damage associated molecular patterns (DAMPS), nutrients and the microbiota. These various self, non self, and quasi self molecules are recognized by receptors of innate immune cells, whose promiscuity allows for many different signals to lead to activation and consequently to inflammation. Examples of stimuli that act as PAMPS include viral and bacterial infection, such as cytomegalovirus and periodontitis respectfully. Examples of DAMPS include misfolded and oxidized proteins, cell debris, and self nucleic acids. Generation of Reactive Oxygen Species In addition to inflammasome activation, with age, cellular components accumulate reactive oxygen species (ROS). These free radicals can damage DNA, lipid, and protein and is able to drive cellular senescence. This is accompanied by a loss in efficiency of DNA damage repair mechanisms. This results in pro-inflammatory cytokine secretion, which contributes to low grade, chronic inflammation in the absence of pathogen or damage, but rather in response to damaged self molecules like oxidized nucleotides. SASP Phenotype Senescent cell populations increase with age and secrete a pro-inflammatory cocktail of chemicals, a condition known as senescence-associated secretory phenotype (SASP). Cells with the SASP are characterized by being in cell cycle arrest, releasing inflammatory factors, and possessing a particular morphology. These cells promote tissue degeneration and are able to spread to other regions by way of the inflammatory secretory molecules released. This contributes to<unk>  as inflammatory secretion contributes to innate immune activation and exhaustion. Functional Decline in Autophagy and Mitophagy Another contribution to<unk>  is a decline in effective autophagy and mitophagy capacity. This is an essential process for cellular housekeeping that prevents protein aggregation and accumulation of damaged mitochondria that produce large quantities of reactive oxygen species. A loss of effective autophagic processes leads to aggregation of damaged proteins. As inflammasome precision declines with age, these aggregates, normally degraded, can be recognizes as a pathogen and lead to an inflammatory response. This contributes to<unk>  and in also involved in many neurodegenerative diseases as well. Other Factors Other possible factors that may lead to<unk>  include insufficient sleep, overnutrition, sensory overload, physical inactivity, altered gut microbiome, impaired intestinal epithelial barrier, and chronic stress occurring in any stage of the individual's life. Cytokines with inflammatory properties can also be secreted by fat tissue.
Inflammaging
Eburnation
Thermal burn
Heat edema
Chemosis
Electrical burn
Virilization
Chemical burn