More recently, it has been recognized that adipocytes also demonstrate intrinsic inflammatory properties, and, like macrophages, they sense the presence of pathogens and inflammation and activate multiple inflammatory signal transduction cascades that result in the secretion of several inflammatory cytokines and acute-phase reactants.
Sepsis is not a single disease, but rather a highly heterogeneous syndrome that is the net result of host and pathogen interactions triggering networks of biochemical mediators and inflammatory cascades in multiple organ systems.
The "inflammatory basis of obesity-associated morbidity" encompasses a particular challenge, since it involves activation of inflammatory cascades in multiple haematopoietic and non-haematopoietic cell types, and includes systemic and local markers of low-grade and chronic inflammatory activation that are all tightly inter-connected.
Furthermore, Schwann cells can potentially modulate multiple aspects of inflammatory cascade [ 14] by producing cytokines and toxic substances [ 78].
IRI is also one of the causes of delayed graft function and acute kidney injury (AKI) after transplantation and is associated with multiple processes, including inflammatory cascade activation, ion accumulation, free reactive oxygen species (ROS) formation, endothelial dysfunction, platelet aggregation with microembolization, and immune activation [ 2].
In severe sepsis and septic shock, endotoxin (lipopolysaccharides [LPS]), IL-6 and complement-activation product 5a (C5a) trigger inflammatory cascades resulting in multiple organ dysfunction and failure of the cell-mediated immune system (immunoparalysis).
Actin exposed at the site of overwhelming injury may act as a sink to exhaust the supply of plasma gelsolin, in turn allowing redundant inflammatory cascades unfettered opportunity to wreak havoc upon multiple organ systems.
This is thought to be secondary to their anti-inflammatory effect, blocking inflammatory cascades triggered in sepsis [2, 3].
Recently, inflammatory cascades have been suggested as a target for epilepsy therapy.
Indeed, hemorrhagic shock precipitates inflammatory cascades that comprise the activation of stress transcriptional factors and up-regulation of cytokines synthesis [ 9, 10] leading to multiple organ failure [ 10].
