Relevance and rationale for the topic
Inflammation is a fundamental and ubiquitous reaction of higher organisms to trauma and infection. The purpose of the inflammatory reaction is to eliminate injured tissues and foreign invaders and to restore the structural and functional integrity of tissues and organs. Therefore, inflammation can be considered as a key element for the preservation of tissue homeostasis.
The inflammatory process consists of many coordinated pathophysiological steps such as changes in the local blood circulation, infiltration, accumulation, and activation of different cell types at the traumatized tissue site, removal of pathogenic organisms, debris, and in-flammatory cells, and finally tissue repair. The quality and quantity of the injury and the type of affected tissue or organ determine the nature of the particular inflammatory reactions to a given pathogen or damaged tissue. Normally, after termination of the inflammatory process the tissue and organ functions are restored. However, in cases when the balance between inflammatory reaction and resolution is disturbed and can not be completed, self-destructive chronic inflammation may develop resulting in defective or loss of organ functions. Due to the dilemma of the absolute requirement of an inflammatory reaction for effective immune defense on the one hand and potential tissue destruction due to the inflammatory reaction on the other hand, it is necessary to tightly regulate and control the inflammatory process.
Inflammation, the immediate immunological consequence of recognition of pathogenic material by the immune system, is considered a necessary, initial component of innate as well as adaptive immunity. Inflammation constitutes a relevant accompaniment of both the humoral as well as the cellular immune response. However, excessive or prolonged inflammatory responses can themselves cause considerable tissue and organ damage. Complete inhibition of the inflammatory reaction in order to prevent secondary damage would leave the organism immune compromised and, therefore, unable to mount an effective immune defense. Consequently, simultaneously with the initiation of an acute inflammatory reaction a coordinated program is initiated, aimed at fine tuning the degree of the immune reaction sufficient for resolution of inflammation. According to this concept of “inflammation-induced termination of inflammation” multiple tightly controlled inhibitory mechanisms selective for individual cellular and molecular reactions of the immune response are required to restore immune homeostasis and permit the development of an adequate immune reaction upon renewed stimulation.
