Inflammation is the body's reaction to invasion by an infectious agent, antigen challenge or even just physical, chemical or traumatic damage.
The mechanism for triggering the response the body to injury is extremely sensitive. Responses are to tissue damage that might not normally be thought of as injury, for example when the skin is stroked quite firmly or if some pressure is applied to a tissue. In addition, the body has the capacity to respond to both minor injuries such as bruising, scratching, cuts, and abrasions, as well as to major injuries such as severe burns and amputation of limbs.
Depending on the severity of the tissue damage resulting from an injury, the integrity of the skin or internal surfaces may be breached and damage to the underlying connective tissue and muscle, as well as blood vessels can occur. In this situation infection can, and frequently does result because the normal barrier to the entry of harmful organisms has been broken. It is obviously most important that the body can respond to injury by healing and repairing the damaged tissue, as well as by eliminating the infectious agents that may have entered the wound and their toxins. It is also important that the appropriate response to the tissue damage and infection can be made: it is no use bringing all of the body's defences into action to repair a minor scratch, just as one would not expect a single mechanism to be able to deal with the sudden loss of a limb or a major infection.
The inflammatory reaction is phylogenetically and ontogeneticaly the oldest defence mechanism. The cells of the immune system are widely distributed throughout the body, but if an infection or tissue damage occurs it is necessary to concentrate them and their products at the site of damage. Three major events occur during this response :
For the possibility of surrounding tissue damage, inflammatory responses must be well ordered and controlled. The body must be able to act quickly in some situations, for example to reduce or stop the lost of blood, whereas tissue repair and reconstruction can begin a little later. Therefore, a wide variety of interconnected cellular and humoral (soluble) mechanisms are activated when tissue damage and infection occur. On the other hand if the injury is negligible, the body must have mechanisms which are able to stop the tissue damage when the injury agent was removed.
The development of inflammatory reactions is controlled by cytokines, by products of the plasma enzyme systems (complement, the coagulation clothing, kinin and fibrinolytic pathways), by lipid mediators (prostaglandins and leukotrienes) released from different cells, and by vasoactive mediators released from mast cells, basophils and platelets. These inflammatory mediators controlling different types of inflammatory reaction differ. Fast-acting mediators, such as vasoactive amines and the products of the kinin system, modulate the immediate response. Later, newly synthesized mediators such as leukotrienes are involved in the accumulation and activation of other cells. Once leukocytes have arrived at a site of inflammation, they release mediators which control the later accumulation and activation of other cells.
However, in inflammatory reactions initiated by the immune system, the ultimate control is exerted by the antigen itself, in the same way as it controls the immune response itself. For this reason, the cellular accumulation at the site of chronic infection, or in autoimmune reactions (where the antigen cannot ultimately be eradicated), is quite different from that at sites where the antigenic stimulus is rapidly cleared.
The nervous system can also participate in the control of inflammation, especially axon reflexes, but inflammation may be realized in denervated tissues as well.
Inflammation can become chronic. In certain settings the acute process, characterized by neutrophil infiltration and edema, gives way to a predominance of mononuclear phagocytes and lymphocytes. This probably occurs to some degree with the normal healing process but becomes exaggerated and chronic when there is ineffective elimination of foreign materials as in certain infections (e.g. tuberculosis) or following introduction of foreign bodies (e.g. asbestos) or deposition of crystals (e.g. urate crystals). Chronic inflammation is often associated with fusion of mononuclear cells to form multinucleated gigant cells, which eventually become granuloma. Chronic inflammation is seen under conditions of delayed hypersensitivity.
Main humoral and cellular components involved in the amplification and propagation of both acute and chronic inflammation are showed in Table 1.1.
Table 1.1: Components of inflammation
