Inflammatory reactions involve a wide variety of interconnected cellular and humoral (soluble) mechanisms.
The major events occur during this response are:
(1) Vasodilation, i.e. widening of the blood vessels to increase the blood flow to the infected area.
(2) Increased vascular permeability, which allows diffusible components to enter the site.
(3) Cellular infiltration by chemotaxis, or the directed movement of inflammatory cells through the walls of blood vessels into the site of injury.
(4) Changes in biosynthetic, metabolic, and catabolic profiles of many organs.
(5) Activation of cells of the immune system as well as of complex enzymatic systems of blood plasma.
(6) Elevation of body temperature followed by the synthesis of acute phase proteins in the liver.
Of course, the degree to which these occur is normally proportional to the severity of the injury and the extent of infection.
Influx of antigen non-specific but highly destructive cells (neutrophils) is one of the earliest stages of the inflammatory response. The inflammatory process may stimulate nerves and cause pain.
Inflammation in different tissues is referred by suffixing “-it is” to the tissue name for eg. “Pancreatitis” – inflammation of pancreas, “myocarditis” – inflammation of the heart, “colitis” – inflammation of the large intestine, “nephritis” – inflammation of the kidneys etc.
According to different criteria, inflammatory responses can be divided into several categories.
The criteria include:
(1) Time – acute and chronic inflammation.
(2) The main inflammatory manifestation – alteration, exudation, proliferation;
(3) The degree of tissue damage – superficial, profound.
(4) Characteristic picture – nonspecific, specific;
(5) Immunopathological mechanisms such as allergic (reaginic) inflammation, delayed-type hypersensitivity reactions etc.
Inflammation classified with reference to time (acute and chronic) is most appropriate to study the reactions in detail.