The mechanisms of defense against infections are organized along several lines. In the first place, there are devices of a purely mechanical nature – such as the skin, whose outer surface is composed of dead cells – which guard against the entrance of bacteria into the body tissues. Other than the skin, these defensive devices – mucous secretions and ciliated cells – are especially massed about the external openings into the interior of the body. These natural openings, such as the mouth and pharynx and respiratory passages, are always potential points of entry for bacteria.
But should these defensive devices, for some reasons, fail in their function and certain kinds of bacteria succeed in penetrating the body tissues, another line of defensive devices work in localizing the intruding infections. Included in this second line of defensive devices is the remarkable occurrence known as inflammation. Simply defined, inflammation is the reaction of living tissues to infections or injuries.
In the immediate vicinity of infections by certain kinds of bacteria, the phenomenon of inflammation takes place. When bacteria lodge in the deeper layers of the skin, they begin to destroy the skin’s tissues. The destruction of skin tissues is caused partly by the toxic products which the bacteria liberate in their metabolism.
Changes soon occur in the adjacent blood vessels, which dilate widely, allowing the flow of a great quantity of blood into the infected area. This occurrence produces the familiar reddening, swelling, pain, and a characterized localized warmth, all of which are characteristics of inflammation.
A boil may very well exemplify the occurrence of inflammation. Here, an increased blood supply to the infected region caused by a dilatation of the arterioles and capillaries is involved. From the blood, fluids escape into the infected area, weakening the bacteria and their toxic products. The plasma fluid, which contains the various blood-clotting elements, causes coagulation to take place. The coagulation is perhaps initiated, to a large extent, by the thromboplastin (a complex enzyme found in platelets) liberated from cells destroyed by the bacteria.
The entire locally infected area is in this way transformed into a jelly-like mass, enmeshed with strands of fibrin (a white insoluble fibrous protein). Fibrous connective tissue forms around the infected area, helping to immure the infection. In some instances, when a boil occurs, the affected person interferes with the natural process by squeezing the boil to allow the pus to ooze out. In so doing, the person incidentally also may break down the limiting barriers of the coagulated mass, causing the spread of more infections. Ordinarily, though, inflammation effectively limits the spread of infections.
Sources:
1. “Defenses Against Infection”, on The Merck Manuals Online Medical Library – http://www.merck.com/mmhe/sec17/ch188/ch188d.html
2. “Definition of Inflammation”, on MedicineNet.com – http://www.medterms.com/script/main/art.asp?articlekey=3979
3. “Inflammation: What You Need To Know”, on The Cleveland Clinic (online) – http://my.clevelandclinic.org/symptoms/Inflammation/hic_Inflammation_What_You_Need_To_Know.aspx
