Inflammation

Inflammation is a defense reaction of the or- ganism and its tissues to injurious stimuli. The
aim is to repair the damage or at least to limit it, and also to remove the cause, for ex- ample,
bacteria or foreign bodies.

Causes of an inflammation can be:

x Microorganisms (→ A), such as
viruses, fungi, or parasites;
x Foreign bodies (foreign protein, e.g., pollen; asbestos or silicon crystals); or
x Tissue destruction with formation of tissue debris, for example, through mechanical dam-
age such as cuts, stabs, scratches or foreign bodies, chemical compounds such as acids or
alkalis, physical influences such as cold, heat, radiation (UV, X-rays, radioactivity), and en-
dogenous causes such as disintegrating tumor cells, extravascular blood, autoimmune reac-
tions (→ p. 56), or crystals of substances pre- cipitated in the body (uric acid, calcium oxa-
late, calcium phosphate, and cholesterol).

An acute inflammation expresses itself as a local reaction associated with the symptoms,
known since antiquity, of pain (dolor), swelling (tumor), reddening (rubor), and warmth (ca-
lor). In addition, there are general inflamma- tory reactions (acute-phase response; see be-
low).

Rapid activation of mast cells (in tissue) or their counterparts in blood, the basophil leuko-
cytes, or basophils, is an example of the occur- rence of a very strong acute inflammatory
re- action (→ A) on which especially type I hyper- sensitivity reactions are based (→ p. 52).
If the body has previously been in contact with an antigen (= allergen in cases of
hypersensitiv- ity), for example, with bee-poison protein, B cells will have been sensitized as
a reaction to it (cooperation with TH2 cells; → p. 47 , B4). The ensuing plasma cells produce
IgE that binds to the Fcε receptors of the mast cells. On renewed contact with the antigen this
is now bound to the antigen-specific Fab-ends of IgE. It seems to be important for further
reactions of the mast cells that the allergen is bound to several IgE molecules (antibody cross-
linking); large antigens that can repeatedly act antigenically with different molecular parts
(polyvalence) are especially effective (e.g., parasites with several bound haptens).

Cross-linking of the antibodies by the anti- gen sets free second messengers in the mast cell
(cGMP, inositol phosphate, Ca2+) that trig- ger a rapid degranulation of the mast cells, i.e.,
exocytosis of the inflammation mediators and chemokines stored within the granules
(hista- mine, interleukin 8[IL-8], eotaxin, neutrophilic chemotactic factor [NCF], etc.). Ca 2+
also acti- vates phospholipase A2 that splits off arachi- donic acid from the phospholipids in
the cell membrane. This is the starting substance for other important inflammation mediators,
namely prostaglandins (E2 etc.) and leuko- trienes (C4, D4 and E4; together also called slow
reacting substance of anaphylaxis [SRS- A], as well as B4). The ether phospholipid platelet
activating factor (PAF), another impor- tant inflammation and hemostatic mediator, is
liberated from the cell membrane of mast cells.