Human Physiology, 14th edition (2016)

The Immune System 501

Histamine and heparin, together with protease enzymes

important in inflammation, are stored in granules within the

mast cells. Either in an allergic reaction or as a normal physi-

ological response to pathogens, mast cells are stimulated to

degranulate. This term refers to the exocytosis of the granules,

which quickly release histamine into the extracellular fluid and

more slowly release the protease enzymes. With a time delay,

pathogens stimulate the mast cells to produce prostaglandins

and leukotrienes (chapter 11; see fig. 11.34) as well as other

pro-inflammatory cytokines. These include tumor necrosis

factor, which acts as a chemokine to recruit neutrophils to the

infected site.

Leukocytes within vessels in the inflamed area stick to the

endothelial cells of the vessels through interactions between

adhesion molecules on the two surfaces. The leukocytes can

then roll along the wall of the vessel toward particular chemi-

cals. As mentioned earlier, this movement, called chemotaxis,

is produced by molecules called chemokines. Complement

and intestinal mucosa. They are identified by their content of
heparin, a molecule that is medically important because of
its anticoagulant ability (chapter 13, section 13.2). However
mast cells are best known for their production of histamine,
a molecule that produces many of the symptoms of allergy
(section 15.6). Histamine binds to its H 1 histamine receptors
in the smooth muscle of bronchioles to stimulate bronchiolar
constriction (in asthma), but produces relaxation of the smooth
muscles in blood vessels (causing vasodilation). In addition,
histamine, serotonin, and other chemicals released by mast
cells and others during an inflammation cause the endothe-
lial cells of capillaries and postcapillary venules to contract
away from each other, creating gaps in the endothelium. This
increases the permeability of the capillaries to allow the escape
of more fluid and plasma proteins into the extracellular space,
producing a local edema. Gaps formed in the endothelium of
postcapillary venules also allow the extravasation of leuko-
cytes into the inflamed area. ( fig. 15.5 ).

Figure 15.5 The
events in a local
inflammation. Antigens on
the surface of bacterial cells
(1) bind to antibodies, which
coat the bacteria. This activates
complement and (2) promotes
phagocytosis by neutrophils
and macrophages. Activation of
complement also
(3) stimulates mast cells to
release histamine and other
mediators of inflammation,
including chemicals that promote
capillary permeability and
(4) extravasation (diapedesis)
of leukocytes, which invade the
inflamed site.

1

2

Epidermis

B lymphocyte

Phagocytic cell

(neutrophil)

Antibodies Antibody-coated

bacterium

Lysosome

Vacuole

Bacteria

Dermis

Dilation, increased Mast cell

permeability of capillary

Capillary

Activation of

complement

Release of

histamine

Extravasation

Phagocytic cell

Lysosomal

enzymes

4

3