Chapter 21
The Immune System: Innate and Adaptive Body Defenses
767
21
fluid. Inflammatory chemicals are released by injured or stressed
tissue cells, and immune cells. Tey can also be formed from
proteins circulating in the blood. For example,
mast cells
, a key
component of the inflammatory response, release the potent
inflammatory chemical
histamine
(his
9
tah-mēn).
Macrophages (and cells of certain boundary tissues such as
epithelial cells lining the gastrointestinal and respiratory tracts)
have special membrane receptors that allow them to recognize
invaders and sound a chemical alarm. Tese surface membrane
receptors, called
Toll-like receptors (TLRs)
, play a central role
in triggering immune responses. Tere are 11 types of human
±LRs, each recognizing a particular class of attacking microbe.
For example, one type responds to a glycolipid in cell walls of the
tuberculosis bacterium and another to a component of gram-
negative bacteria such as
Salmonella
. Once activated, a ±LR
triggers the release of inflammatory chemicals called
cytokines
.
Other inflammatory chemicals include
kinins
(ki
9
ninz),
prostaglandins
(pros
0
tah-glan
9
dinz), and
complement
. All
inflammatory chemicals dilate local arterioles and make local
capillaries leakier, as we discuss next. In addition, many attract
leukocytes to the injured area and some have individual inflam-
matory roles as well
(Table 21.1)
.
Vasodilation and Increased Vascular Permeability
Vasodilation accounts for two of the cardinal signs of inflam-
mation. Te
redness
and
heat
of an inflamed region are both due
to local
hyperemia
(congestion with blood) that occurs when
local arterioles dilate.
± cells (described fully on p. 789). NK cells also secrete potent
chemicals that enhance the inflammatory response.
Inflammation: Tissue Response to Injury
Describe the inflammatory process. Identify several
inflammatory chemicals and indicate their specific roles.
Te
inflammatory response
is triggered whenever body tissues
are injured by physical trauma (a blow), intense heat, irritating
chemicals, or infection by viruses, fungi, or bacteria. Te in-
flammatory response has several beneficial effects. It:
Prevents the spread of damaging agents to nearby tissues
Disposes of cell debris and pathogens
Alerts the adaptive immune system
Sets the stage for repair
Te four
cardinal signs
of short-term, or acute, inflammation
are
redness, heat
(
inflam
5
set on fire),
swelling
, and
pain
. Some
authorities consider
impaired function
to be a fi²h cardinal sign.
For instance, movement in an inflamed joint may be hampered
temporarily, forcing it to rest, which aids healing.
Figure 21.3
summarizes the inflammatory process and shows how these
cardinal signs come about.
Inflammatory Chemical Release
Te inflammatory process begins with a chemical “alarm”—a
flood of inflammatory chemicals released into the extracellular
Lysosome
Phagosome
(phagocytic
vesicle)
Acid
hydrolase
enzymes
(a) A macrophage (purple) uses its cytoplasmic extensions
to pull rod-shaped bacteria (green) toward it.
Scanning
electron micrograph (4800
m
).
(b) Events of phagocytosis.
1
Phagocyte adheres
to pathogens or debris.
2
Phagocyte forms
pseudopods that
eventually engulf the
particles, forming a
phagosome.
3
Lysosome fuses with
the phagocytic vesicle,
forming a phagolysosome
4
Lysosomal enzymes
digest the particles,
leaving a residual body.
5
Exocytosis of the
vesicle removes
indigestible and
residual material.
Innate defenses
Internal defenses
Figure 21.2
Phagocytosis.
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