Maintenance of the Body
Te respiratory tract mucosae also have structural modifi-
cations that counteract potential invaders. ±iny mucus-coated
hairs inside the nose trap inhaled particles, and cilia on the mu-
cosa of the upper respiratory tract sweep dust- and bacteria-
laden mucus toward the mouth, preventing it from entering the
lower respiratory passages, where the warm, moist environment
provides an ideal site for bacterial growth.
Although the surface barriers are quite effective, they are
breached by everyday nicks and cuts, for example, when you
brush your teeth or shave. When this happens and microorgan-
isms invade deeper tissues, your
innate defenses—the
second line of defense—come into play.
Check Your Understanding
What distinguishes the innate defense system from the
adaptive defense system?
What is the first line of defense against disease?
For answers, see Appendix H.
Internal Innate Defenses:
Cells and Chemicals
Explain the importance of phagocytosis and natural killer
cells in innate body defense.
Te body uses an enormous number of nonspecific cellular and
chemical means to protect itself, including phagocytes, natural
killer cells, antimicrobial proteins, and fever. Te inflamma-
tory response enlists macrophages, mast cells, all types of white
blood cells, and dozens of chemicals that kill pathogens and
help repair tissue. Tese protective tactics identify potentially
harmful substances by recognizing (binding tightly to) surface
carbohydrates present on infectious organisms (bacteria, vi-
ruses, and fungi) but not on human cells.
Pathogens that get through the skin or mucosae into the
underlying connective tissue are confronted by
, the most abundant type of white
blood cell, become phagocytic on encountering infectious
material in the tissues. However, the most voracious phago-
cytes are
(“big eaters”), which derive from white
blood cells called
that leave the bloodstream, en-
ter the tissues, and develop into macrophages.
Free macrophages
wander throughout the tissue spaces in
search of cellular debris or “foreign invaders.”
Fixed macro-
, like
stellate macrophages
in the liver, are permanent
residents of particular organs. Whatever their mobility, all mac-
rophages are similar structurally and functionally.
A phagocyte engulfs particulate matter much the way an
amoeba ingests a food particle. Flowing cytoplasmic extensions
bind to the particle and then pull it inside, enclosed within a
membrane-lined vesicle
(Figure 21.2a)
. Te resulting
then fuses with a
to form a
in Figure 21.2b).
Phagocytic attempts are not always successful. In order for a
phagocyte to ingest a pathogen, the phagocyte must first
or cling to that pathogen, a feat made possible by recognizing the
pathogen’s carbohydrate “signature.” Many bacteria have external
capsules that conceal their carbohydrate signatures, allowing them
to elude capture because phagocytes cannot bind to them.
Our immune systems get around this problem by coating
pathogens with
. Opsonins are complement pro-
teins (discussed shortly) or antibodies that provide “handles”
to which phagocyte receptors can bind. Any pathogen can be
coated with opsonins, a process called
(“to make
tasty”), which greatly accelerates phagocytosis of that pathogen.
Generally, neutrophils and macrophages kill ingested prey
by acidifying the phagolysosome and digesting its contents
with lysosomal enzymes. However, some pathogens such as
the tuberculosis bacillus and certain parasites are resistant to
lysosomal enzymes and can even multiply within the phagoly-
sosome. In this case, other immune cells called helper ± cells
release chemicals that stimulate the macrophage, activating ad-
ditional enzymes that produce a lethal
respiratory burst
. Te
respiratory burst promotes killing of pathogens by:
Liberating a deluge of highly destructive free radicals (in-
cluding superoxide)
Producing oxidizing chemicals (H
and a substance iden-
tical to household bleach)
Increasing the phagolysosome’s pH and osmolarity, which acti-
vates other protein-digesting enzymes that digest the invader
Neutrophils also pierce the pathogen’s membrane by using
, the antimicrobial peptides we mentioned earlier.
When phagocytes are unable to ingest their targets (because of
size, for example), they can release their toxic chemicals into the
extracellular fluid. Whether killing ingested or extracellular targets,
neutrophils rapidly destroy themselves in the process, whereas
macrophages are more robust and can go on to kill another day.
Natural Killer (NK) Cells
Natural killer (NK) cells
, which “police” the body in blood and
lymph, are a unique group of defensive cells that can lyse and
kill cancer cells and virus-infected body cells before the adaptive
immune system is activated. Sometimes called the “pit bulls” of
the defense system, NK cells are part of a small group of
granular lymphocytes
Unlike lymphocytes of the adaptive immune system, which
only recognize and react against
virus-infected or tumor
cells, NK cells are far less picky. Tey can eliminate a variety of
infected or cancerous cells by detecting general abnormalities such
as the lack of “self” cell-surface proteins called MHC, described on
p. 774. Te name “natural” killer cells reflects their nonspecificity.
NK cells are not phagocytic. Tey kill by directly contacting
the target cell, inducing it to undergo apoptosis (programmed
cell death). Tis is the same killing method used by cytotoxic
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