627
CHAPTER SIXTEEN
Lymphatic System and Immunity
tors. Most infl ammation is a tissue response to pathogen inva-
sion, but physical factors (heat, ultraviolet light) or chemical
factors (acids, bases) can also cause it.
White blood cells accumulate at the sites of infl amma-
tion, where some of them help control pathogens by phago-
cytosis. Neutrophils are the F
rst to arrive at the site, followed
by monocytes. Monocytes pass through capillary walls (dia-
pedesis), becoming macrophages that remove pathogens
from surrounding tissues. In bacterial infections, the result-
ing mass of white blood cells, bacterial cells, and damaged
tissue may form a thick fl
uid called
pus.
Tissue fl
uids (exudate) also collect in infl
amed tissues.
These fluids contain fibrinogen and other clotting factors
that may stimulate formation of a network of F brin threads
in the affected region. Later, F
broblasts arrive and secrete
F
bers around the area, enclosing it in a sac of connective
tissue. This walling off of the infected area helps inhibit the
spread of pathogens and toxins to adjacent tissues.
Once an infection is controlled, phagocytic cells remove
dead cells and other debris from the site of infl ammation.
Cell division replaces lost cells.
Table 16.2
summarizes the
process of infl
ammation.
Phagocytosis
Phagocytosis
(fag
o-si-to
sis) removes foreign particles from
the lymph as it moves from the interstitial spaces to the blood-
stream. Phagocytes in the blood vessels and in the tissues of
the spleen, liver, or bone marrow usually remove particles
that reach the blood. Recall from chapter 14 (p. 533) that the
most active phagocytic cells of the blood are
neutrophils
and
monocytes.
Chemicals released from injured tissues attract
these cells (chemotaxis). Neutrophils engulf and digest
smaller particles; monocytes phagocytize larger ones.
Monocytes that leave the blood become macrophages,
which may be
free
or
F
xed
in various tissues including lymph
nodes, the spleen, the liver, and the lungs, or attached to the
inner walls of blood and lymphatic vessels. A macrophage
can engulf up to 100 bacteria, compared to the twenty or
so bacteria that a neutrophil can engulf. Monocytes, mac-
rophages, and neutrophils constitute the
mononuclear
phagocytic system
(reticuloendothelial system).
intestinal epithelium, the urogenital tract, the kidneys, and
the skin. Recognition of a nonself cell surface or viral par-
ticle triggers the expression of genes that encode defensins.
Some defensins make holes in bacterial cell walls and mem-
branes, crippling the microbes.
Collectins
are proteins that
provide broad protection against bacteria, yeasts, and some
viruses. These proteins home in on slight differences in the
structures and arrangements of sugars that protrude from the
surfaces of pathogens. Collectins detect not only the sugar
molecules, but the pattern in which they are clustered, grab-
bing on much like velcro clings to fabric, thus making the
pathogen more easily phagocytized.
Complement
(kom
ple
˘-ment) is a group of proteins
(complement system), in plasma and other body fl uids, that
interact in a series of reactions or cascade. Complement acti-
vation can rapidly occur by the
classical pathway
when a
complement protein binds to an antibody attached to its spe-
ciF c antigen (discussed later in this chapter, p. 636), or more
slowly by the
alternative pathway
triggered by exposure to
foreign antigens, in the absence of antibodies. Activation of
complement stimulates infl
ammation, attracts phagocytes,
and enhances phagocytosis.
Natural Killer (NK) Cells
Natural killer (NK)
cells are a small population of lympho-
cytes that are distinctly different from the lymphocytes that
provide adaptive defense mechanisms. NK cells defend the
body against various viruses and cancer cells by secreting
cytolytic (“cell-cutting”) substances called
perforins
that
lyse the cell membrane, destroying the infected cell. NK cells
also secrete chemicals that enhance infl
ammation.
Infl
ammation
Inflammation
produces localized redness, swelling, heat,
and pain. The redness is a result of blood vessel dilation that
increases blood fl ow and volume in affected tissues (hyper-
emia). This effect, coupled with an increase in permeability of
nearby capillaries and subsequent leakage of protein-rich fl uid
into tissue spaces, swells tissues (edema). The heat comes as
blood enters from deeper body parts, which are warmer than
the surface. Pain results from stimulation of nearby pain recep-
TABLE
16.2
|
Major Actions of an InF
ammation Response
Action
Result
Blood vessels dilate. Capillary permeability increases and f
uid leaks into
tissue spaces.
Tissues become red, swollen, warm, and painFul.
White blood cells invade the region.
Pus may Form as white blood cells, bacterial cells, and cellular debris accumulate.
Tissue f
uids containing clotting Factors seep into the area.
A clot containing threads oF ±
brin may Form.
²ibroblasts arrive.
A connective tissue sac may Form around the injured tissues.
Phagocytes are active.
Bacteria, dead cells, and other debris are removed.
Cells divide.
Newly Formed cells replace injured ones.
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