The Immune System: Innate and Adaptive Body Defenses
neutrophils encounter these CAMs, they slow and roll along
the surface, eventually achieving an initial foothold. When
activated by inﬂammatory chemicals, CAMs on neutrophils
bind tightly to endothelial cells.
refers to this
phenomenon of phagocytes clinging to the inner walls (mar-
gins) of the capillaries and postcapillary venules.
Continued chemical signaling prompts the
neutrophils to ﬂatten and squeeze between the endothelial
cells of the capillary walls—a process called
Inﬂammatory chemicals act as homing devices,
or more precisely
. Neutrophils and other
WBCs migrate up the gradient of chemotactic agents to the
site of injury (positive
). Within an hour aFer the
inﬂammatory response has begun, neutrophils have collected
at the site and are devouring any foreign material present.
As the body’s counterattack continues, monocytes follow neu-
trophils into the injured area. Monocytes are fairly poor phago-
cytes, but within 12 hours of leaving the blood and entering the
tissues, they swell and develop large numbers of lysosomes, be-
coming macrophages with insatiable appetites. Tese late-arriving
macrophages replace the neutrophils on the battleﬁeld.
Macrophages are the central actors in the ﬁnal disposal of
cell debris as an acute inﬂammation subsides, and they pre-
dominate at sites of prolonged, or
, inﬂammation. Te
ultimate goal of an inﬂammatory response is to clear the in-
jured area of pathogens, dead tissue cells, and any other debris
delivers important proteins such as complement and clotting
factors to the interstitial ﬂuid (±igure 21.3).
Te clotting factors form a gel-like ﬁbrin mesh (a clot) that
acts as a scaﬀold for permanent repair. Te mesh also isolates
the injured area and prevents bacteria and other harmful agents
from spreading. Walling oﬀ the injured area is such an impor-
tant defense strategy that some bacteria (such as
have evolved enzymes that break down the clot, allowing them
to invade surrounding tissues.
Soon aFer inﬂammation begins, phagocytes ﬂood the dam-
aged area. Neutrophils lead, followed by macrophages. If path-
ogens provoked the inﬂammation, a group of plasma proteins
known as complement is activated and elements of adaptive
immunity (lymphocytes and antibodies) also arrive at the
illustrates the four steps in which
phagocytes are mobilized to inﬁltrate the injured site.
Injured cells release chemicals called
. In response, neutrophils enter
blood from red bone marrow and within a few hours, the
number of neutrophils in blood increases four- to ﬁve-
the increase in white blood cells
(WBCs), is characteristic of inﬂammation.
Inﬂamed endothelial cells sprout cell adhe-
sion molecules (CAMs) that signal “this is the place.” As
blood from bone
to capillary wall.
and squeeze out of
site act as