Chapter 18
The sequence of local events in a typical nonspecifi c
infl ammatory response to a bacterial infection—one caused,
for example, by a cut with a bacteria-covered knife—is sum-
marized in
Table 18–3
. The familiar signs of tissue injury and
infl ammation are local redness, swelling, heat, and pain.
The events of infl ammation that underlie these signs are
induced and regulated by a large number of chemical media-
tors, some of which are summarized for reference in
(not all of these will be described in this chapter). Note
in this table that some of these mediators are cytokines. Any
given event of infl ammation, such as vasodilation, may be
induced by multiple mediators. Moreover, any given media-
tor may induce more than one event. Based on their origins,
the mediators fall into two general categories: (1) peptides
(kinins, for example) generated in the infected area by enzy-
matic actions on proteins that circulate in the plasma; and
(2) substances secreted into the extracellular fl uid from cells
that either already exist in the infected area (injured cells or
mast cells, for example) or enter it during infl
ammation (neu-
trophils, for example).
Let us now go step by step through the process summa-
rized in Table 18–3, assuming that the bacterial infection in
our example is localized to the tissue just beneath the skin. If
the invading bacteria enter the blood or lymph, then similar
infl ammatory responses would take place in any other tissue or
organ the blood-borne or lymph-borne microorganisms reach.
Vasodilation and Increased Permeability to Protein
A variety of chemical mediators dilate most of the microcircu-
lation vessels in an infected and/or damaged area. The medi-
ators also cause the local capillaries and venules to become
permeable to proteins by inducing their endothelial cells to
contract, opening spaces between them through which the
proteins can move.
The adaptive value of these vascular changes is two-
fold: (1) the increased blood fl ow to the infl
amed area (which
accounts for the redness and heat) increases the delivery of
proteins and leukocytes; and (2) the increased permeability
to protein ensures that the plasma proteins that participate in
infl ammation—many of which are normally restrained by the
intact endothelium—can gain entry to the interstitial fl
Table 18–2
Features of Selected* Cytokines
Target Cells
Major Functions
Interleukin 1, tumor
necrosis factor, and
interleukin 6
Antigen-presenting cells
such as macrophages
Helper T cells; certain brain
cells; numerous systemic
Stimulate IL-2 secretion and IL-2 receptor
expression; induce fever; stimulate systemic
responses to infl ammation, infection, and injury
Interleukin 2
Most immune cells
Helper T cells; cytotoxic T
cells; NK cells; B cells
Stimulate proliferation
Promote conversion to plasma cells
Most cell types
Most cell types
Stimulate cells to produce antiviral proteins
(nonspecifi c response)
NK cells and activated
helper T cells
NK cells and macrophages
Stimulate proliferation and secretion of cytotoxic
Damaged cells, including
endothelial cells
Neutrophils and other
Facilitate accumulation of leukocytes at sites of
injury and infl
Bone marrow
Stimulate proliferation of neutrophils and
This list is not meant to be exhaustive. There are >100 known cytokines.
Table 18–3
Sequence of Events in a Nonspecifi
Local Infl ammatory Response to
1. Entry of bacteria into tissue; injury to tissues causes release
of chemicals to initiate the following events
2. Vasodilation of the microcirculation in the infected area,
leading to increased blood fl ow
3. Large increase in protein permeability of the capillaries
and venules in the infected area, with resulting diffusion of
protein and fi ltration of fl uid into the interstitial fl
4. Chemotaxis: Movement of leukocytes from the venules into
the interstitial fl uid of the infected area
5. Destruction of bacteria in the tissue either through
phagocytosis or by other mechanisms
6. Tissue repair
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