Immunology of Inflammation - Slides

IMMUNOLOGY OF INFLAMMATION.
• Learning objectives.
• Types of inflammation
• Causes of inflammation
• Stimuli for inflammatory processes
• Cellular events- Leukocyte extravasation
and phagocytosis.
• Chemical mediators of inflammation.
• Termination of inflammatory response.
1
Introduction.
• In vascularized tissues, exogenous and
endogenous stimuli provoke a host of
response called inflammation.
• The unique feature of the inflammatory
process is the reaction of blood vessels,
leading to the accumulation of fluid and
leukocytes in extravascular tissues.
• Inflammatory response is closely intertwined
with the process of repair.
2
Thus:
• Inflammation serves to destroy, dilute, or wall
off the injurious agent, and it sets into
motion a series of events that try to heal and
reconstitute the damaged tissue.
• Inflammation is fundamentally a protective

response, the ultimate goal of which is to rid
the organism of both the initial causes of cell
injury (e.g., microbes, toxins) and the
consequences, of such injury (e.g., necrotic
cells).
3
NB: Inflammation and repair may be
potentially harmful, however:
Inflammatory reactions, for example,
underlie common chronic diseases, such
as rheumatoid arthritis, atherosclerosis,
and lung fibrosis, as well as life
threatening hypersensitivity reactions.
4
Phases of inflammatory response:
• Inflammatory response consists of two

components: a vascular reaction and a
cellular reaction.
• The circulating cells include neutrophils,
monocytes, eosinophils, lymphocytes,
basophils and platelets.
5
Inflammation is divided into:
• Acute inflammation - rapid in onset (seconds or

minutes) and is of relatively short duration.
• Its main characteristics are the exudation of fluid
and plasma proteins, and the emigration of
leukocytes, predominantly neutrophils.
• Chronic inflammation - is of longer duration and is

associated with the presence of lymphocytes and
macrophages, proliferation of blood vessels,
fibrosis, and tissue necrosis.
6
• The vascular and cellular reactions of both
acute and chronic inflammation are
mediated by chemical factors that are
derived from plasma proteins or cells, and
are produced in response to or activated
by the inflammatory stimulus.
7
Acute inflammation.
• Is a rapid response to an injurious agent

that serves to deliver mediators of host
defense- leukocytes and plasma proteins-
to the site of injury.
8
• Major components:
Alterations in vascular caliber that lead to an
increase in blood flow
Structural changes in the microvasculature that
permit plasma proteins and leukocytes to leave
the circulation
Emigration of the leukocytes from the
microcirculation, their accumulation in the focus of
injury, and their activation to eliminate the
offending agent.
9
Stimuli for acute inflammation.
• Varied and include, among others:
Infections (bacterial, viral, parasitic) and
microbial toxins
Trauma (blunt and penetrating)
Physical and chemical agents (thermal injury,
e.g. , burns or frostbite; irradiation, e.t.c).
Immune reactions (also called
hypersensitivity)
10
Homing and movement of cells from
peripheral blood into tissue during
inflammatory response.
11
Vascular changes:
• Increased vascular permeability (vascular
leakage):
Leading to the escape of a protein-rich
fluid (exudate) into the extravascular
tissue.
12
Elicited by :
histamine,
bradykinin,
leukotrienes (naturally produced eicosanoid
lipid mediators, which may be responsible for
the effects of an inflammatory response)
Cytokines (IL-1, TNF, IFN-gamma);
Many other chemical mediators.
13
Cellular events: leukocyte extravasation
and phagocytosis.
• Useful to deliver leukocytes to the site of
injury and to activate the leukocytes to
perform their normal functions in host
defense.
• Leukocytes ingest offending agents, kill
bacteria and other microbes, and get rid of
necrotic tissue and foreign substances.
14
However:
• A price paid for the defensive potency of

leukocytes is that they may induce tissue
damage and prolong inflammation, since
the leukocyte products that destroy
microbes and necrotic tissues can also
injure normal host tissue.
15
Leukocyte adhesion and transmigration.
• Are regulated largely by the binding of

complementary adhesion molecules on the
leukocyte and endothelial surfaces,
and
• chemical mediators- chemo attractants and
certain cytokines- affect these processes by
modulating the surface expression or avidity of
such adhesion molecules.
16
• The adhesion receptors involved belong to 4
molecular families:
• The selectins (e.g. E-selectin, mucin-like

glycoproteins- GlyCAM-1, CD34)
• The immunoglobulin superfamily (e.g. ICAM,
VCAM)
• The integrins
• Mucin-like glycoproteins (e.g. heparan sulfate)
17
18
Acute Inflammatory Response.
Cytokines produced Leukocytes move to Blood clotting occurs

periphery of blood Leukocyte extra
by Macrophages vasate at the site of in the micro vessels.
cause dilation of vessels as a result of
increased expression infection
small
blood vessels of adhesion
molecules
19
Symptoms of Inflammatory
response
Wheal Response
Pain
Redness
Heat
Swelling
20
Chronic inflammation.
• Macrophages-
Interferon gamma (IFN-gamma)
Tumor necrosis factor alpha (TNF-alpha)
21
Anti-inflammatory agents.
• Reduce Extravasation
- Anti-LFA antibodies
• Corticosteroids
- Immune-suppressive, induce apoptosis.
• Non-steroidal anti-inflammatory drugs
(NSAID)-
- Aspirin, ibuprofen, phenylbutazone,
acetameniophen.
22

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IMMUNOLOGY OF INFLAMMATION.

• Inflammation is fundamentally a protective

• Inflammatory response consists of two

• Acute inflammation - rapid in onset (seconds or

• Chronic inflammation - is of longer duration and is

• Is a rapid response to an injurious agent

• A price paid for the defensive potency of

• Are regulated largely by the binding of

• The selectins (e.g. E-selectin, mucin-like

Cytokines produced Leukocytes move to Blood clotting occurs

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