Chapter 3 Inflammation - Lecture1

Inflammation and Repair
Learning Objectives:
• 1. Describe the sequence of vascular changes in acute inflammation
(vasodilation, increased permeability) and their purpose.
• 2. Know the mechanisms of increased vascular permeability. Know

which vessels are affected in the immediate transient response.
• 3. Describe the steps involved in extravasation of leukocytes from the

blood to the tissues. Know the steps at which selectins and integrins
act.
• 4. Define the terms edema, transudate, and exudate.
• 5. Describe the meaning and utility of chemotaxis. Understand the

role that chemokines play in inflammation.
• 6. Describe the steps involved in phagocytosis and the role of IgG

and C3b as opsonins and receptors. Know the leukocyte receptors
for these opsonins. Understand the role that collectins play in
phagocytosis.
Learning Objectives:
• 7. Chemical mediators of inflammation are numerous). You should learn the
cellular sources and major effects of the mediators and, conversely, list the
most likely mediators of each of the steps of inflammation (There is no need to
memorize all the information.)
• 8. Compare and contrast acute vs chronic inflammation with respect to

causes, nature of the inflammatory response, and tissue changes.
• 9. Compare and contrast the clinical settings in which different types of

inflammatory cells (eg, neutrophils, eosinophils, monocyte-macrophages, and
lymphocytes) accumulate in tissues. Compare and contrast the contents of
neutrophil and eosinophil granules.
• 10. Describe the differences between the various cell types (ie, labile, stable,
and permanent cells) in terms of their regeneration potential. List examples of
each cell type.
• 11. Distinguish between fibrinous, purulent, and serous inflammation. Define

an abscess.
• 12. Describe the systemic manifestations of inflammation and their general

physiology, including fever, leukocyte left shift, and acute phase reactants.
Inflammation:
• Definition: The reaction of vascularized living
tissue to local injury.
• Inflammation serves to destroy, dilute or
isolate the injurious agent (microbes, toxins)
and eliminate the necrotic cells and tissues
arising as a consequence to such injury.
• It also starts a series of events which leads as
far as possible to the healing and
reconstitution of the damaged tissue.
Inflammation
• During repair, the injured tissue is replaced by:
 Regeneration of native parenchyma cells

 Filling of the defect by fibroblastic tissue or
both
• Inflammation and repair are protective

response, however they may induce harm e.g.,
anaphylactic reaction, rheumatoid arthritis,
atherosclerosis or pericarditis.
Components of Inflammation
Tissues and cells involved in inflammatory response:
The fluid and proteins of plasma, circulating cells, blood
vessels and connective tissue
• The circulating cells: neutrophils, monocytes,
eosinophils, lymphocytes, basophils, and platelets.
• The connective tissue cells are the mast cells, the
connective tissue fibroblasts, resident macrophages and
lymphocytes.
• The extracellular matrix, consists of the structural
fibrous proteins (collagen, elastin), adhesive
glycoproteins (fibronectin, laminin, nonfibrillar collagen,
tenascin, and others), and proteoglycans.
• The basement membrane is a specialized component
of the extracellular matrix consisting of adhesive
glycoproteins and proteoglycans.
The
connective
tissue cells
The circulating cells:
The
extracellular
matrix
Cellular components of inflammation
Inflammation
• Inflammation is divided into:
 Acute inflammation.
 Chronic inflammation.
Acute inflammation Chronic inflammation
• •Is rapid in onset (seconds or
is of longer duration
minutes)
• Is associated histologically with the presence of lymphocytes
• of relatively short duration,
and macrophages,
lasting the proliferation of blood vessels, fibrosis,
for minutes, several
and tissue
hours, necrosis.
or a few days
• • itsLess
mainuniform.
characteristics are
the exudation of fluid and
plasma proteins (edema)
and the emigration of
leukocytes, predominantly
neutrophils.
 The inflammatory response consists
of two main components:
 a vascular reaction
 a cellular reaction.
Chemical Mediators - Inflammation
• The vascular and cellular reactions of both acute and
chronic inflammation are mediated by chemical
factors that are derived from plasma proteins or cells
• These chemical factors are produced in response to

or activated by the inflammatory stimulus.
• Such mediators, acting singly, in combinations, or in

sequence, then amplify the inflammatory response
and influence its evolution.
• Necrotic cells or tissues themselves-whatever the

cause of cell death-can also trigger the elaboration of
inflammatory mediators e.g. acute inflammation after
myocardial infarction.
Inflammation -Termination
• Inflammation is terminated when the offending agent
is eliminated and the secreted mediators are broken
down or dissipated.
• In addition, there are active anti-inflammatory
mechanisms that serve to control the response and
prevent it from causing excessive damage to the
host.
Acute Inflammation
1. Acute inflammatory reactions are triggered by a
variety of stimuli:
• Infections (bacterial, viral, parasitic) and microbial toxins
• Trauma (blunt and penetrating)
• Physical and chemical agents (thermal injury, e.g., burns
or frostbite; irradiation; some environmental chemicals)
• Tissue necrosis (from any cause)
• Foreign bodies (splinters, dirt, sutures)
• Immune reactions (also called hypersensitivity reactions).
2. Acute inflammation has three major components:
• Vasodilation
• Vascular leakage and edema
• Leukocyte emigration (mostly PMNs)
Acute Inflammation
• Local clinical signs of acute inflammation :
 Heat (calor)
 Redness (rubor)
 Swelling 9tumor)
 Pain (dolor)
 Loss of function (functiolaesa)
Redness
Swelling
Swelling
Acute Inflammation
• 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.
• Acute inflammation has three major components:

(1) alterations in vascular caliber that lead to an increase in
blood flow
(2) structural changes in the microvasculature that permit
plasma proteins and leukocytes to leave the circulation
(increased vascular permeability)
(3) emigration of the leukocytes from the microcirculation,
their accumulation in the focus of injury, and their
activation to eliminate the offending agent

Chapter 3 Inflammation - Lecture1

Uploaded by

Copyright:

Available Formats

Chapter 3 Inflammation - Lecture1

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Chapter 3 Inflammation - Lecture1

Uploaded by

Copyright:

Available Formats

Inflammation and Repair

• 2. Know the mechanisms of increased vascular permeability. Know

• 3. Describe the steps involved in extravasation of leukocytes from the

• 5. Describe the meaning and utility of chemotaxis. Understand the

• 6. Describe the steps involved in phagocytosis and the role of IgG

• 8. Compare and contrast acute vs chronic inflammation with respect to

• 9. Compare and contrast the clinical settings in which different types of

• 11. Distinguish between fibrinous, purulent, and serous inflammation. Define

• 12. Describe the systemic manifestations of inflammation and their general

 Regeneration of native parenchyma cells

• Inflammation and repair are protective

The circulating cells:

• These chemical factors are produced in response to

• Such mediators, acting singly, in combinations, or in

• Necrotic cells or tissues themselves-whatever the

• Acute inflammation has three major components:

You might also like