04.inflammation 4-ChronicInflammation

Inflammation 4
Department of pathology
A 7 year old boy with fever and sore throat, on clinical examination,
was found to have purulent exudate covering his tonsillar area.
Which among the following mediators is most likely responsible for
accumulation of pus?
1. Complement C3b
2. Lymphotactin
3. RANTES
4. IL-8
5. bradykinin
• Which of the following is MOST responsible for the anti-
inflammatory activity of corticosteroids?
1. Release of TGF – beta from macrophages
2. Inhibition of Phospholipase A2
3. Induction of NOS (nitric oxide synthase)
4. Inhibition of cyclooxygenase
5. Inhibition of lipoxygenase
Acute Inflammation Morphological types
1. Serous inflammation
2. Fibrinous inflammation
3. Suppurative inflammation
4. Pseudomembranous inflammation
5. Catarrhal inflammation
6. Serosanguinous inflammation
Inflammation Serous Inflammation
Blister
This example of serous exudate
collection, a blister of the skin, occurs
after minor burns or friction.
Inflammation Fibrinous Inflammation
Here, the pericardial cavity has been

opened to reveal a fibrinous pericarditis
with strands of stringy pale fibrin
between visceral and parietal
pericardium (fibrinous exudate is rich in
fibrin). Fibrin may organise into fibrous
tissue giving raise to adhesive
pericarditis
Suppurative Inflammation
The abdominal cavity is opened at

autopsy here to reveal an extensive
purulent peritonitis that resulted from
rupture of the colon. The exudate is
Pus (purulent). It is thick, yellow fluid
rich in neutrophils
A purulent exudate is seen beneath the

meninges in the brain of this patient
with acute meningitis from
Streptococcus pneumoniae infection.
The exudate obscures the sulci.
Pseudomembranous Inflammation
This yellow-green exudate on the surface

of an inflamed, hyperemic (erythematous)
mucosa (bowel & throat) consists of many
neutrophils along with fibrin and
amorphous debris from dying cells. This
type of exudate forms a pseudomembrane
in Clostridium difficile caused colitis &
Diphtheria
Serosanguinous Catarrhal
Inflammation Inflammation
Here is an example of bilateral
pleural effusions. Note that the
fluid appears reddish, because
there has been hemorrhage into
the effusion. This is a
serosanguinous effusion.
Catarrh is the inflammation of the

mucous membrane, especially in
the nose and throat, accompanied
by increased production of mucus.
It is most commonly associated
with the common cold.
Abscess
(Localised collection of pus)

is the result of a Liquefactive necrosis of the
parechyma caused by pyogenic organism
resulting in the formation of one or more
cavities filled with pus (purulent exudate).
It has a central necrosis, rimmed by
neutrophils and surrounded by fibroblasts.
If pus collects within pleural cavity, gall
bladder, it is callled empyema
Carbuncles Cellulitis
Sometimes boils occur in clusters

called carbuncles. Although anyone
can develop, people who have
diabetes, a suppressed immune
system are at increased risk.
an infection of the skin and

underlying tissues caused most
commonly by group A
Streptococcus and
Staphylococcus aureus.
Ulcer
An ulcer is a local defect/discontinuity

of mucosal lining produced by
shedding of necrotic tissue. Superficial
ulcers are called erosions
Acute Inflammation Outcome
Inflammation Chronic
1. Inflammation of prolonged duration in which active inflammation,

tissue destruction and attempts at repair are going on
simultaneously
2. Although it may follow acute inflammation, chronic inflammation

frequently begins insidiously, as a low-grade, smoldering, often
asymptomatic response.
Chronic Inflammation Causes
1. Persistent infections
• Organisms of low toxicity (M. Tuberculosis, treponema,
viruses, fungi, parasites elicit delayed hypersensitivity and
sometimes cause granulomatous inflammation)
2. Prolonged exposure to potentially toxic agents, either exogenous
or endogenous
• Inanimate, non-degradable particles like silica; athersclerosis
3. Autoimmunity
Chronic Inflammation Morphological
1. Infiltration with mononuclear cells, which include macrophages,

lymphocytes, and plasma cells.
2. Tissue destruction, induced by the persistent offending agent or by

the inflammatory cells.
3. Attempts at healing by connective tissue replacement of damaged

tissue, accomplished by proliferation of small blood vessels
(angiogenesis) and, in particular, fibrosis
Mononuclear Phagocyte
Chronic Inflammation System
Functions of
Chronic Inflammation Macrophage
Mononuclear
Chronic Inflammation Phagocyte System
1. Monocytes appear at the site of injury within 48 hours

2. Recruitment of monocytes from circulation (chemotactic stimuli
from CHC chemokines, C5a, PDGF, fibronectin, TGFβ)
3. There is Local proliferation & Immobilisation of macrophage
4. In short-lived acute inflammation they disappear after irritant is
eliminated
5. In chronic inflammation they persist
Functions of
Chronic Inflammation Macrophage
• The products of activated

macrophages serve to eliminate
injurious agents such as microbes
and to initiate the process of repair,
and are responsible for much of the
tissue injury in chronic
inflammation.
• Tissue destruction is one of the

hallmarks of chronic inflammation.
Chronic Inflammation Other Cells
1. Lymphocytes:
• in immune reactions and some non-
immune inflammations
• T cells release factors that activate
macrophages, other T cells & B cells
Chronic Inflammation Other Cells
1. Plasma cells: derived from B cells;
seen in syphilis, many other non-
specific inflammations; produce Ab
against persistent Ag or damaged
tissue components
2. Eosinophils: in parasitic & allergic
inflammation; eotaxin is the
chemoattractant; MBP is toxic to
parasites
3. Mast cells: Have receptor for IgE;
so participate in type 1
hypersensitivity; release factors
that promote fibrosis
Chronic Inflammation Types
1. Granulomatous
2. Non-specific (perivascular interstitial)
Chronic Inflammation granulomatous
• A granuloma is a focus of chronic

inflammation consisting of a
microscopic aggregation of
macrophages that are transformed
into epithelium-like cells
surrounded by a collar of
mononuclear leukocytes, principally
lymphocytes and occasionally
plasma cells.
Chronic Inflammation Granulomatous
Granulomas are of two types:

1. Immune granuloma (also called
tubercles)
• Result of cell mediated immune
response (type 4
hypersensitivity)
2. Foreign body granuloma
• Incited by inert, non-degradable
foreign particles (talc, sutures
etc.)
Immune granulomas are of two

types:
1. Non-caseating granulomas (hard
tubercle)
• E.g., sarcoidosis
2. Caseating granulomas (soft
tubercle)
• E.g., tuberculosis
Chronic Inflammation Interstitial
Certain etiologic agents such as viruses

are more likely to lead to chronic
inflammation characterized by the
presence of the inflammatory
infiltrates in the interstitium (within
tissues mostly perivascular) without
being exudative (above surfaces or in
spaces) like acute inflammation.
Differences between Acute & Chronic Inflammation
Acute Chronic
Long (weeks to months)
Duration/Onset Short (days); Acute
Insidious
Specific (where immune
Specificity Nonspecific
response is activated)
Lymphocytes, plasma cells,
Inflammatory cells Neutrophils, macrophages
macrophages, fibroblasts
Active vasodilation, New vessel formation
Vascular changes
increased permeability (granulation tissue)
Exudate + –
Cardinal signs + –
Leucocytosis Neutrophilic Lymphocytic/monocytic

Exception
Typhoid is an example of acute

inflammation which induces
leucopenia with relative lymphocytosis
Local Clinical Effects of Acute And Chronic Inflammation
1.Loss of organ secretory / metabolic function

e.g. hepatitis, thyroiditis, pancreatitis,
2. Damage and Loss of vital functioning tissues causing organ failure

e.g. acute / chronic pneumonitis, hepatitis,
glomerulonephritis
3. Compression of vital organs

nerves, blood vessels, lymphatics
Local Clinical Effects of Acute And Chronic Inflammation
4. Interferences with normal mechanical function:

a. post-burn scarring over joints
b. scarring of articular joints in rheumatoid arthritis (RA)
c. adhesions in peritoneal cavity and pericardial cavity
5.Hemorrhage:
Ulcer
Damaged blood vessels
6. Obstruction of vital organ passages:

a- inflammatory exudate
B- fibrous tissue formation (scarring) leading to stricture formation
Inflammation Systemic effects
Elevated ESR: In presence of

acute phase proteins
(fibrinogen) erythrocytes
aggregate due to loss of their
negative charge with
Increased ESR
Leucocytosis: a direct effect

of IL-1 and IL-6 on bone
marrow neutrophil stores, is
the simplest indicator of
acute inflammation;

04.inflammation 4-ChronicInflammation

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Inflammation 4

Here, the pericardial cavity has been

The abdominal cavity is opened at

A purulent exudate is seen beneath the

This yellow-green exudate on the surface

Catarrh is the inflammation of the

(Localised collection of pus)

Sometimes boils occur in clusters

an infection of the skin and

An ulcer is a local defect/discontinuity

1. Inflammation of prolonged duration in which active inflammation,

2. Although it may follow acute inflammation, chronic inflammation

1. Infiltration with mononuclear cells, which include macrophages,

2. Tissue destruction, induced by the persistent offending agent or by

3. Attempts at healing by connective tissue replacement of damaged

1. Monocytes appear at the site of injury within 48 hours

• The products of activated

• Tissue destruction is one of the

• A granuloma is a focus of chronic

Granulomas are of two types:

Immune granulomas are of two

Certain etiologic agents such as viruses

Leucocytosis Neutrophilic Lymphocytic/monocytic

Typhoid is an example of acute

1.Loss of organ secretory / metabolic function

2. Damage and Loss of vital functioning tissues causing organ failure

3. Compression of vital organs

4. Interferences with normal mechanical function:

6. Obstruction of vital organ passages:

Elevated ESR: In presence of

Leucocytosis: a direct effect

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