- Inflammation is the body's protective response to injury or infection that involves increased blood flow, immune cell activity, and release of chemical mediators. It has both acute and chronic forms. - The cardinal signs of inflammation are redness, heat, swelling, pain, and loss of function. It involves vascular changes like increased permeability and leukocyte emigration from blood vessels. - Leukocytes like neutrophils, macrophages, and lymphocytes are involved. Chemical mediators regulate the inflammatory response. Acute inflammation typically resolves in a few days while chronic inflammation persists long-term.

1. Inflammation-1
"Opportunities are usually
disguised by hard work, so
most people don't recognize
them."
- Ann Landers
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2. Inflammation-2
INFLAMMATI0N
Dr. SHAHILA JALEEL
Histopathology
SZH,Lahore
Shashi-Mar 2000

3. Introduction:
“Inflame” – to set fire.
 Inflammation is “dynamic
response of vascularised tissue to
injury.”
 Is a protective response.
 Serves to bring defense & healing
mechanisms to the site of injury.

4. INTROD……….
 Injurious stimuli cause a protective
vascular connective tissue reaction
called “inflammation”
• Dilute
• Destroy
• Isolate
• Initiate repair
 Acute and chronic forms

6. Lewis Triple Response:
 Flush: capillary dilatation.
 Flare: arteriolar dilatation.
 Weal: exudation, edema.

7. Gastric Ulcer:

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Laryngitis:
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9. Acute Enteritis:

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Pneumonia
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Cardinal Signs of Inflammation
 Rubor : Redness – Hyperaemia.
 Calor : Warm – Hyperaemia.
 Dolor : Pain – Nerve, Chemical
med.
 Tumor: Swelling – Exudation
 Loss of Function:
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12. The 5 Cardinal Signs of
Heat Redness Swelling Pain Loss Of Func.

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Inflammation
Two main components:
vascular reaction
cellular reaction
Two main types:
acute
chronic
Chemical mediators
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Cells of inflammation
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15. Circulating cells

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22. Connective tissue matrix
 Made up of :
 A)collagen fibers
 B)elastic fibers
 C)glycoproteins
 D)proteoglycans

23. Connective tissue cells

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Acute Inflammation - Mechanism
1.Alterations in
vascular calibre
leading to
increased blood
flow
2.Microvasculature
structural changes
3.Leukocyte
emigration
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Vascular changes
 A Inconstant transient
vasoconstriction of arterioles for few
seconds followed by vasodilation
Accounts for warmth and redness
Opens microvascular beds
 Increased intravascular pressure
causes an early transudate (protein-
poor filtrate of plasma) into
interstitium (vascular permeability
still not increased yet) DR EJAZ WARIS

30.  Vascular permeability (leakiness)
commences
Transudate gives way to exudate
(protein-rich)
Increases interstitial osmotic pressure
contributing to edema (water and ions)
 slowing of circulation (increased
permeability of the vasculature)
 stasis
 Leukocyte migration

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Vascular changes continued
 B)increased vascular permeability
vascular leakage leading to escape of
protein rich fluid into the interstitium is
the hall mark of acute inflammation
exudate
transudate
edema
pus
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32.  An exudate is an extravascular fluid that
has a
 high protein concentration
 cellular debris
 high specific gravity.
 Its presence implies an increase in the normal
permeability of small blood vessels in an area of
injury .
 A transudate is a fluid with
 low protein content (most of which is albumin)
 little or no cellular material
 low specific gravity
 It is essentially an ultrafiltrate of blood plasma that
results from osmotic or hydrostatic imbalance across
the vessel wall without an increase in vascular
permeability

33.  Edema denotes an excess of fluid
in the interstitial tissue or serous
cavities; it can be either an
exudate or a transudate.
 Pus, a purulent exudate, is an
inflammatory exudate rich in
leukocytes (mostly neutrophils),
the debris of dead cells and, in
many cases, microbes.

36.  IMMEDIATE TRANSIENT RESPONSE – RESPONSE
TO
MINOR INJURY
 IMMEDIATE SUSTAINED RESPONSE – RESPONSE
TO
MORE SERIOUS INJURY, CONTINUES FOR
SEVERAL
DAYS, DAMAGE TO VESSELS
 DELAYED RESPONSE – INCREASES IN CAPILLARY
PERMEABILITY, DELAYED 4-24 HR, RADIATION
INJURIES, SUNBURN

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How does endothelium becomes
leaky in inflammation?
 1)formation of endothelial gaps in
venules
 2)cytoskeletal reorganization
 3)increased transcytosis
 4)direct endothelial injury
 5)leukocyte dependent injury
 6)delayed prolonged leakage
 7)leakage from new blood vessels
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Mechanism of Inflammation:
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Leukocyte emigration/extravasation
 Sequence of events in the journey of
leukocytes from the lumen to the
interstitial tissue
 Margination
 Pavementing
 Rolling
 Adhesion
 Transmigration/diapedesis
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42. Adhesion molecules
 Play an important role in acute
inflammation
 4 families
 Family no 1: Selectins
E-selectin,P-selectin,L-selectin
Family no 2:Ig-family adhesion
proteins
ICAM-I,ICAM-II,PECAM-I,VCAM-I

43. Adhesion molecules
Family no 3:Integrins
LFA
MAC-1
VLA-4
Family no 4:Mucin like glycoproteins
CD-34
Glycam-1

44. Margination and Rolling
 Early rolling adhesion mediated by
selectin family:
• E-selectin (endothelium), P-selectin
(platelets, endothelium), L-selectin
(leukocytes) bind other surface
molecules (i.e.,CD34, Sialyl-Lewis X-
modified GP) that are upregulated on
endothelium by cytokines (TNF, IL-1) at
injury sites

45. Adhesion
 Rolling comes to a stop and adhesion
results
 Other sets of adhesion molecules
participate:
• Endothelial: ICAM-1, VCAM-1
• Leukocyte: LFA-1, Mac-1, VLA-4
(ICAM-1 binds LFA-1/Mac-1, VCAM-1 binds VLA-
4)
 Ordinarily down-regulated or in an inactive
conformation, but inflammation alters this

46. Transmigration (diapedesis)
 Occurs after firm adhesion within the
systemic venules and pulmonary
capillaries via PECAM –1 (CD31)
 Must then cross basement
membrane
• Collagenases
• Integrins

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Neutrophil Margination
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Vascular changes
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Pneumonia - Exudation
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53. "Each time you are honest and conduct
yourself with honesty, a success force will
drive you toward greater success. Each
time you lie, even with a little white lie,
there are strong forces pushing you
toward failure."