INFLAMATION :

Cellular Process

Oleh:
dr. Rahma Triliana, S.Ked. M.Kes.
Block : Cellular Moleculer Biology
PPD UNISMA
Nopember 2008
 Definitions of
Inflammation
 It’s a part of Wound Healing process
 Protective respons induced by
cellular/tissue injury to;
1. minimize the threat to body by: diluting,
localising, destroying, & removing of insult or
injury
2. repairing damage
3. restoring normal function
 It‘s a dynamic vascular & cellular response
to insult or injury
 can be:
 beneficial & protective - if regulated
 injurious - if unregulated
WHEN CELLs EXPOSED TO
INJURY
 CAUSES
 microorganisms & toxins
 parasites
 chemical & biochemical damage
 physical damage:
 heat
 cold
 radiation
 trauma -electrical -mechanical
 immunologic: types I, III, IV
hypersensitivity
 SIGN
Complex Reactions
vascular
immunological
cellular

Clinical Signs
Redness/Rubor
Swelling/Tumor
Heat/Kalor
Pain/Dolor
loss of function/Functiolesa
 TYPES
ACUTE CHRONIC
Causative Pathogens, Injured Persistant inflam e.c. non
Tissue degradable pathogens,
foreign bodies,
Major Macrophages (as autoimmune
Mononuclear
Cells APC), Neutrophils (makrophages,
Involved lymphocytes, plasma
Primary Vasoactive Amines, cells),
IFN-γ &Fibroblast
other Cytokines,
Mediators eucosanoids Growth factors, ROS,
Hydrolytic Enzymes
Onset Immediate Delayed
Duration Few Days Up tp Months or years
Outcome Healing, Abcess Tissue destruction,
s Form., Chronic Fibrosis
 Mediated by:
1. Cellular products/cell derived
mediators:
 vasoactive amines: histamine, 5-
hydroxytryptamine
 mast cells, basophils & platelets
 leads to vasodilatation & increased vascular permeability  

 Cytokines & Chemokines (from macrophages &

lymphocytes)
 polypeptides leads to increased vascular permeability &
dilatation
 regulate cellular activity in inflammation
 
 leukocyte products (enzymes & O2 radicals)
 proteinases leads to degradation of membranes. & collagen
 also chemotaxis
 H2O2, O2-, OH. -highly destructive

 products of arachadonic acid metabolism

(eicosanoids)
EUCOSANOID
FORMATION
 Mediated by…..

2. Plasma components/derived
Mediators:

 kinins (e.g. brady kinin)

 protease-activated plasma proteins
 potent vasodilators, increased vasc. permeability & induce
pain
 
 clotting & fibrinolysis system (fibrinopeptides)
 e.g. fibrinogen, fibrin, thrombin (coagulation system),
plasmin (fibrinolysis system), F-XII/Hageman Factor (active
by kinin, fibrinolysis & coagulation system)
 chemotactic factors & increased vasc. permeability
 
 complement cascade
 protease-activated plasma proteins
 mediate lytic destruction of cells
 chemotaxis, histamine release, increased vascular
C C
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EVENTS/STEPS
IN
INFLAMMATION
 SEQUENCE
Clinical
Event Mechanism
Response
1)
- release of vasoactive substances from REDNESS &
Changes in
damaged & aggregating cells HEAT
Blood Flow
2)
Permeability - contraction of lining cells
changes
- widening of endothelial junctions SWELLING
- fluid leakage (edema) PAIN
-sensory nerve irritation

3) - local occlution of blood in capillaries &

Hemostasis venules LOSS OF
- congestion FUNCTION
decreased blood flow leads to hypoxia
 Sequence….

Clinical
Event Mechanism
Response
• Chemotaxis:
• Migration of WBC to area (neutrophils
•mononuclear cells) -escape from vessels

4) • Phagocytosis:
WBC responses • WBCs indentify, attack, ingest & dispose
PAIN
-Chemotaxis of foreign matter
-Phagocytosis • enzymes, O2 radicals, inflam. Mediators
- removal of noxious agent, tissue debris &
fibrin
•leads to further tissue damage
5) • connective (scar) tissue formation
LOSS OF
Repair and • growth of new blood vessels
FUNCTION
Regeneration • replacement of destroyed cells
WBC RESPONSES
NFLAMMATION CAN BE GIVE LOCAL & SYSTEMIC RESPONS
 SYSTEMIC RESPONSES
 Release acute phase proteins (C-reactive
proteins, serum Amyloid A & P,
Vasopressin & glucocorticoids)
 Fever
 Increase Blood Pressure
 Decrease sweating
 Malaise
 Loss Of Appetite
 Somnolence
 Increase Leucocyte numbers/count
(leukocytosis), some can decrease
(leukopenia)
 HARMFUL
POTENTIALS
Response Examples
- Altered blood supply - Anoxia, infarcts, ischemia,
- Space occupying shock
lesions - Edema in lungs, abscesses
- Further tissue damage - Inflam. mediators, Cytolysis,
- Altered kinetic function WBC enzymes, free radicals
- Altered metabolic - Arthritis, arteriosclerosis
functions - Pyrexia, secretion
- Pain
Involved in pathogenesis of- Disuse
:
Allergic reactions/Hypersensitivities disorder, myopathies,
immune disorders (autoimune diseases), cancer,
atherosclerosis (CHD, Stroke), other degeneratives
diseases,

armful effects necessitate therapeutic interventi

Inflamation in time can resolved in
-Chronic Inflammation  Inflammation With Chronic
Sign (Inflammation with partial healing)
-Repair/Healing  wound Healing
-Resolution  Rehabilitation/proliferation back to N
state
 Progress of Wound
-Bleeding/cell damage after injury (within hours)
-Inflammation process  5 Cardinal sign of Inflammation (within 1 –
7 Day)
-Proliferation  Cell & tissue repair process begin (Days – Weeks)
-Remodelling  Tissue remodelling & getting back to function
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