THE INFLAMMATORY PROCESS

The Imflammatory
Process

1. Increased vaskular
permeability
2. Emigration of leukocytes
3. Phagocytosis of antigen
and debris
 ad.Increase Vascular Permeability

injury
Vasodilation Precapillary arterioles
vasoconstriction

Release of Realese of
Leukotrienes Histamin & Prostaglandin

Endothelial cells Vasodilation

contraction

Cardinal sign
Increasing capillary
permeability

Increase of Pushes fluid into

Hydrostatic pressure the tissue
The cardinal sign of
acute inflammation
The Arachidonic acid and roles in inflammation
ad.Emigration of Leukocytes
Emigrasi / diapedesis leukosit  proses perpindahan neutrophil
dari vaskuler kedalam jaringan radang melalui dinding vaskuler
(capillary endothelial)

vasodilation
Inflamed
tissue
Increased
permability

Chemotaxis : neutrophils eosinophils NK cells

1.Bacterial toxins
2.C5a complement
3.Degenerative
product of the 1.Production of 1. Hydrolase
inflamed tissue collagenase 2. Peroxidase
2.Phagocytosis
1. Recognizing virally
Inflammatory Infected cells
Break down dead tissue process 2.Opzonized microbes
Emigration of Leukocytes

Capillary
endothelial
 ad.Phagocytosis
Ingestion and destruction of
phatogens by leukocytes
 Mechanism of phagocytosis
Microbe
The small
microbe

Ingestion

Macrophages

Phagosome

Lysosome
Hydrolitic enzymes

Digestion of microbe
 Mechanism of phagocytosis
Neutrophils and macrophages
specialize in collagen and
extracellular matrix degradation
The large microbe

monocytes (macrophages) ingestion

neutrophils the neutrophil to

release its degradative
enzymes extracellularly.
produce digest protein structures:
lysozyme, neutral proteases,
collagenase, elastase, and acid
hydrolases

Peptide bonds are cleaved in the extracellular matrix

by collagenase, elastase, proteinase, and gelatinase
 Oxidizing agents, the most destructive of
the inflammatory cell products, are formed as
a result of the phagocyte oxidase enzyme
system on the membrane of the lysosome

Neutrophils  oxidizing agents

 oxygen radicals:
= superoxide (O2- ),
= hydrogen peroxide (H2O2)
= hydroxyl ions (OH")

Oxidizing agents directly attack cell

membranes and thereby increase permeability

Nitric oxide products may also be produced

by inducible nitric oxide synthase (iNOS) and function in
concert with oxygen radicals to attack microbial molecules
 acute inflammation can inhibitor of inflammatory
cause severe tissue damage damage is a antiprotease

Antiproteases are made in the liver and

circulate continuously in the blood stream

Neutrophils have a limited When phagocytosis is

capacity to phagocytose incomplete, a collection of
foreign and inflammatory dead neutrophils, bacteria,
debris and cellular debris, called
PUS, may form at the site

Macrophages are left with the job of removing spent

neutrophils and preparing the site for healing

A predominance of monocytes and macrophages in an

inflamed area signals the beginning of chronic inflammation.
INFLAMMATORY EXUDATES

Exudate is fluid that leaks out of blood vessels, combined with

neutrophils and the debris from phagocytosis. Exudates may vary
in composition, but all types have similar functions, including :
(1) transport of leukocytes and antibodies,
(2) dilution of toxins and irritating substances, and
(3) transport of the nutrients necessary for tissue repair.

Serous exudate is watery, has a low protein content,

accompanies mild inflammation. permeability of the blood
vessels is not greatly changed. As a result, only some protein
molecules escape from vessels

Fibrinous exudate is sticky and thick and may have to be removed

to allow healing; otherwise, scar tissue and adhesions may
develop. However, in some instances fibrinous exudate may be
beneficial. In the case of acute appendicitis, fibrinous exudate
may actually wall off and localize the infection and prevent its
spread.
Purulent exudate is called pus. Purulent exudate generally occurs in
severe inflammation accompanied by bacterial infection and is
primarily composed of neutrophils, protein, and tissue debris.
Large pockets of purulent exudate, called abscesses, must
generally be removed or drained for healing to take place.

Hemorrhagic exudate has a large component of red blood cells.

This type of exudate is usually present with the most severe
inflammation. Hemorrhagic exudate occurs with severe leakage
from blood vessels or after necrosis or breakdown of blood
vessels.
SYSTEMIC MANIFESTATIONS OF INFLAMMATION

Three macrophage-derived
cytokines: By raising the set point for body
= IL-1, temperature, these cytokines induce
= IL-6 conservation of heat through
= TNF-a vasoconstriction, as well as increased
heat production through shivering

Systemic responses include:

TNF-a and IL-1 act on the brain to:
= fever,
= Raise body temperature
= neutrophilia
= Induce sleep
= lethargy, and
= Suppress appetite
= muscle catabolism.

IL-1 is responsible for stimulating the

release of neutrophils from bone marrow
storage sites, thus producing neutrophilia

All three cytokines act on skeletal muscle to enhance protein

catabolism, which provides an available pool of amino acids for
efficient antibody production by plasma cells
Acute phase proteins
 cytokines
IL-1,
IL-6, the liver
TNF-a

release acute phase proteins

= C-reactive protein (CRP) complement clotting factors

= serum amyloid component
= protease inhibitors

controlling inflammation to prevent

excessive tissue damage
inflammation process &
lysis cells
Fibrinogen coats the surface of
red blood cells  aggregate
A blood test called the erythrocyte sedimentation rate (ESR,
"sed. rate") provides a simple measure of the level of
inflammation in an individual. Thus an elevated ESR indicates
the presence of inflammation in the body. The greater the
inflammation, the faster the red blood cells settle to the
bottom of a test tube and the higher the ESR. The ESR is a
nonspecific but clinically useful indicator of inflammation.
Serum CRP activity is also used as a nonspecific indicator of
inflammation in a manner similar to the ESR.
Chronic Inflammation Macrophages are essential
for wound healing because
of their phagocytic and
Macrophages debridement functions

proteases thromboplastin peptide growth factors

removing facilitate hemostasis and

foreign protein stimulate fibroblast angiogenic factor
from the wound activity

encourages the growth

Healing wound of new blood vessels
preparing

Prolonged inflammation  impair healing 

accumulation of macrophages, fibroblasts, and
collagen  a granuloma Fibrosis and scarring
 fibrous tissue.
WOUND HEALING

fibroblasts myofibroblasts. endothelial cells

angiogenic
Macrophages
connective tissue
= lactate
= growth factors develop capillary beds

collagen wound edge and tissue repair and

proteoglycans wound contraction. wound healing
fibronectin
contribute to
continuing edema
cellular growth

WOUND HEALING
 Wound remodeling

process of collagen deposition and lysis with debridement of

the wound edges.

Wound remodeling by fibroblasts, macrophages, neutrophils, and

eosinophils. During this phase the wound changes color from
bright red to pink to whitish. As long as a wound is pink, the
maturation phase is not completed.