中國醫(yī)科大學病理學外文翻譯課件6

we

saw

how

various

exogenous

and

endogenous

stimulican

cause

cell

injury.Invascularized

tissues,

these

same

stimulialso

provoke

a

host

response

called

inflammation.

A

local

physiological

response

to

tissue

injury.a

manifestation

of

disease.Chapter

4.

InflammationZhao

YueInflammation

is

a

complexreaction

to

injurious

agents

such

as

microbes

and

damaged,

usually

necrotic,

cells

that

consists

of

vascular

responses,migration

and

activationof

leukocytes,

and

systemic

reactions.The

unique

feature

of

the

inflammatory

process

is

the

reaction

of

blood

vessels,

leading

to

the

accumulation

of

fluid

and

leukocytes

inextravascular

tissues.Section

1.

Introduction1.

Definition:Inflammation:

adefensive

reaction

inliving

tissue

with

vascular

system

toinjurious

stimuli.Reaction

of

BVs

is

the

central

link limiting

and

killing

injured

factor eliminating

and

absorbing

necrotic

tiThe

inflammatory

responses

is

closelyintertwined

with

the

process

of

repairInflammation

is

fundamentally

a

protective

response,

the

ultimate

goal

ofwhich

is

to

rid

the

invading

microrganism

and

the

walling-off

of

anabscess

cavity,

thus

preventing

spread

of

infection.

Without

inflammation,

infections

would

go

unchecked,

wounds

would

never

heal,

and

injuredorgans

might

remain

permanent

festering

sores.Inflammation

and

repair

may

be

potentially

harmful,

however.

Inflammatory

reactions,

for

example,

underlie

commonchronic

diseases,

such

asrheumatoid

arthritis,

atherosclerosis,

and

lung

fibrosis,

as

well

as

life-threatening

hypersensitivity

reactions

to

insect

bites,

drugs,

and

toxins.Repair

by

fibrosis

may

lead

to

disfiguring

scars

or

fibrous

bands

that

cause

intestinal

obstruction

or

limit

the

mobility

of

joints.4)

SignificanceBeneficial

:

without

inflammationInfections

would

go

uncheckedinjured

organs

might

remain

permanent

festering

soreswound

would

never

healHarmful

:hypersensitive

reactions

to

drugs,

toxinsunderlie

common

chronic

diseases→

rheumatoid

arthritis,atherosclerosis,

and

lung

fibrosisfibrous

repair

→

disfiguring

scars

or

fibrous

bands

that

cauintestinal

obstruction

or

limit

the

mobility

of

joints.Inflammatory

reactions

are

triggered

by

a

variety

of

stimuli:Infections

(bacterial,

viral,

parasitic)

and

microbial

toxinsTrauma

(blunt

and

penetrating)Physical

and

chemicalagents

(thermal

injury,

e.g.,

burns

or

frostbite;

irradiation;

some

environmental

chemicals)Tissue

necrosis

(fromany

cause)Immune

reactions

(also

called

hypersensitivity

reactions)2.

Causes

of

inflammationBiologic

factors:bacteria,

Virus,

fungi,

parasites→the

most

commonChemical

factors

Exogenous:

drugs,

acEndogenousPhysical

agents:

trauma,

burnAllergic

reaction:

GN,

TBlupusEach

of

these

stimulimayinduce

reactions

with

some

distinctive

features,

but

allinflammatory

reactions

share

the

same

basic

features.3.

Basic

pathologic

changes1.

AlterationDegeneration,

necrosisof

local

tissue

and

ceParenchymal

C

cellular

swellingfatty

changecoagulative,

liquefactive

necroMesenchymal

Cmucoid

changeamyloid

changefibrinoid

necrosishyaline

change2.

Exudation:In

inflammatory

foci,

the

escape

of

fluid,

prote(fibrin),

blood

cells

from

vascular

wallinto

interstitial

tissue,

body

cavities

orsurface

of

the

body

and

mucosa3.

ProliferationParenchymal:

epithelium,hepatocyteMesenchymal:

fibroblast,

EC,

histocyteclassified

according

to

its

time

course

as:Acute

inflammation

is

rapid

in

onset

(seconds

or

minutes)

and

is

of

relatively

short

duration,

lasting

for

minutes,

several

hours,

ora

few

days;

itsmain

characteristics

are

the

exudation

of

fluid

and

plasma

proteins

(edema)

and

the

emigration

of

leukocytes,

predominantly

neutrophils.Chronic

inflammation

is

oflonger

duration

and

is

associated

histologically

with

the

presence

of

lymphocytes

and

macrophages,

the

proliferation

ofblood

vessels,

fibrosis,

and

tissue

necrosis.They

also

characterised

by

different

in

the

cell

types

taking

part

in

the

inflammatory

response.4.

Clinical

typesAcute

inflammationRelatively

short

duration,

lasting

for a

few

days

or

a

few

weeksLesions

exudation

of

fluid

,

neutrophils degeneration,necrosis2)

Chronic

inflammationlonger

duration

for

a

few

months

or

yearsLesions

Proliferation:

BV,

fibrosis LC

,PC,

Macrophage

infiltration病例六病史：男性，40歲，頸部患“癤”，紅、腫、

熱、痛，10天后局部紅腫發(fā)展至手掌大，體溫38℃，局部手術切開引流。當晚即惡寒、高熱、頭痛，次日體檢發(fā)現(xiàn)病人輕度黃疸，肝脾腫大，體溫39℃，WBC計數(shù)21.0G/L。思考題：用所學的炎癥知識，作出病理診斷并解釋上述臨床表現(xiàn)。Since

the

two

major

mechanisms

of

host

defense

against

microbes-antibodies

and

leukocytes-are

normally

carried

in

the

bloodstream,

it

is

notsurprising

that

vascular

phenomena

play

a

major

role

in

acute

inflammation.Acute

inflammation

has

three

major

components:Section

2.

Acute

inflammationTwo

major

mechanisms

of

host

defense

:AntibodyLeukocytesmajor

components:Changes

of

hemodynamicsFluid

exudationLeukocyte

extravasation

and

phagocytosiagainst

microbesThe

major

local

manifestations

of

acute

inflammation,

compared

to

normal.(1)

Vascular

dilation

and

increased

blood

flow

(causingerythema

and

warmth),(2)

extravasation

and

deposition

of

plasma

fluid

and

proteins

(edema),(3)

leukocyte

emigration

and

accumulation

in

the

site

of

injury.Changes

in

vascular

flow

and

caliber

begin

early

after

injuryand

develop

at

varying

rates

depending

on

the

severity

of

the

injury.

The

changesoccur

in

the

following

order:Vasodilation

is

one

of

the

earliest

manifestations

of

acute

inflammation;sometimes,

it

follows

a

transient

constriction

of

arterioles,

lasting

a

few

seconds.Vasodilationfirst

involves

the

arterioles

and

then

results

in

opening

of

new

capillarybeds

in

the

area.Thus

comes

about

increased

blood

flow,

which

is

the

cause

of

the

heat

and

the

redness

.I.

Changes

of

hemodynamics1.

Alteration

in

vascular

flow

and

calibTransient

vasoconstriction

of

arterilasting

for

a

few

seconds.Vasodilation

and

increased

blood

floArteriolar

dilationopening

of

new

cap

beds

increased

blood

flowinflammatory

hyperemiaVasodilationis

induced

by

the

action

of

several

mediators.Vasodilation

is

quickly

followed

byincreased

permeability

of

the

microvasculature,

with

the

outpouring

of

protein-rich

fluid

into

the

extravasculartissues;The

loss

of

fluid

results

in

concentration

of

red

cells

in

small

vessels

and

increased

viscosity

of

the

blood,

reflected

by

the

presence

of

dilated

smallvessels

packed

with

red

cells

and

slower

blood

flow,

a

condition

termed

stasis.(2)

Related

to

the

factors

of:Body

fluid:

chemical

mediatorNervous:

axon

reflection3)

Slowing

of

blood

flow:increased

permeability

of

the

microvasculatureoutpouring

of

fluid

into

extracellular

tissuconcentration

of

RBC

and

increased

viscosity

of

bstasis

of

blood

flowNormal

blood

flowVasodilationincreased

blood

floSlowing

of

blood

flStasis

of

blood

flExtravasation(fluid

and

leukocyNormal

fluid

exchange

and

microvascular

permeability

are

criticallydependent

on

anintact

endothelium.

How

then

does

the

endothelium

becomeleaky

in

inflammation?The

following

mechanisms

have

been

proposedFormationof

endothelial

gaps

in

venules.This

is

the

most

common

mechanismof

vascular

leakage

and

is

elicited

by

histamine,

bradykinin,

leukotrienes,

the

neuropeptide

substance

P,

andmany

other

classes

of

chemical

mediators.

Itoccurs

rapidly

after

exposure

to

the

mediator

and

is

usuallyreversible

and

short-lived

(15

to

30minutes);

it

is

thus

knownas

the

immediate

transient

response.

Classically,

this

type

of

leakage

affects

venules,

leaving

capillaries

and

arteriolesunaffected.2.

Increased

vascular

permeabilitIncreased

permeability

→the

most

important

causeresulting

in

exudation

of

fluid

and

proteinMechanism

of

Increased

permeability1)

EC

retractionFormation

of

endothelial

gaps

in

venulesImmediate

transient

response:occurs

rapidly

after

exposure

to

the

mediator

and

isusually

reversible

and

short-lived

(15

to

30

minutemost

common

mechanism

of

vascular

leakage

and

iselicited

by

:histamine,

bradykinin,substance

P,

leukotrieneCytokines

such

as

interleukin-1

(IL-1),

tumor

necrosis

factor

(TNF),

and

interferon-γ

(IFN-γ)

also

increase

vascular

permeability

by

inducing

astructural

reorganization

of

the

cytoskeleton,

such

that

the

endothelial

cells

retract

fromoneanother.Increased

transcytosis

across

the

endothelial

cytoplasm.Transcytosis

occurs

across

channels

consisting

of

clusters

of

interconnected,

uncoated

vesicles

and

vacuoles

called

the

vesiculovacuolar

organelle,many

of

which

are

located

close

to

intercellular

junctions.

Certain

factors,

for

example,

vascular

endothelial

growth

factor

(VEGF),

appear

to

cause

vascular

leakage

by

increasing

the

number

and

perhaps

the

size

of

these

channels.

It

has

beenclaimed

that

this

is

also

a

mechanismofincreased

permeability

induced

by

histamine

and

most

chemical

mediators.2)

Cytoskeletal

reorganizationDelayed

prolonged

responseinduced

by

cytokines(IL-1,

TNF,

IFN-γ),increased

permeability

after

a

delay

of

4

to

6

hourslasting

for

more

than24

hoursinvolves

venules

as

well

as

cap.the

endothelial

cells

retract

from

one

another3)

Increased

transcytosis

across

the

endothelial

cytoplasmBytranscytoplasmicchannelVEGF,

histamine,

bradykinin,Increasing

the

number

and

the

size

of

channelsDirect

endothelial

injury,

resulting

inendothelial

cell

necrosis

and

detachment.The

reaction

is

knownas

the

immediate

sustained

response.This

effect

is

usuallydue

to

direct

damage

to

the

endothelium

by

the

injurious

stimulus,

as,

for

example,

in

severe

burns

or

lytic

bacterial

infections.In

most

instances,

leakage

starts

immediately

after

injury

and

is

sustained

at

ahigh

level

for

several

hours

until

the

damaged

vessels

are

thrombosed

or

repaired.All

levels

of

the

microcirculation

are

affected,

including

venules,

capillaries,

and

arterioles.4)

Direct

endothelial

injuryImmediate

sustainedresponse:severe

burn,

purulent

Bacteriaresult

in

EC

necrosis

and

detachmentleakage

starts

immediately

after

injurysustained

at

a

high

level

for

several

hoursuntil

damaged

BV

thrombosed

and

repairedLeukocyte-mediated

endothelial

injury.Delayed

prolonged

leakage.

Such

leakage

is

caused,

for

example,

by

mild

to

moderate

thermal

injury,

x-radiation

or

ultraviolet

radiation,

andcertainbacterial

toxins.This

is

acurious

but

relatively

common

type

of

increased

permeability

that

beginsaftera

delay

of

2

to

12

hours,

lasts

for

several

hours

or

even

days,

and

involves

venules

as

well

as

capillaries.

Late-appearing

sunburnisa

good

example

of

a

delayed

reaction.

Leukocytes

adhere

toendothelium

relatively

early

in

inflammation.

As

discussed

later,

such

leukocytes

may

be

activated

in

the

process,

releasing

toxic

oxygen

speciesand

proteolytic

enzymes,

which

then

cause

endothelial

injury

or

detachment,

resultingin

increased

permeability.5)

Leukocyte-mediated

endothelial

injuryMild-to-moderate

thermal

injury,

toxin,

x-radiincreased

leucocyte

infiltrationinvolves

venules

as

well

as

cap.Leukocyte

adhere

to

EC

activatedReleasingtoxic

species

and

proteolytic

enzymesLeakage

fromnewblood

vessels.

As

described

in

Chapter3,

duringrepair,

endothelial

cells

proliferate

and

formnew

blood

vessels,

a

processcalled

angiogenesis.New

vessel

sprouts

remain

leaky

until

the

endothelial

cells

mature

and

form

intercellular

junctions.In

addition,

certain

factors

that

cause

angiogenesis

(e.g.,

VEGF)

also

increase

vascular

permeability,And

endothelial

cells

in

foci

ofangiogenesis

have

increased

density

of

receptors

for

vasoactive

mediators,

including

histamine,

substance

P,

andVEGF.All

these

factors

account

for

the

edema

that

is

characteristic

of

the

early

phases

of

healing

that

follow

inflammation6)

High

permeability

of

new

capsduring

repair,

endothelial

cells

proliferate

andnew

blood

vessels①

New

vessels

sprouts

remain

leaky

until

ECsdifferentiate

and

form

intercellular

juncti②

Certain

factors

that

cause

angiogenesis(VEGF)

increase

permeability③

Increased

density

of

receptor

for

vasoactivemediators

in

the

surface

of

ECIn

summary,

in

acute

inflammation,

fluid

loss

fromvessels

with

increased

permeability

occurs

indistinct

phases:(1)

an

immediate

transient

response

lasting

for

30

minutes

or

less,

mediated

mainly

by

the

actions

ofhistamine

and

leukotrienes

on

endothelium;(2)

adelayed

response

starting

at

about

2

hours

and

lasting

for

about

8

hours,

mediated

by

kinins,

complement

products,

and

other

factors;(3)

a

prolonged

response

that

is

most

noticeable

after

direct

endothelial

injury,

for

example,

after

burns.Diagrammaticrepresentation

of

fivemechanisms

of

increasedvascular

permeability

ininflammation(Vascular

Leakage)A

hallmark

of

acute

inflammation

is

increased

vascular

permeabilityleading

to

the

escape

of

a

protein-rich

fluid

(exudate)

into

the

extravasculartissue.The

loss

of

protein

from

the

plasma

reduces

the

intravascular

osmotic

pressure

and

increases

the

osmotic

pressure

of

the

interstitial

fluid.

Together

with

the

increased

hydrostatic

pressure

owing

to

increased

blood

flow

throughthe

dilated

vessels,

this

leads

to

a

marked

outflow

of

fluidand

its

accumulation

in

the

interstitial

tissue.

The

net

increase

of

extravascular

fluid

results

in

edema.II.

Fluid

exudation1)

Major

causes:①

Increasedvascularpermeability

→escape

of

aprotein-rich

fluid

into

the

interstitiu②

The

loss

of

proteinreduces

intravascular

colloid

osmotic

pressurincreases

the

colloid

osmotic

pressure

of

theinterstitial

fluidBlood

pressure

and

plasma

colloid

osmotic

forces

innormal

and

inflamed

microcirculation.A,

Normal

hydrostatic

pressure

(red

arrows)

is

about

32

mm

Hg

at

the

arterial

end

of

a

capillary

bed

and

12

mm

Hg

atthe

venous

end;

the

meancolloid

osmotic

pressure

of

tissues

is

approximately

25

mm

Hg

(green

arrows),

which

is

equal

to

the

mean

capillary

pressure.

Although

fluid

tendsto

leave

the

precapillary

arteriole,

it

is

returned

in

equal

amounts

via

the

postcapillaryvenule,

so

that

the

net

flow

(black

arrows)

in

or

out

is

zero.B,

Acute

inflammation.

Arteriole

pressure

is

increased

to

50

mm

Hg,

the

mean

capillary

pressure

is

increased

because

of

arteriolar

dilation,

and

the

venous

pressure

increases

to

approximately

30

mm

Hg.

At

the

same

time,

osmotic

pressure

is

reduced

(averaging

20

mm

Hg)

because

ofprotein

leakage

across

the

venule.

The

net

result

is

an

excess

of

extravasated

fluid.Blood

pressureand

plamacolloid

osmoticforces

in

normaland

inflammedmicrocirculatioexudation

:The

escape

of

fluid,

proteins,

and

blood

cellthe

vascular

system

into

the

interstitial

tissue

or

bodyExudate:

an

inflammatory

extravascular

fluid

that

has

aprotein

concentration,

cellular

debris,

and

a

higher

graIt

implies

significant

alteration

in

the

normal

permeabismall

blood

vessels

in

the

area

of

injury.Transudate:

a

fluid

with

low

protein

content

(most

of

whialbumin)

and

a

lower

gravity.It

is

essentially

an

ultrafiltrate

of

blood

plasma

that

rfrom

osmotic

or

hydrostatic

imbalance

across

the

vesselThe

escape

of

fluid,

proteins,

and

blood

cells

from

the

vascular

system

into

the

interstitial

tissue

or

body

cavities

is

knownas

exudation.An

exudate

is

an

inflammatory

extravascular

fluid

that

has

a

high

protein

concentration,

cellulardebris,

and

a

specific

gravity

above

1.020.

It

implies

significant

alteration

in

the

normal

permeability

of

small

blood

vessels

in

the

area

of

injury.In

contrast,

a

transudate

is

a

fluid

with

low

protein

content

(most

of

which

is

albumin)

and

a

specific

gravity

of

less

than

1.012.

Itis

essentially

an

ultrafiltrate

of

blood

plasma

that

results

fromosmotic

or

hydrostatic

imbalance

across

the

vessel

wall

without

an

increase

in

vascular

permeability.

Edema

denotes

an

excess

of

fluid

in

the

interstitial

or

serous

cavities;

it

can

be

either

an

exudate

or

a

transudate.2)

Distinguish

between

exudate

and

transudTransudateNormal<

30g/LAlbuminExudateIncreased>

30g/LKinds

of

proteinNegative

(-)

Positive

(+)No

HaveVascular

permeabilityProtein

concentrationProtein

typeRivalta

testFibrinSpecific

gravity<

1.018Cell

numberAutoagglutinationAppearance<

300×106

/LNoClear>

1.018>

1000×106/LYesCloudy3)

Functions

of

exudate:Dilute

local

toxins

→reduce

the

injury

to

tiBring

in

the

nutritional

substance

for

leukocarry

off

the

metabolicproductsin

infla

focikill

the

pathogen

:

Ab,

complementFibrinmesh:limit

the

spreading

of

pathogenic

organismslimit

the

removing

of

MφThe

sequence

of

events

in

the

journey

of

leukocytes

from

the

vessel

lumen

to

the

interstitial

tissue,

called

extravasation,

can

be

divided

into

thefollowing

stepsIn

the

lumen:

margination,

rolling,

and

adhesion

to

endothelium.Vascular

endothelium

normally

does

not

bind

circulatingcells

or

impede

their

passage.

In

inflammation,

the

endothelium

has

to

be

activated

topermit

it

to

bind

leukocytes,

as

a

prelude

to

their

exit

from

the

blood

vessels.Transmigration

across

the

endothelium

(also

called

diapedesis)Migration

in

interstitial

tissues

toward

a

chemotactic

stimulusIII.

Leukocyte

extravasationand

phagocytosis1)

Leukocyte

extravasation:

leukocyte

passthrough

vascular

wall

into

the

site

of

injury.Divided

into

following

steps:Margination

and

rollingAdhesionTransmigration

and

chemotaxisIn

normally

flowing

blood

invenules,

erythrocytes

are

confined

to

a

central

axialcolumn,

displacing

the

leukocytes

toward

the

wall

of

the

vessel.Because

blood

flow

slows

early

in

inflammation

(stasis),

hemodynamic

conditions

change

(wall

shear

stress

decreases),

and

more

white

cellsassume

a

peripheral

position

alongthe

endothelial

surface.

This

process

of

leukocyte

accumulation

is

called

margination.Subsequently,

individualand

then

rows

of

leukocytes

tumble

slowlyalong

the

endothelium

and

adhere

transiently

(a

process

called

rolling),

finallycoming

to

rest

at

some

point

where

they

adhere

firmly.

In

time,

the

endothelium

can

be

virtuallylined

by

white

cells,

an

appearance

calledpavementing.(1)

Margination

and

rollingleukocyte

in

central

axial

columnBV

dilation,

speed

of

blood

flow↓marginationrollingpavementing

appearanceThe

multistep

process

of

leukocyte

migration

through

blood

vessels,

shown

here

for

neutrophils.

The

leukocytes

first

roll,

then

become

activatedand

adhere

to

endothelium,

thentransmigrate

across

the

endothelium,

pierce

the

basement

membrane,

and

migrate

toward

chemoattractantsemanating

from

the

source

of

injury.

Different

molecules

play

predominant

roles

indifferent

steps

of

this

process-selectins

in

rolling;

chemokines

inactivatingthe

neutrophils

to

increase

avidityofintegrins

(in

green);

integrins

in

firm

adhesion;

and

CD31

(PECAM-1)

in

transmigration.Leukocytic

emigrationLeukocyte

adhesion

and

transmigration

are

regulated

largely

by

the

binding

of

complementary

adhesion

molecules

on

the

leukocyte

andendothelial

surfaces,

and

chemical

mediators-chemoattractants

and

certaincytokines-affect

these

processes

by

modulatingthe

surfaceexpression

or

avidity

of

such

adhesion

molecules.The

adhesion

receptors

involved

belong

to

four

molecular

families-the

selectins,

the

immunoglobulin

superfamily,

the

integrins,

and

mucin-likeglycoproteins.The

immunoglobulin

family

molecules

include

two

endothelial

adhesion

molecules:ICAM-1

(intercellular

adhesion

molecule

1)

and

VCAM-1(vascular

cell

adhesion

molecule

1).

Both

these

molecules

serve

as

ligands

for

integrins

found

on

leukocytes.Integrins

are

transmembrane

heterodimeric

glycoproteins,

made

up

of

α

and

β

chains,

that

are

expressed

on

many

cell

types

and

bind

to

ligandson

endothelial

cells,

other

leukocytes,

and

the

extracellular

matrix.(2)

Adhesion:By

binding

ofcomplementary

adhesionmolecules

on

the

leukocyte

and

endothelialsurfacesAdhesion

molecules

:The

immunoglobulin

family:

I(V)CAM-1IntegrinsselectinsThe

recruitment

of

leukocytes

to

sites

of

injury

and

infection

is

a

multistep

process

involvingattachment

of

circulating

leukocytes

to

endothelialcells

and

their

migrationthrough

the

endothelium.

The

first

events

are

the

inductionof

adhesion

molecules

on

endothelial

cells,

by

a

number

ofmechanism.P-selectin

,which

is

present

in

endothelium

and

platelets.

Mediators

such

as

histamine,

thrombin,

and

platelet

activating

factor

(PAF)

stimulatethe

redistribution

of

P-selectin

from

its

normal

intracellular

stores

in

granules

(Weibel-Palade

bodies)

to

the

cell

surface.P-selectin

was

first

identified

in

the

secretorygranules

of

platelets,

hence

the

designation

P.

Ithas

since

been

found

in

secretory

granules

ofendothelial

cells,

called

Weibel-Palade

bodies.

Whenendothelial

cells

or

platelets

are

stimulated,

P-selectin

is

translocated

within

minutes

to

thecell

surface.

On

reachingthe

cell

surface,

P-selectin

mediates

binding

of

neutrophils,

T

lymphocytes,

and

monocytes.c.

Mechanisms

of

adhesive

process:i)

Redistribution

of

adhesion

moleculesto

the

cell

surface:For

example

:

P-selectinNormally

present

in

W-

P

body

of

ECHistamine thrombin,

PAFRedistributed

to

the

cell

surfaceBinding

to

the

receptor

of

leukocyteResident

tissue

macrophages,

mast

cells,

and

endothelial

cells

respond

to

injurious

agents

by

secreting

the

cytokines

TNF,

IL-1,

and

chemokines.TNF

and

IL-1

act

on

the

endothelial

cells

of

postcapillaryvenules

adjacent

to

the

infectionand

induce

the

expression

of

several

adhesionmolecules.

Within

1

to

2

hours,

the

endothelial

cells

begin

to

express

E-selectin.ii)

Induction

ofadhesion

molecules

synSome

inflammatory

mediators,

(IL-1,

TNF)induced

the

synthesis

and

surface

expressionofendothelial

adhesionmol