Suppressive effect of topical FK506 on irritant and allergic contact dermatitis in mice

JSID Abstracts/J.

Dermatol.

013

016

SUPPRESSIVE

EFFECT

DERMTITIS

IN

OF TOPICAL FKMG

orev~ous

dernat!tls

I”

mace.

at

lower

and

suppressive

effect

Dermatolw~,

awl,c.t~on

a macrolide

c~closwr~n

of

topical

,nduced

to the ear of

graft

to FK506

In

on

oil

known

rejectton

CYA.

by croton

IS

study.

irrufant

and

contact

as

after

this

A (CYA)

allergic

and

a potent

organ

we

trans-

investigated

allergic

contact

dinitrofluorobenrrne

showed that topical

BALE/c mice InhibIted

awlIcatIon

(DNFB).

of FK506 (O.OOl-

the ear swellIns

relwnse

dose-depndent

mm”er. Thus, FKSOBcwy be useful as I toolcal

treatment for

lntlamnatorv skin dtseases.

in a

asent I” the

MODULATION

OF

MINE

CONTACT HYPERSENSITIVITY

REACTION

BY

STAPHVLOCOCCAL ENTEROTOXIN B ABE.

M.

NATSUAKI.

of kdlclne.

Y.

KITANO.

N,ah
Staohvlococcal

of

it

1 cells

IS

in this

study. we tnvestlgated

day

6.

0.

mace.

chaIIen&ed

on day

SEE-Injection

rnhabltlon

was

to

mice

with

I,,

v,tro

study,

erat,ons

to

,ndlcate

that

BALB/c

on dry

mediated anerzy lymph

SEE.

but

to

known

Oermatolosv.

Hyogo

College

exotoxlns which

5 and 0

were

followins senslt,zed

ear

swel

inhIbIted

not

did cells from cells

l,ng the

necrosis

SEE-resDond,ng

VB elerrntr

15 Induced

normal

SEE-injected 0l.y

reseonses

the

reaction were

a key

of However,

mice role

showed did in

(CHR)

evaluated

the

this

SEB-tvectron effect.

SIgnItIcaot not.

on

CHR and

Imwnonmdulatory

m,ce

I”

actlvatlon.

dnnitrotluorobenzene

sens,tIzation

factor-a.

shw

trcm

wfth

have

of 1 cell

the transient

These

rmdulation

In wolltresults of

MUTATION OF LEU lz2 TO PHE AT A HIGHLY CONSERVED HYOROPHOBlC RESIDUE IN THE HELIX INlTlATlON MOTlF OF KERATIN 14 IN EPIOERMOLYSIS EULLOSA SIMPLEX

Kyoto.

Epldsrmolysis bullosa simplex (EBS) has been shown to arise from mutations of the genesfw ti kareWmK5 and K14. To-lhsmuta%ons of the keratln genes. vs desIgned a dotssib systsm using PCR and automatedseqwndng. me sbqwncssin whlchmerspo~hot~of~ke~n~rn~~~~a~~~~R using the primers one of tihieh was 5’-pMsphwylated. After dlgssllon of tha amplified S-p~ed DNA by cexonuclwse. UN remaining ringIs-arendad DNA was used as a template for didsow sswsndn~ with a fluorescant prlmsr. DNA sequenoes wsfs [email protected]@tRd DN& ssq-r. When a cnss of KMmer type EBS was analyzsd. w found a mutatlon of LB&W to Phe of K14 by a pant mutation of C to T transitIonin one of the Wslas. There vmrs no mutations in the members d the patlenc’s tamlly s”d nofmsl controls. Thu, (hlscsse was diagnosed as a sporadic case of EBS by a nsw mulation otK14 gene with a possible dominant lnherhance. Our detection method Is useM fa screening of the muwdions of K14 and K5 genes In EBS and *nil be applkaMe

to prenata! dmgnosis of EBB.

CHR.

018

015 ACUTE BARRIER DISRUPTION BY ACETDNIZ AUGMENTS OF MURINE CONTACT HYPERSENSITIVITY.

A NOVEL

M. MATSUKI, K. KONISHI, K. YAMANISHI, and H. YASUNO Oeparimant of Oennatology. Kyoto Prefectural University of Medicine, Japan

stimulate

the contact hvpersensitlvltv

mice

SEE those

surerantigens

to the suwrant~.Wn

T cells

by tumor

node

that

have particular

(anerey)

of the stimulated

I” SEB-!n,ected on day

well

uhlch

receptors and “nres~ns!venes~ the pwulatlon

of

0 (SEE) IS one of bacterIaI

Prwxrtles. nun&r

Department

Japan

enterotoxnn

*“Pera”tl&en a Iarle

Tenascin is an extracellular matrix protein and is induced in wound healing of the skin. We investigated the expression of tenascin in allergic contact dermatitis of the mouse skin induced by epicutaneous application of 2,4-dinitmfluorobenzene @NFB). In the normal ear skin, tenascin was found in the periphery of the cartilage and in the subcutaneous tissue of the inner-side skin. In the swollen ear skin of tie allergic contact dermatitis. no remarkable induction was observed. However. in the dermis of the regenerating skin, abundant tenascin was detected. which disappeared with healing of skin damage. These results suggest that tenascin is involved in the healing of skin damage after allergic contact dermatitis.

017

014

K.

INDUCTION OF TENASCIN IN CONTACT DERMATITIS Y. KOYAMA”‘, K. NOROSE’ and M. KUSAKABE’, ’ Nippi Research Institute of Biomarix, Japan, and *Latwatory of Cell Biology, The Institute of Physical and Chemical Research (RIKEN), Japan

HYO.SO College

of

antlbiotIc,

against

conmared

The results

respectrely.

of

towcal

ettcctlve

doses

,n m,ce

0.1~)

that

FK506.

Inwnoswcwessant

derratltis

Department

Jawn

sntlammatory res~onaes of crr,tant and

the

the

Kl TANO.

sfudles showed

,nhib,ted

plantataon

ON IRRITANT AND ALLERGIC CONTACT

MICE

n. NATSUAKI. K. ABE. Y. of kd,clne. Nlshlnomlva. Our

Sci 8 (1994) 54-88

RESPONSIVENESS

T. NISHUIMA ‘, Y. TOKURA ‘, G. IMOKAWA 2 and M. TAKIGAWA I, 1 Depanment of Dermatology, HmnamatsuUniversity School of Medicine, Japanand * Insdtute for Fundamental Research.Kao Coqwetion. Japan Stratum -urn has permeable barrier function, whose disruption may caosevarious skin rexdons. We examined whether acutebarrier disruption influencesthe nsponsivmss of inurine contxt hypersensitivity (CHS). Miie were sensitizedwith 0.5% DNFB painting a, days 0 and 1 and elicited on day 5 with 0.05.0.1 w 0.2% DNFB a! chcerrlobes. Acute barrier disruption was perfomwd by treatmentof earlobes with acetonebcfwe clullenge. When mice wete challenged with 0.1% DNFB. treatment with zxelIxK 24 hoursbefcsechallenge signitlundy augmentedear swelling responses comparedwith thosewithout @tone pretreatment.while suchenhancementof CHS responsewas not found by acetonetreatment 0.5 or 48 hoofs before elicitation. On the other hand.no signiti &il&nce was obsetwd betweenacetcw-tmaicd and con-aared groupsin mice chalknged with 0.2% or 0.05% DNFB. l?us, acute banier disruption affectedCHS at M Bppopripv concenaetia~ of spplied hapten. Flow cytometric analysesrevealedthat Lang&ins cells &C) that were t&en from cpidcmris mated with acetoneexpressedhiHC classII molecules at kvelr significantly highu than those without m btabnent. The uament plso affected IL-1 prcducdonby epidtrmal cells as assessedby bioacdvity in adture supanauna of tishly isolated &Is. These resultsindicate that llcute banier disruption inducesalteration of CHS at least partly via influencing antigen-presentingability of LC and keratin@@c cytokine poduction.

MODULATION AN0

OF PLASMA

PEMPHIGOIO

LEVELS

PATIENTS

OF CYTOKINES

TREATED

IN

I. KANAIZUKA, Y. SUGITA, S. ICHIYAMA. T. NAGATANI H. NAKAJIMA. Department of Dermatology. Yokohama University School of Medicine, Yokohama, Japan Although

the

mechanism

is uncsrtain.

the

pemphigoid.

The

studied.

Cytokine

diseases.

therapy

and

has

modulation

beneficial

been of

interaction

Therefore,

pemphigus

of the

effect

performed

cytokines

cytokine

pemphigoid

were

by

measured

the

using

ELISA

of TNF ct. IFN Y. IL - 2R and

psmphlgus

plasmapheresis and

pemphigoid.

wara

and was

inflammatorV patients

before

levels

of

plasmapheresis pamphigus

role for in

plasmapheresis

cycle

such

and City

plasmapherasis

IL - 6.

Plasma

kits

levels

of for

has an impOrtant

the

PEMPHIGUS

BY PLASMAPHERESIS

and

with after

as TNF cr. IFN y. IL - 2R and

daoreased

in

the

IL - 6 after patients

one with