JSID Abstracts/J. Dermatol. Sci. 8 (1994) 54-M

073 CANDIJJA ALBICANS PFCOTEINASE IS CIEMOTACTIC FOR HUMAN PERIPHERAL NEUTROPHILS AND LYMPHOC~

Y. Ran. K. Unno. R. Twboi, K. Iw&uchi*, 1. Nagaoka* &II. Ogawa

Oepaunent of Dermatology nod Sexad Depamwnt of Bioctwoistry’. School of

Medicine Juntendo Uivetsity, my”.

w previously de- dtat an acid pmteinase tiom CaJbicum is importam for

invasion sod multiplicaion of the organisms in host tissues. However. dw mechanism of the n&on of the host tissues to the pmtebwe has not ken elucidated. In his study,

we investigated wheti the pudtled pmteioase frcm C.&cans has a chemotactic

activity for human @p&ml neotrophils and lympbccytes. Human peripheral

oeutrophils and lymphayvs wem is&ted by a ceoeifugation m&cd, and 3~10~ /ml of

the cells rhm M, The cbem~c activity was a&z& by a modified Boyden

chamber method IL-8 at JO’ M was used as a positive camel. The pmteimw showed

the strongest chemotacdc activity to the oeutmphils at 0.48 pM, which was a similar

potency to dw induced by IL-S. This chomotaic activity disappand when heated at

100” C for 10 min or treated with I@/ml pepstadn. However, little &mot&c

activhy was observed for lympbacytes. These findings suggest that Cdbicm

pfoainw plays a role not only as a hydrolytic enzyme for invasion but also as B

chemoatuxtan~ for neuuophils. which subsequently pbagocyte the organisms.

075 THROMBOMODULIN COMPARISON WITH VARIOUS MACROPHAGE-

MARKERS IN CHRONIC GRANULOMATOUS INFLAMMATION

Y. llZlJh41’. S. IZAKI’, K. KIT-’ AND 1. MARUYAMA’. ‘Department of Dermatology, Saifama Medical Cmta. Saitama Medical S&ml and ‘Department d Laboratory Medicine, Kagoshima Voiversity School of Mediane

%vmbomcxiulin gu) is a newly desczibed marker glympotein for

monocyceslmacrophages in granuJomatou.9 intlammation. We hex ccinpwd

immun~stihemical expression of TM with various maaophage-markers. such as

CDllb (MAC-J). CD14. CLI16. CD33, CD68, MAC387 and lysozyme in sarmidosis,

lupus miliaris disseminatw faciei and deep mycosis. Monocyiic nod epitbetioid

bmtiocytes tiltmting into the “&sue were CDllb (MAC-l) positive. TM-positive

intlammatory cells were observed smrouoding tie granuimoas but “01 observed in tbc

center of orgaoized granulomas Lysozyme-p-wove and CD 6S-pwtive epithcboid and

multiouckated cells wre fotmd in dw center d gmuulomas. 0th~ mmxqh&% markers showed vanable rw&.~ between types of gmnulomatous intlammaoon. In conclusicm.

TM is a umque and useful immuomnarker for monocytic bistiocyles surrounding

ep&elioid ceJJ graoulomas

076 CHANGES OF NEGATIVE CHARGE DISTRIBUTION ANL.J SUSCEPTIBILITY ‘IQ THE EXFOLIATIVE TOXIN IN THE COURSE OF DEVELOPMENT OF THE MOUSE EMBRYONAL. SKIN

EIICHI MAKINOI, MASAYOSHJ NAMBAzand JIRi) ARATA’, J Jkpariment of

Dermatology and 2 Cell Biology, Okayama Universily Medical School, Japan

Exfoliative toxin (E:r) is considered to be one of the pathogenic factors of cleR for- mation within the granular layer of human and moose epidermis. ET specific receptor, which has not be ever identified, is supposed to be on the granular cell. The ski” of hu- man, neonatal and embxyonal mouse was used to explore the mechanism of cleft for- mation. Mouse embryonal skin develops rapidly during a short period of time. On day 12 of embryonal life, the epidermis consists of a single layer of undifferentiated cells. Stratification and mmiiic%tion develop between 12 and 16 days of the embryonal age. llte keralohyaline granules appear in the uppemwsl layer by 18 days of age. The negali- ve charge (NC) distribution within the epidermis was examined. The results revealed that no NC WBF detectable within the skin of lZ-dav-old cmbrvos. .md that the NC emerged in the whole layers of the epidermis excepi the basal jay& by 16 days of age. ll~lhe NC is loalized withii the aranula~ layer of the skin of l&day-old mouse embryos, and is also observed whhin 1hc~gmnol.w l&r of human and neon& mouse skin. ET induced cleft formation in the mouse embryonal slain, and it cccuned within the supm- basal law which was below the mawJar Jaw. these data wozest that cellular changes such as ihe NC distribution in the-course of bevelopment of &kin, might be associ-- ated with susceptibility of the skin to ET. The experbnental system using the mouse embryonal ski” is useful 10 investigate the mechanism of action of ET to the epidermis.

077 DECREASED RELEASE OF INTERFERON-r BY PERIPHERAL BLOOD MONONUCLEAR CELLS OF CHRONIC DERMATOPHYTOSIS PATIENTS IN AESPONSE TO STIMULATION WlTH TRICHOPHYTIN

T. KCGA , 5. TOGHlTANI ’ , ii. ISHIZAKI ? T. MATStJM2TO”and Y. HCFtl ’ ’ ~alt”f !Jwmt&gy. Sohoolof Medkine, Pukucka University. Fukuoka Japan. 2 Kanazava Medial University. Iuhikam. s To&&a Haspit& Tokyo. ’ Fecuily of Madick-m, Kyushu Univenity Fukuoka

llwpmactknof intwlwon. I (IPN-7) in reapan~~tostimulation wh ttichopnytin ~1s c!+wawd in the ~pheml b&d momnuclur calls (PBMC) obtakmd from patimta who had had clwwic darrmtophyte iniectti #mn con-&wed Hith wn-chronkally inlscted patknts. This findog indiites that peripMral T-tymphocyies cd the pat&&s tih chonk titophyte infection have reduced abilityt”producelFN - 7, tilchomy plny arolein thedevobpmunt aldelayed typ hyparsensttttity (DTH) reaction in the skin. By mansuing the rslplre of cytdtiiw which is one of the key functional parameters d tnvmma response, this study suppMIs the hypothssi that a partial defect in tb DTHres~~ to dwm&@yte anttgen may be responsible for the establishment of chronicdenatophytosis

078 EFFECTS OF ANTIFUNGAL DRUG ON INTRACELLULAR CALCIUM CONCENTRATION IN TRICHOPHYTON RUBRUW.

K. OSADA, I. INOUE. M. SEISBIMA, and Y. KITAJIYA, Dept. of Deraatology. Gifu Univ. School of Medicine, Gifu

Prior studies have indicated that intracellular calcium concentration ([&.‘*I ,) is involved in fungsl cell growth. It has not been known whether antifungal drugs affe;; ;;;;I transduction via calcium or not in fungal cells. context, re examined the effect of an antifungal drug. ittsconazol, on [I%“], in Trichophyton rubrum. ‘I. rubrum on the glass cover-slips w.s loaded with fura-t/AM. and then [Cas’Ii was determined in single cell by measuring fluorescence ratio (F340/F360) with a videomicroscope. Itraconazol (5ng/ml) induced a rapid and transient [Ca”l. increase in hyphal cells of T. rubrum, but not in spores. Slow phase of [Ca”‘], increse by itraconazol was decreased by chelating extracellular calcium vith EGTA. Itraconazol induced a explosive and sustained calcium increase in spores at long/ml and lOOng/sl. At the concentration of Ing/ml, no [Ca”]. increase was caused in both hyphal and spore cells. These findings suggest that signal transduction via calcium might be involved in the effect of itraconazol on T. rubrum.