Immunomodulating actions of met-enkephalin

WS16-9

*9

IMMUNOMODULATING ACTIONS OF MET-ENKEPHALIN S.X. Yang and X. Y. Li Shanghai Inst. Materla Medlca, Chinese Academy of Sciences, Shanghai, China Experimental

evidence indicated that endogenous opioid peptides are involved

in the modulation of immune functions. (10 - 9 ~ I0-3M)

Studies in vitro showed that Met-Enk

enhances mouse splenocyte transformation stimulated by subop-

timal concentrations

of Con A and PHA; on the other hand, Met-Enk was found

to inhibit the splenocyte blastogenesis stimulated by LPS and PFC formation against SRBC. significantly

Met-Enk(10-12~10-6M)

in vitro or 0 . I ~ 0 . 6

mg/kg ip in vivo

increase IL-I production induced by LPS(4 Bg/ml)

neal exudative macrophages.

from peroto-

However, it is not certain in some cases the

above effects of Met-Enk are blocked by naloxone,

a specific antagonist,

because naloxone per se also affect immune responses.

Our results suggest

that Met-Enk is a potential neuroimmunomodulator.

WS16-10

"10 IMUTHIOL PREVENTS AGAINSTTHE DEPRESSIONOF T-CELL ACTIVmES INDUCED BY 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE(MPTP). G.RENOUX, M. RENOUX, K. BIZIERE,Labomtoire d'iTlTlunoIogie, Facult6 de ML~lecine, Tours, France. MFTP (30 rn~g), a dopamine (DA) neurotoxin, depresses T cell n ~ and acidities in mice, and increases B cell numbers and responses. A concomi~rt Irealmert w ~ 25

n ~ o of p ~

sodium d~J~,~m~<~ace

( m u m ~ . a T ~Ii sl~ci'~

Irnmunostlmulant ancl a p-dopamlne hyOroxylase inhbltor, restores T cell-dependent responses and striatal DA levels, but not the levels of DA melatx>li~s. In conlrast, deprenil, a MAO-2 inhibitor, restores both DA and DA rnetabolite levels and maintains high B cell values, yet do not influenceon It~ T-cell responses. The _d=i~suggest ~ DA, which strlalal levels are malrmlned by mub'liol, is among I~e neuro Imnsmlters Involved In pathway from neocortex to the immune systs~ to control T cell activities, and that DA mdabolites may anlagonize these elfeds.

WS16-11 MECHANISM OF POLYMORPHONUCLEAR LEUKOCYTES(PMNs) MIGRATION FROM THE PERITONEUM IN THE TREATMENT OF MALIGNANT ASCITES BY OK-432 M. Inoue, H. Kate, Y. Yamamura, M. Tanigawa, H. Sane, S. Sugino, M. Kondo First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan Participation of PMNs was investigated in carcinomatous peritonitis and pleuritis with i.p. injection of 0K-432. We applied OK-432 with or without normal human serum(NHS) or fresh frozen plasma(FFP) to generate complement -derived chemotactic factors C3a and C5a for accumulation of PMNs into the cavity. Here, we tried to demonstrate the mechanism of PMNs migration from the peritoneum, when 0K-432 and/or NHS with inhibitors to complements or arachidonic acid cascade reacted through filter membranes on the turned peritoneum in rats. Histological examination showed the movement of PMNs from small vessels in the peritoneum to the mesothelium by the treatment of 0K-432 for 3hrs. Then PMNs came into the peritoneal cavity. FOY and K76COOH dose-dependently prevented the migration of PMNs judging by the counts of PMNs on the filter membranes after staining. Prednisolone, OKY046, AA-861, and Azelastin also did. It was concluded that PMNs migrated from the peritoneum into the peritoneal cavity and chemotactic factors derived from complements and arachidonic acid cascade play a significant role on the migration of PMNs into the peritoneal cavity.

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