Clinical rheumatology, 1982, 1, N ~ 2, 140-152 Fourth European Workshop on inflammation Wilrijk March 1982 At the fourth European Workshop on the role of the complement system, endotoxins and intravas- cular coagulation in inflammation held at Wilrijk Belgium on 15-16 March 1982, the following abs- tracts were submitted. Inflammatory stimuli augment synthesis of complement component C3 by macrophages. H.P. Hartung, D. Bitter-Suermann, U. Hadding, Inst.f.Med.Microbiology, Hochhaus Augustplatz D-65 Mainz, FRG Macrophages (mo) are major producers of complement. We investigated whether inflamma- tory stimuli applied in vivo affect synthesis and release of complement components C3, C2 and C4. Peritoneal mo were harvested from guinea pigs either untreated or intraperitoneally injected with serum albumin or C. parvum 4/7 days be- fore sacrifice, ma cultured under serumfree con- ditions for 12 hrs, and supernatants tested for C3 by ELISA, and C2/C4 by hemolytic titration em- ploying serum fron C2/C4 deficient guinea pigs. In addition, secretion of N-acetylglucosaminidase was determined. Mo from untreated animals re- leased about 70 ng/106 cells C3 into culture su- pernatant, albumin elicited mo 88ng and C.par- vum stimulated ma 183 ng. Secretion of C2 rang- ed from 0.99 x 108SFU to 2.66 x 108 in albumin - and 3.93 x 108SFU in C.parvum-stimulated mo, corresponding values of C4 release being 1.9 x 108; 3 x 108; 4.1. x 108 SFU/106 cells. By employing an ELISA we could demonstrate that in vivo application of inflammatory stimuli augments synthesis and release of C3, the most abundant complement component. These changes were paralleled by alterations in C2, C4 and Iysosomal enzyme secretion. Our findings show that ma can be induced to enhance synthes- is and release of complement at sites of inflam- mation. Human platelets, after their contact with in- fluenza virus, activate the complement system in autoiogous serum. F. Maillet, C. Lambrd, M. Kazatchkine. INSERM U 28 and U 139. H6pital Broussais 75014 Paris, France. Guinea pig erythrocytes that have been exposed to influenza virus activate the human alternative pathway through virus-induced desialation of the cells. Neuraminidase treatment of rabbit platelets enhances their clearance in vivo. Washed human platelets were prelabeled with 51Cr and resus- pended in Tyrode's solution containing Influenza virus Hong-Kong/1/68 for 15 min at 4~ After elution of the virus at 37~ the platelets were washed and resuspended in autologous serum that had been dialyzed against Veronal buffered saline containing Ca + § and Mg § § (VBS § +), VBS containing 8mM/EGTA and 2mM Mg § § (VBS-MgEGTA) or VBS containing 20mM ED- TA (VBS-EDTA) for 45 min at 37~ Four point nine per cent 51Cr release and no complement consumption were observed in VBS-EDTA se- rum. In contrast, 9 ~ 51Cr release with 50 ~ de- crease in C3 and B hemolytic activities occured in VBS-MgEGTA serum and 20,5 ~ 51Cr release with 60 070 decrease in C2 hemolytic activity oc- cured in VBS +§ serum. These results suggest that Influenza virus may alter the platelet surface in such a way that both complement pathways might be recruited and the cells be lyzed in autol- ogous serum. Contact activation by bacterial fragments. E.S. Kalter, W.C. van Dijk, A. Timmermans, J. Ferhoef, B.N. Bouma, University Hospital, 3511 GV Utrecht, The Netherlands. To investigate whether bacterial cell wall frag- ments activate the contact system of plasma we incubated a mixture of purified human Factor XII, Prekallikrein (PK) and High Molecular Weight kininogen each at its plasma concen-