PROLONGED AND PRERIATURE RUPTURE OF THE AIERIBRANES (PPRORI) AND ITS RELATIONSHIP TO CHRONIC RESPIRATORY RIORBIDITY 35 Thompson P, Greenough A, Blott &I, Nicolaides K, Icing's College Hospital, London PPRORl is frequently associated with pulmonary hypo- plasia. Some infants, however, do survive and our aim was to determine the incidence of impaired lung grorvth and its relationship to chronic respiratory morbidity in these children. 53 pregnancies com- plicated by PPROR.1 before 32 weeks gestation were studied. Of these, there were 2 termination, 2 spontaneous abortions, 1 utrauterine death, 22 neonatal deaths, and 26 were discharged home. Of these 26, 5 were lost to follow up. The remaining 21 had a mean gestation of 32 weeks (range 25-41), mean rupture of membranes (RORI) at 24 weeks (range 15-32) and mean duration of ROhl of 8 weeks (range 1-20). The mean length of follow up was 15 months (range 6-22). Only 5 infants (4 of whom were ventilated) had recurrent respiratory problems. These infants were born more pre- maturely than the asymptomatic infants (p<O.05). Only 3 children required hospital admission for chest related disorders and all 3 suffered with re- current respiratory symptoms. No relationship was found between either recurrent symptoms or hospital admission and duration or length of mem- brane rupture. At one year, abnormal lung vol~imes were only found in the symptomatic ventilated infants, except for 2 infants who had very early onset and prolonged duration of RORI. IVe conclude that chronic respira- tory morbidity following PPROAI relates to the gestation at birth and neonatal ventilation and only in extreme cases to the duration and onset of membrane rupture. STUDIES OF ENDOTOXIN (LPS) INDUCED HUAIAN RIACROPHAGE (arm) PRODUCTS WHICH INDUCE POLY- AIORPHONUCLEAR LEUKOCYTE (PMNL) RECRUITLIEMT 36 DURING IPIFLALIRIATION. ~kl J. Megyeri and Andrew C. Issekutz, Szent-Gyoryyi Albert Rledical School,Szeged, Hungary, Dept of Pediatrics and Rlicrobiology Dalhousie Univ, Halifax, N.S., Canada Previously we reported that LPS induced rabbit RIBS release protein factors which recruit PLINLs into rabbit skin as measured with 51cr labelled leuko- cytes. Here we report that in vitro stimulation of human monocyte de- rived nibs with LPS (3-100 ng/rnl for 1-24 hours) results in their secretion of at least one protein factor capable of attracting PMNLs into the skin of rabbits following intradermal injection. The predominant PRlNL re- cruiting activity (PRA) had a molecular weight on gel filtration (Sephadex- 100, Superose-12) of 40-45 Kd. The production of the PRA was inhibited by cycloheximide (2 pg/ml) and the PRA was found to be relatively heat stable (43% loss of activity at 56O C 30 min) and had no in vitro chemo- tactic activity for PRlNLs. The gel filtration fractions m o s t t i v e for PRA had 7-20 U/ml TNF and no detectable IL-1 (<0.2 U/ml) activity. The active gel filtrntion fractions were tested after treating them with neutral- izing polyclonal anti-human IL-lo( and IL-I+ ' and with neutralizing mono- clonal anti-TNFa antibody. This combined treatment decreased the & * PRA activity by only 16%. These results suggest that LPS stimulated human hlbs secrete a yet unidentified 40-45 Kd component (PRA) which can be distinguished from TNFd , IL-1 and macrophage derived factors chemotactic for PRINLs 5 u. FOLLOY UP AND CCUPARISW OF IMMUNOLOGICAL PARAXETERS IN HIV-INFECTED AND HIV-A0 NEGATIVE HIV-EXPOSED INFANTS C.Rorerdah1, U.Uintergerst, E.Fahrenheim, E.Eir1, B.H. Belahradsky Imrdefekt-Antxllanz der Universitars-Kinderklinikm, Linduurmstr.4, 8000 3 7 Mrn,h," 2, FRG Introduction: Infants with AIDS-related c~nplex(ARC) or AIDS following vertically acquired nlv-infection develop severe 0- ard T-cell defects. The imological paramterr and clinical r m t m of the H1V-infected children uere studied and conpared u i t h those of the HIY-exposed infants, who becam HIV-Ab negative and were Otherwise healthy. m: 35 children could be evaluated for clinical, inmawlogical, serological, end virological parameters regularly. The following innunologic data mere investigated: Total wmter of COL. C08. COZO ~sitive cells, stimulation virh phytohamgglutinin (PHI). MT3, pokeweed nitogen (PHI), staphylococcus aurws protein (SAC) and the antigens -, tberculin, vaccinia, streptolysin 0, and tetanustoxoid. 15 HlV-infected children cwld be C-red uith 12 children, who lost HIV-Antibodies and seem clinically, serologically, and virologically M r infected. In 8 further children the infectian is still uncertain. -: until the age of 20 mnths there war M detectable d i f f e r m e in the i-ological firdings of childrm uith, withcut or vith wcerraln HIV-infection (children uith full blown AIDS excludes). The t o t a l n-r of CD4 psifive cells decreases in older infected childrm, especially in those uith AIDS, despite IVIG- andlor Lidondine-therapy. The pathological results of the lpwi7ocyte-rtirmlation with PHI and OK73 correlate with the declining course of C04 cell cwnt and CD4/CD8 ratio StirmlaCiM uith PVW in infected children is already low uhm C04 cell covlts are still mrmal. In all childrm under 20 rnrnthr the antigenic rtirmlation could not be dnncnrtrated. Cmclu110n: uith CBU~~WS interpretation of our data. PW seem To be the earliest immlogical marker for HIV-infection. For rourim imnunological surveillance of HIV- infected children the determination of the CD4/CD8-ratio is sufficient. Uith Pupport of the Goverrmnt of the FRG) LOCAL T CELL RESPONSE IN POSTINFECTIOUS ENCEPHALOMYELITIS H. W. Kreth, G. W. Hofmann and F. Hashimoto 38 Univ.-Kinderklinik, D-8700 Wuerzhurg, FRG Postinfectious encephalomyelitis (PE) is a well- known complication of viral infections such as measles, rubella or varicella. The pathogenesis of these com- plications is still unclear. The absence of infectious virus or viral antigens from cerebrospinal fluid (CSF) and brain tissues led to the assumption that PE night be a T cell-rnedia- ted autoallergic process resembling experimental autoallergic encephalitis (EAE) . In this study, we have investigated the local T cell response in 5 children with PE (2 x measles encephalitis, 1 x rubella encephalitis, 2 x varicella cerebellitis). T cells Hero directly cloned from CSF exudate cells by limiting dilution in the presence of irradiated feeder cells and ZL-2. A variable pro- portion of T cell clones and lines bras found to react specifi- cally t o viral. antigens in either cytotoxicity o r prolifera- tive assays. Responses t o brain antigens (myelin basic protein, qalactocerebrosides, ganqliosides) !/ere not seen. These ob- servations strongly argue against the autoallergic hypothesis. The results are nuch more compatible with the direct invasion of the CNS by the infecting viruses. IN VIVO AND IN VITRO IMMUNE REACTIONS INDUCED BY BOVINE SURFACTANT (SF-RI 1) 39 P.Bartmann*, U.Bamberger**, F.Pohlandt*, L.Gortner* 'University of Ulm, Dept. of Pediatrics, D-7900 Ulm, FRG, **Dr.K.Thomae GmbH, D-7950 B i b e r a c h , FRG We performed a multicenter randomized trial to investigate the effect of a bovine surfactant preparation (SF-RI 1) on the treat- ment of respiratory distress syndrome in 69 preterm infants less than 30 weeks of gestation. 34 infants were treated with 50 mg/kg birth weight of SF-RI 1 with a maximum of 4 doses. Sera of all children were collected before as well as 2, 4 and 6 weeks after the initial treatment. 71% of the exspected number of sera was obtained and tested for the presence of anti-surfactant antibodies using an ELISA with a detection limit of 10 ng/ml spe- cific antibody. Anti-surfactant antibodies could not be detected in any of the serum samples. T-cells from patients with surfactant treatment were tested by 3H- thymidine incorporation for the induction of a proliferative res- ponse t o SF-RI 1 2 to 70 days after the in vivo application. SF- RI 1 alone did not stimulate T-cells from these patients in vitro. Mitogen induced T- and B-cell activation in vitro was found to be altered in the presence of SF-RI 1. Conclusion: No immune responses could be detected after in vivo application of SF-RI 1 though in vitro immune functions are al- tered in the presence of bovine surfactant. PATTERNS OF ABNORMAL CEREBRAL ENERGY METABOLISM FOLLOWING BIRTH ASPHYXIA. James M o o r c r a f t , N i c h o l a s M. Bolas, Peter L. Ho e, N. Kevin Ives. Bheeshma 40 Rajagopalan, Philip S:tton, George K. Radda. Universitv of Oxford. John Radcliffe Hosoital. Deot o f P a e d i a t r i c s , and MAC Clinical Magnetic Resonance Unit, Oxford, England. Phase modulated rotating frame imaging (PMRFI) was used t o study 23 asphyxiated neonates of gestation 34-42 (median 40) weeks by phosphorus magnetic resonance spectroscopy (MRS) a t 1-16 (med. 4) days of age. Six infants with severe encephalopathy had global phosphocreatine/inorganic phosphate (PCr/Pi) ratios of 0.18-0.86 (med. 0.59) and global Pi/adenosine triphosphate (Pi/ATP) ratios of 0.5-1.59 (med. 0.64). PMRFI data showed a progressive rise in Pi/ATP in slices 1 and 2 cms below super- ficial brain tissue. Seventeen infants with mild or moderate asphyxia had median global PCr/Pi of 1.62 and Pi/ATP of 0.35, and PMRFI did not show any consistent pattern of changing energy metabolism with depth. However, many individual infants (e.g. Infant A, global Pi/ATP 0.27) had focal areas of impaired rneta- bolism although ultrasound and conventional MRS were normal. Superficial Lcm deep 2cm d e e p Ned. Pi/ATP severe asphyxia 0.41 0.83 0.95 Med. Pi/ATP mildhod. asohvxia 0.35 0.45 0.34 . . Pi/ATP Infant A o.% 0.75 o.i8