339 DEFICIENT RESPONSES TO POLYSACCHARIDE ANTIGENS AND TO BACTERIOPHAGE 4 X 174 IN ASSOCIATION WITH FUNCTIONAL ASPLENIA. .A.D. Gaines, M.D. and R.H. Buckley, M.D., Durham, North Carolina.

Immunologic evaluation of a 2 11/12 year old black boy with history of recurrent H. influ- enzae and oneumococcal sepsis and disseminated varicella revealed the following normal data: I& 580, IgGl 480, IgG2 59, IgG3 27, IgG4 12, IgA 140, IgD 5.8 mg/dl; IgE 210 u/ml; CH50 39 u/ml; 45% CD2+, 36% CD3+; PHA 115,337, Con A 117,073, PWM 68,678, tetanus 69,328, candida 78,871, varicella 57,843 cpm; and tetanus and diphtheria titers both 1:19,683. Antibody to HIV was not detected in the patient or his mother. The CD4:CD8 ratio was reversed at 0.63. In addition, he had no significant antibody response to HIB (50 pre- and 33 rig/ml post- immunization) or Pneumovax (75, 77, 63 & 190 pre- and 75, 84, 59 & 220 rig/ml post-immuniza- tion for serotypes 3, 7, 9 and 14, respective- ly) * His spleen appeared normal on sonogram, but lack of splenic uptake of radionuclide indicated functional asplenia, the etiology of which could not be identified. While his slight- ly low IgM (25 mg/dl, nl 32-131) and abnormal response to intravenously administered 4 X 174 (peak 0.04 Kv, nl >8) are in keeping with de- fective splenic function, his lack of response to polysaccharide antigens contrasts with normal responses to these antigens in patients with functional asplenia from a hemoglobinopathy or with surgical asplenia. These observations sug- gest that this infant's functional asplenia could have been present throughout his life and is responsible for his defective antibody pro- duction and undue susceptibility to infection.

340 IMMUNOMODULATION OF GLUTEN AND GLIADIN ADCC BY OM-89 W K P dl . . eski,

M.D., Ph.D. and J.R. Allman, SOS., Denver. Colorado.

Host response toward ingestant anti- gens (bacteria, helminths, foods) is frequently mediated by ADCC. Normal human white blood cells (nWBC) armed with anti- body through Fc receptor recognize tar- get antigen and disintegrate in the pro- cess of autologous lysis (Allergy, 1985, 40,166). In vitro measurement of this antibody-zpendent autocytotoxic (ACT) phenomenon was accomplished using fluorescence markers; acridine orange and ethidium bromide among 10 nWBC donors. ACT effect was demonstrated when human RAST positive sera toward wheat were incubated for 2h, at 37"C, in the presence of gliadin and gluten. Preincu- bation of nWBC with immunomodulating fraction of E. coli, OM-89 (OM Lab., Geneva, Swit55rland), resulted in dose- dependent inhibition of ACT. New fluor- escent methodology confirms that OM-89 exerts immunomodulation in antibody- dependent ACT (Int. J. Immunopharmaco- logy,1987,9,349). Helminthic and food antigenic determinants may operate through common mechanisms of allergic inflammation. However, antigenic compe- tition of OM-89 could contribute to protective immunity.

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ALLERGIC SENSITIZATION TO ENZYMES IN A MEAT PROCESSING PLANT. D.I. Bernstein, S. Galson, 3. Gallagher, J. Boiano, A.B. Smith, Cincinnati, Ohio.

A cross sectional study was performed on 91 workers (W) in a meat portioning facility where beef is treated with tenderizers. In order to determine possible IgE mediated sensitization, skin prick and RAST testing were performed with purified enzyme reagents. Skin prick testing (ST) was also done to a battery of 5 aero- allergens to define atopic status. Of 91 subjects 21 (23%) reacted to either purified P, B or F. Fourteen (15%) exhibited cutaneous reactivity to purified'p; 13 (14%) to purified Br; and 11 (12%) to purified 1. Significant RAST binding ( >3 S.D. above X of 10 controls) was detected in 7 of 14 (50%) P reactive workers. In contrast, RAST reactivity was found in only 3 (23%) of 13 Ws with skin reactivity to B and in 1 (9%) of 11 Ws with cutaneous sensitivity to F. There were 9 (10%) of 91 Ws who exhibited positive S.T. to 2 or more aeroallergens. Of 21 enzyme sensitive Ws, 5 (23%) were atopic vs. 4 (6%) of 70 W with negative S.T. to P, F or B. Concurrent cutaneous sensitization to 2 or more enzymes was found in 8 (38%) of 21 enzyme reactive Ws. This study demonstrated that IgE mediated sensitization to multiple enzymes can occur in this industrial setting. The RAST was less sensitive than S.T. for detecting enzyme sensitivity. The prevalence of atopy was increased among workers sensitized to enzymes.

FOOD INPJCED ALLERGIC RHINITIS (FUR) IN CHINA.Shih-Tai Yeh(Shi-Tai Ye) M.D., Beij%ng,China

Food may cause. ski& hives has been documented in ancient Chinese literature 3000 B.C.The total prevslence of sller- gic diseases in general Chinese popula- tions is as high as 37.7g.However IXAR has not yet been reported previousEy.In the past 3 yeas,21 cases of typical FUR were encountered in oyr clinic.Male 8,Femsle 13.&e ranging 36- 8.9.Seven of them' provided a history of fsmily sller- gy.lO-gave a history of other eliexgic ailments themselves..Food sllergens como- lained by the patients end com&xmed by skin testing or food ingestkon chalPenge vere:Seseme seed 6 cases,peanut 3,Xenti.l 3,soybean 2,broad beam2,sunfEower seed 2 ,walnut 2, rioe 'j,wheat 3,corn li,Chinese cabbage 2,tomato 1 ,green Chinese onion 1 ,ge.rlic 1,peach 2,apple V,lychee(a kind of fruit commomly grow in south ChLna)1, egg 3,sea fish 3,shrinps 3,pork 1,fresh water fish1 1,milk l&Bleven of them rhi- nitis was triggered by multiple foods.

Three. Dossible mechanisms of FUR were. proposed:l.Food allergen absorbed in G.I.tract then transfered to nasal mucosa to excite symptoms. 2.Food eller- gen absorbed end cause mediator release in elementary canal,mediators were then carried to nasal mucosa to provoke symp- toms. 3.Food allergen may act as an in- helent factor due to their special odors to cause nasal. symptoms.

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