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I I I I I i I I I I I I I I I I I I ~75 AUTHOR: MACKENZIE, J.S. AND R.L.P. FLOWERS .p.~:1979 ~T_J.T~: THE EFFECT OF LONG-TERM EXPOSURE TO CIGARETTE SMOKE ON THE HEIGHT AND SPECIRCITY OF THE SECONDARY' IMMUNE RESPONSE TO INFLUENZA VIRUS IN A MURINE MODEL SYSTEM. CITATIQN= JOURNAL OF HYGIENE, CAMBRIDGE 83, 135-141 (1979) .~;TU DY DESIGN;. The effect of long-term exposure to cigarette smoke on the height and specificity of the secondary humoral immune response to influenza was investigated in a murine model system. C3H/HeJ Inbred female mice were exposed to fresh cigarette smoke in a Hamburg II small animal smoking machine set to deliver a mixture of smoke: air (1:7) at a puff volume of 35 ml. This corresponded, by body weight, to 20-30 cigarettes per day of human consumption. The mice were exposed daily for approximately 8 min over a period of 36 weeks. Age-matched control mice were kept over the same period of time. Influenza virus strains A/MEL (HON1), A/CKS (HON1), and A/BEL (HON1) were employed in this study. Mice were inoculated by intranasal route with 25 pl virus diluted to give a dose of 0.1 LD 50. Control mice were inoculated with diluent only. .FINDINGS/RESULTS: It was shown that if mice were pre-immunized with a sub-lethal infection of influenza virus and then exposed to cigarette smoke daily for 36 weeks, they were able to mount a secondary immune response of normal height on subsequent challenge with the homologous virus strain. However, the response was less specific than that elicited in control mice, with high titres of cross-reacting antibody by haemagglutination-inhibition to the following strain in the same antigenic series. Recall of antibody to the previous strain in the antigenic series was not observed in either control or smoke-exposed animals. The results obtained in this study serve to correct an earlier discrepancy between the murine system and human studies in which the response to influenza infection in mice was depressed by prolonged exposure to cigarette smoke, whereas in man the response of smokers did not differ significantly from that of non-smokers. This apparent discrepancy had been caused by a lack of previous experience of influenza in the mice, which had therefore mounted a primary response, compared with the secondary response observed in human studies. cq