INTERACTION OF MYCOPLASMA PULMONIS WITH MOUSE PERITONEAL MACROPHAGES AND POLYMORPHONUCLEAR LEUCOCYTES

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Abstract
MYCOPLASMA PULMONIS produces persistent respiratory disease and arthritis in mice (Barden and Tully, 1969; Lindsey and Cassell, 1973). A major histological feature of both diseases is the large number of polymorphonuclear (PMN) leucocytes and macrophages in the lesions at all stages (Lindsey and Cassell, 1973; Taylor, Taylor-Robinson and Keystone, 1978). Clearance of M. pulmonis from the alveoli coincides with the influx of phagocytic cells and development of specific antibody in respiratory secretions (Cassell, Lindsey and Baker, 1974). This observation and that of the presence of mycoplasmas within PMN leucocytes (Organick, Siegesmund and Lutsky, 1966) have led to the suggestion that immune phagocytosis may be important in resistance. However, after clearance from the alveoli, mycoplasmas remain localised on the bronchial epithelium where they persist despite the presence of phagocytic cells and specific antibody. Resistance to M. pulmonis-induced arthritis and respiratory disease in mice can be transferred by convalescent serum (Cassell et al., 1973; Taylor and Taylor-Robinson, 1976, 1977), and it has been suggested that the protective effect may be due, in part, to the ability of serum to promote phagocytosis of the mycoplasmas (Taylor and Taylor-Robinson, 1977). Resistance to M. arthritidis-induced arthritis in rats and mice can also be transferred to some extent by convalescent rat or mouse serum (Cole et al., 1971; Cole and Ward, 1973a) but such sera did not promote in-vitro phagocytosis of M. arthritidis by rodent macrophages (Cole and Ward, 1973b). In contrast, specific antiserum produced in rabbits was very efficient at promoting phagocytosis of M. arthritidis. Although it is known that rabbit antiserum promotes the phagocytosis of M. pulmonis by mouse macrophages in vitro (Jones and Hirsch, 1971), the opsonic capacity of convalescent mouse serum for M. pulmonis has not been examined. The following investigations were therefore undertaken to examine the ability of convalescent mouse serum to promote phagocytosis of M. pulmonis by mouse peritoneal macrophages and polymorphs in vitro. In addition, factors were examined that may contribute to the persistence of M. pulmonis, despite the presence of large numbers of phagocytic cells and antibody at the sites of infection.