Kinetics and maintenance of acquired resistance in mice to Listeria monocytogenes

Abstract

In the mouse system, acquired resistance to Listeria monocytogenes can only be demonstrated after immunization with viable microorganisms. A successful state of immunity cannot be elicited with formalin-killed organisms or bacterial cell-derived products. Viable, serologically cross-reactive organisms (not mouse pathogenic) do not induce a state of immunity as measured by acquired resistance. The duration of immunity, once established, is dose independent, and the absolute interval of its existence is not extended by secondary challenge with large numbers of viable organisms. The decline of immunity in actively immunized animals is not altered by antigenic challenge with formalin-killed cells or cell products. This indicates that the cellular requirements for the development of host resistance are similar for induction as well as maintenance. In vitro measurements of cellular immunity by migration inhibition indicate that formalin-killed organisms as well as cell products were recognized by actively sensitized lymphocytes obtained from immune animals.

Course of infection and development of immunity in experimental infection of mice with Listeria serotypes

“…It could be shown by the passive transfer of spleen cells that the mechanism of protective immunity is basically identical to the mode of action first described by Miki and Mackaness (12). Protective immunity, however, is rather short lived after primary infection with L. innocua, a finding that has been described by Kearns and Hinrichs (7) for infection with L. monocytogenes serotype 1/2b. The dose dependency of protective immunity after primary infection with L. innocua furthermore suggests that immunity can be acquired only when the animal host contains great numbers of microorganisms.…”

Induction of immunity with avirulent Listeria monocytogenes 19113 depends on bacterial replication

“…Generation of acquired cellular resistance (ACR) to listerias characteristically requires immunization by sublethal inoculation of viable, virulent L. monocytogenes (7,10). However, Wirsing von Koenig et al (23) reported that extremely large doses of avirulent Listeria strains can stimulate host resistance to challenge from a virulent Listeria strain.…”

“…These virulent Listeria strains are able to replicate within professional phagocytes, as demonstrated during in vitro and in vivo studies (10,13). In contrast, exposure to either apathogenic Listeria strains or nonviable virulent L. monocytogenes fails to promote a protective immune response (1,3,6,7,12,22,23) unless associated with an adjuvant (19)(20)(21). Furthermore, antigen preparations derived from listerias fail to induce acquired resistance as well.…”

Expression of systemic protection and delayed-type hypersensitivity to Listeria monocytogenes is mediated by different T-cell subsets

“…The initial arguments which proposed that these two phenomena are direct manifestations of the same cell population were based on observations which showed an apparent inseparability of ACR and DTH during the immune response (17)(18)(19). This association is highlighted by the need for an active infection to induce both ACR and DTH, unless special immunizing techniques are applied (4, 14,21,29,[31][32][33]. Also, the kinetics of development and longevity of these responses are similar (17,24,26).…”