CELLULAR RESISTANCE TO INFECTION

doi:10.1084/jem.116.3.381

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The Journal of Experimental Medicine, Vol 116, 381-406, Copyright, 1962, by The Rockefeller Institute

ARTICLE

CELLULAR RESISTANCE TO INFECTION

G. B. Mackaness M.B.¹

¹ From The Department of Experimental Pathology, John Curtin School of Medical Research, Australian National University, Canberra

The mouse was found to be natively susceptible to Listeriamonocytogenes. Its susceptibility was attributed to the capacityof the organism to survive and multiplying in host macrophages.During the first 3 days of a primary infection the bacterialpopulations of spleen and liver were found to increase at aconstant rate. On the 4th day of infection the host became hypersensitiveto Listeria antigens and at the same time bacterial growth ceased.A rapid inactivation of the organism ensued.

Convalescent micewere resistant to challenge, but no protective factor couldbe found in their serum. Histological evidence suggested thatacquired resistance was the result of a change occurring inthe host's mononuclear phagocytes. When challenged in vitro,the macrophages of convalescent mice were found to resist infectionwith Listeria monocytogenes. Listeria-resistant cells appearedduring the course of infection at a time which correspondedwith the development of the antibacterial mechanism in the spleen.They persisted for as long as the antibacterial mechanism remainedintact in this organ.

This period of absolute resistance toListeria lasted about 3 weeks. Thereafter, the host remainedhypersensitive but unable to inactivate a challenge inoculumof Listeria. However, it remained capable of producing an acceleratedresponse to reinfection. This was thought to depend upon anability to generate a new population of resistant cells froma residuum of specifically sensitized macrophages or macrophageprecursors still surviving in the tissues as a result of theimmunological activation which occurred during the primary infection.

Submitted on March 5, 1962

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