Peritoneal macrophages recovered from chickens 15 to 20 days after inoculation with fowlpox virus and showing a delayed hypersensitivity reaction against fowlpox antigens demonstrated an enhanced antimicrobial effect against fowlpox virus as well as unrelated viruses and bacteria. Inoculation of normal chicken macrophage cultures with fowlpox virus resulted in approximately a 200-fold increase in virus titer by 96 h, whereas the virus showed less than a fourfold increase in macrophage cultures from fowlpox-immune chickens. Similarly, the titer of Newcastle disease virus increased by more than 1 log in cultures of normal macrophages, whereas the titer decreased by approximately 1 log after infection of fowlpox-immune macrophages. Vaccinia, vesicular stomatitis, and herpes simplex viruses, which are not natural pathogens of chickens, failed to replicate in cultures of either normal or fowlpox-immune macrophages. By using Salmonella gallinarum , it was further demonstrated that the antimicrobial activity of fowlpox-immune macrophages encompassed not only nonspecific viruses but also bacteria. Infection of normal macrophages with Salmonella resulted in intracellular replication of the organism between 0 and 24 h as determined by microscope examination and viable bacteria counts. In contrast, cultures of fowlpox-immune macrophages failed to show an increase in intracellular organisms and showed a marked decrease in viable bacteria. In conclusion, these studies clearly showed that cellular immunity, previously demonstrated in mammalian species, develops in chickens after infection with fowlpox virus.

Tumors were induced in adult and newborn rabbits by inoculation of fibroma virus. After 10 to 14 days, oil-induced peritoneal macrophages were harvested, purified, and tested in vitro for interferon synthesis after stimulation with specific and nonspecific viruses. Peritoneal macrophages from adult rabbits that had initiated tumor regression produced high levels of interferon (titers ranged from 160 to 640) after stimulation with fibroma virus, whereas macrophages from normal adult rabbits failed to produce significant levels of interferon under the same conditions (titers ranged from <10 to 10). Furthermore, fibroma-immune macrophages responded to vaccinia virus and Newcastle disease virus with higher levels of interferon than did normal macrophages. In contrast, macrophages from newborn tumor-bearing rabbits that showed no evidence of tumor regression failed to respond to fibroma virus stimulation with higher levels of interferon (titers ranged from <10 to 10). These macrophages did, however, yield significantly more interferon than newborn control macrophages when stimulated with a good interferon inducer, Newcastle disease virus (titers ranged from 10 to 80). These data suggest that interferon production may be an expression of macrophage activation to fibroma antigens and that macrophage activation is impaired in newborn rabbits with progressive growing tumors.