Monocytogenes-infected Mice Research Articles

Effect of splenectomy on production of interferon and colony-stimulating factor in Listeria monocytogenes-infected mice.

Splenectomy of mice genetically susceptible to Listeria monocytogenes genetically susceptible mouse strains increased their resistance to L. monocytogenes infection but had no effect on the course of infection in L. monocytogenes-resistant mice. However, splenectomy led to a dramatic decrease in the production of colony-stimulating factor and interferon after L. monocytogenes infection in all mouse strains examined.

Decreased resistance to Listeria monocytogenes in mice injected with killed corynebacterium parvum: association with suppression of cell-mediated immunity.

To investigate the therapeutic potential of killed Corynebacterium parvum, its effects on the course of Listeria monocytogenes infection in mice was studied. Mortality in mice given C. parvum after L. monocytogenes infection was greater than in mice given C. parvum before infection or infected with only L. monocytogenes. C. parvum alone resulted in no mortality. Spleens from infected mice given C. parvum had increased numbers of L. monocytogenes. Peritoneal macrophages from mice infected with only L. monocytogenes were activated by four days after infection, whereas those from mice given L. monocytogenes plus C. parvum were not. By seven days macrophages from both were activated. Delayed hypersensitivity and in vitro lymphocyte transformation in response to L. monocytogenes antigen were strikingly suppressed in infected mice given C. parvum. The increased susceptibility of L. monocytogenes-infected mice given C. parvum may have been due to delayed macrophage activation resulting from suppression of thymus-derived lymphocyte responses.

Role for activated macrophages in resistance against Trichinella spiralis.

To determine whether activated macrophages are important in resistance against the intestinal phase of nematode parasites, we studied Trichinella spiralis infections in mice with normal macrophages and in mice with macrophages activated by either chronic Toxoplasma gondii or acute Listeria monocytogenes infections. The peak T. spiralis adult worm burden in the intestines of normal C57BL/6 or Swiss Webster mice occurred from 6 to 14 days after infection. Subsequent expulsion of worms from the intestines occurred from 8 to 20 days after infection. C57BL/6 mice chronically infected with T. gondii and then challenged with T. spiralis larvae had significantly lower peak intestinal worm burdens (P < 0.05) than normal C57BL/6 mice similarly challenged. Swiss Webster mice infected 7 or 13 days earlier with L. monocytogenes and then challenged with T. spiralis larvae had significantly lower peak worm burdens (P < 0.01) than uninfected mice. The time of expulsion of adult worms was not affected by either infection. Swiss Webster mice infected 42 days earlier with L. monocytogenes (i.e., possessing lymphocytes sensitized to L. monocytogenes but not possessing activated macrophages) did not have a lower worm burden than uninfected mice. Serum factors (e.g., antibody) did not appear to play a role because normal mice injected with serum from L. monocytogenes-infected mice had worm burdens similar to those of mice injected with normal serum. The histopathology of intestines of mice infected with T. gondii or L. monocytogenes was the same as that of normal mice. When T. spiralis larvae were incubated with normal macrophages or macrophages from T. spiralis-infected mice in vitro for 24 h, the number of larvae with adherent T. spiralis macrophages was significantly (P < 0.005) greater than the number of larvae with adherent normal macrophages. These studies suggest a role for activated macrophages in resistance to T. spiralis.

Plasma enzyme changes in Listeria monocytogenes-infected mice.

ported by numerous investigators (reviewed by Seeliger, 1961; Gray and Killinger, 1966). In contrast, until recently there has been very little known about the biochemical and physiological changes occurring during Listeria monocytogenes infections. Mcllwain et al (1964) described changes such as abnormalities in electrocardiogram tracings, hyperglycemia followed by hypoglycemia, and increases in blood pyruvate and lactate in rabbits following injection with a proteinaceous fraction of L. monocytogenes. Alterations of serum proteins, including haptoglobin and transferrin, in mice infected with Listeria were reported by Sword (1966a). Subsequent studies showed that iron compounds caused a reduction in the LD50 of Listeria for mice and were stimulatory for the in vitro growth of the pathogen. Growth of L. monocytogenes and mortality from experimental infection appeared to be correlated with availability of iron to the bacteria and suggested the possibility that host iron metabolism plays a part in the in-

Mechanisms of acquired resistance in mouse typhoid.

Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular S. typhimurium pretreated with immune serum, cells from infected animals killed virtually all ingested organisms and did so at an accelerated rate. Macrophages from Listeria monocytogenes-infected mice were shown to possess similarly enhanced microbicidal activity against S. typhimurium. Furthermore, the growth of S. typhimurium in the liver and spleen was more effectively restricted in Listeria-infected mice than in animals vaccinated with heat-killed S. typhimurium, even though the Listeria-infected animals possessed no demonstrable cross-reacting antibody to S. typhimurium. The lack of resistance in the mice vaccinated with heat-killed organisms could not be attributed to any deficiency of humoral factors, since the serum from these animals was as effective at promoting phagocytosis and killing by macrophages as serum from actively infected (and demonstrably resistant) mice. Conversely, Salmonella-infected mice were totally resistant to intravenous challenge with L. monocytogenes. The level of resistance in individual animals was related to the numbers of residual Salmonellae remaining in the tissues; mice with heavier residual infections being the more resistant. Specific antiserum from mice vaccinated with heat-killed S. typhimurium was found to be significantly protective only when the intraperitoneal route of challenge was employed. The foregoing studies have been interpreted to mean that enhancement of the microbicidal ability of macrophages is the mechanism of major importance in acquired resistance to S. typhimurium infection in mice.