Delayed hypersensitivity and acquired cellular resistance in guinea pigs infected with Listeria monocytogenes

Randomly bred guinea pigs were infected with Listeria monocytogenes using the intracardial, intravenous, and intraperitoneal routes of infection. Doses of Listeria ranged from 5 to 1,000 x the 50% lethal dose based on the 50% lethal dose for intracardially injected Listeria. A complete necropsy was performed on all animals that died after infection. Gross and microscopic examination of tissues revealed major pathological features which include myocarditis, edema and congestion with interstitial pneumonitis present in the lungs, and fatty hepatic changes with focal necrosis. For all or a majority of the animals, large numbers ofListeria were likewise recovered from these organs and from lymph nodes, spleen, kidneys, and adrenal gland tissue. Of the three routes of infection used, guinea pigs were most susceptible to Listeria injected via the intracardial route. The relatively high lethal dose of Listeria for the guinea pig, however, suggests that the organism is a low-grade pathogen for this species.

“…Samples (1 ml) of this suspension were stored at -70'C (frozen stock cultures). The 50% lethal dose for intracardially injected Listeria was 1.2 x 105 as reported previously (6).…”

supporting

confidence: 68%

“…Use of Listeria infection in guinea pigs for the purpose of in vitro and in vivo characterization of acquired cellular resistance, delayedtype hypersensitivity, and lymphokine production has been under investigation in this laboratory (5,6). A very limited number of studies so far have employed Listeria in the potentiation of tumor immunity (1,2,12,13).…”

mentioning

confidence: 99%

Bacteriological and histopathological evaluation of guinea pigs after infection with Listeria monocytogenes

Dustoor¹,

Croft²,

Fulton³

et al. 1977

“…Listeria monocytogenes in the mouse and rat suggest that the development of acquired cellular resistance is dependent upon the development of delayed-type hypersensitivity (DTH) (9,10). Studies in this laboratory (5) showed that, in guinea pigs infected with one-half a 50% lethal dose of Listeria, bacterial multiplication occurs only during the first 24 h after infection. Listeria-infected animals are also resistant to a small challenge dose of Listeria given 48 h, 7 days, or 2 weeks after the primary infection.…”

Section: Studies Of Acquired Cellular Resistance Tomentioning

confidence: 99%

“…The skin tests were read at 2, 4, 8, 12, 24, and 48 h. Cutaneous reactivity was measured by using three parameters: (i) degree of erythema, (ii) mean diameter of erythema, and (iii) changes in double skin thickness at the reaction site. The degree of erythema was scored arbitrarily as described previously (5). Induration was measured using a Schnelltester (System Kroplin, type A, 2T, H. C. Kroplin, Schliictern, Hessen, Germany).…”

Section: Studies Of Acquired Cellular Resistance Tomentioning

confidence: 99%

Blastogenesis as an in vitro correlate of delayed hypersensitivity in guinea pigs infected with Listeria monocytogenes

Fulton¹,

Dustoor²,

Kasinski³

et al. 1975

Self Cite

Randomly bred guinea pigs of both sexes were injected intracardially with one-half a 50% lethal dose of Listeria monocytogenes. When these animals were skin tested with 30 ,g of a water-soluble extract of sonically disrupted Listeria, animals had uniformly detectable levels of delayed-type hypersensitivity (DTH) 6 days after infection. Histological examination of skin test reaction sites, after fixation in Helly fixative and Giemsa staining, revealed a classical tuberculintype infiltrate consisting primarily of mononuclear cells with few polymorphonuclear cells. Many of the small vessels showed perivascular cuffing. When purified peritoneal exudate lymphocytes from these animals were cultured in vitro in the presence of various concentrations of Listeria antigen, it was found that the optimal antigenic dose for specific antigen-induced incorporation of [3H Ithymi- MATERIALS AND METHODSAnimals. Randomly bred albino guinea pigs of both sexes were obtained from local suppliers. The 647 on July 15, 2020 by guest http://iai.asm.org/ Downloaded from

“…ACR against L. monocytogenes is usually measured by the pattern of elimination of challenge bacteria from the spleen (13,14,24), and DH is assayed by delayed footpad reaction (15,19) or by the macrophage migration inhibition test (6). There are many reports showing that ACR is expressed in association with DH (7,15,19), and it seems that many investigators regard DH to be essential for the expression of ACR. However, several reports have shown the dissociated development of ACR and DH (10,25).…”

mentioning

confidence: 99%

Direct correlation between delayed footpad reaction and resistance to local bacterial infection

Mitsuyama¹,

Nomoto²,

Takeya³

1982

The resistance to bacteria was studied at the site of delayed footpad reaction in mice immunized with Listeria monocytogenes. When a challenge injection of listeria was given into the footpad of immune mice, no enhancement of bacterial elimination was observed before the generation of delayed footpad reactivity. After the generation of delayed reactivity, an enhanced elimination of listeria or Salmonella typhimurium was observed only at the site of strongly positive delayed footpad reaction elicited with listerial antigen. Such an enhancement in bacterial elimination was also found at the site of delayed footpad reaction induced by immunization with heterologous erythrocytes. Both delayed footpad reaction and local resistance could be transferred locally by immune spleen cells in a dose-dependent fashion, but were completely abrogated when recipient mice were treated with carrageenan or whole-body X irradiation. Macrophage accumulation was an important factor in the expression of resistance at the reaction site. These results suggest that the delayed footpad reaction contributes to host defense by enhancing the local resistance to bacteria.