Immune T cells sorted by flow cytometry confer protection against infection with Treponema pallidum subsp. pertenue in hamsters.
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The role of cell-mediated immunity against infection with Treponema pallidum subsp. pertenue in humans or experimental animals is unclear. Hamsters injected subcutaneously in the hind paws with 4 x 10(6) unfractionated lymph node cells or enriched lymph node T cells (immunoglobulin negative, Ia negative) from T. pallidum subsp. pertenue-immune hamsters were resistant to challenge with T. pallidum subsp. pertenue. The popliteal lymph nodes of hamsters that received immune cells weighed less and had significantly fewer treponemes than did lymph nodes from hamsters infused with cells from nonimmune donors. Furthermore, recipients of immune T cells failed to develop antitreponemal antibodies 21 days after challenge. Enriched T cells were obtained by flow cytometric separation by using monoclonal anti-Ia antibody 14-4-4s, which identified hamster B cells. Flow cytometric analysis by two-color immunofluorescent staining with anti-hamster-immunoglobulin and monoclonal anti-Ia antibody 14-4-4s confirmed that monoclonal anti-Ia antibody 14-4-4s recognized B cells. In addition, lymph node cells obtained after treatment with anti-Ia monoclonal antibody 14-4-4s and complement were 97% T cells, as determined by monoclonal antibody 20, a hamster T-cell marker. These results demonstrated that highly enriched T cells (immunoglobulin negative, Ia negative) from T. pallidum subsp. pertenue-immune hamsters conferred partial protection on hamsters against infection with T. pallidum subsp. pertenue. (+info)
Diarrhea induced by Treponema hyodysenteriae: a young chick cecal model for swine dysentery.
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The experimental infection of 25 young chicks with Treponema hyodysenteriae was carried out. Treponemes were isolated from 21 of 25 chicks on day 21 after inoculation. The ceca of chicks infected with treponemes were atrophied. The lumen was filled with a white watery fluid instead of digested feed. In some infected chicks, a cecal core was observed with the fluid in the cecum. The cecal core was grayish, hard, and rod shaped. It consisted of eroded cells and debris of treponemes and resembled the pseudomembrane. Bloody mucus was also observed in one chick. The thickness of the mucosae in 17 of 25 chicks were markedly increased. The histological changes were classified into two types. In the case of regressive changes of epithelial cells which mean severe erosion, the laminae propriae were exposed. Hemorrhage, edema, and heterophil infiltration in the laminae propriae were also confirmed. Numerous treponemes were observed within the edematous area under the remaining epithelia and also invaded the epithelial cells and laminae propriae. In the other case, progressive changes, that is, hyperplasia of mucosal epithelial cells and elongation of the crypt, were observed. The epithelia consisted mainly of cuboidal basophilic cells, mitotic cells, and goblet cells. The mitotic cells increased in number and were also observed near the superficial luminal surface of the ceca. Mucous goblet cells were also considerably increased in number. The erosion of superficial luminal epithelial cells was not so severe, but edema in laminae propriae was frequently observed. Electron-microscopic observation demonstrated that the basophilic epithelial cells were polyribosome rich, mitochondria poor, and lipid droplet poor. Furthermore, tonofibril-like structures under the terminal web in cytoplasms were lost, and numerous membrane-bound vesicles at the terminal web with free ribosomes were observed. In places, a number of vesicles were observed between microvilli, and some vesicles were released from the apical cytoplasm of epithelial cells. Microvilli also became scarce and irregular. The junctional complexes between cuboidal cells became unclear, the interdigitations between cuboidal cells became loose, and the intercellular spaces were widened. In conclusion, the appearance of numerous membrane-bound vesicles at the terminal web and the dilated intercellular space indicates increased secretion of water and electrolytes, and the abnormal proliferation of such immature epithelial cells indicates impaired absorption. On the basis of our findings, we can say that diarrhea induced by T. hyodysenteriae can be developed by synergism between impaired absorption and increased secretion by intestinal mucosae with hyperplastic immature epithelial cells.(ABSTRACT TRUNCATED AT 400 WORDS) (+info)
Effect of Treponema hyodysenteriae infection on mucosal mast cells and T cells in the murine cecum.
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The pathogenic mechanisms responsible for the development of lesions in swine and mice after infection with Treponema hyodysenteriae have not been fully characterized. The release of inflammatory mediators from mast cells has been postulated to play a role in lesion development during swine dysentery. Therefore, C3H/HeN mice were infected with T. hyodysenteriae, and mucosal mast cell (MMC) numbers were examined in cecal sections. An initial increase in MMC numbers from 13 to 22 per 50 crypt villus units was observed, but at 20 days postinfection the numbers significantly decreased (P less than 0.05) to 5 MMC per 50 crypt villus units. Immunohistochemical analysis performed on cecal sections failed to show a significant change in lamina proprial T-lymphocyte subsets. Numbers of T. hyodysenteriae CFU recovered from the cecum were stable throughout the experimental time period. Mast cell-deficient W/Wv mice and their mast cell-sufficient littermates were also infected to determine whether MMCs were necessary for the occurrence of T. hyodysenteriae-induced lesions. W/Wv mice were as susceptible to infection as their normal littermates and developed similar macroscopic and microscopic lesions. These results indicate that changes in MMC numbers can be detected after an infection with T. hyodysenteriae; however, on the basis of observations of infected W/Wv mice, mast cells are not required for lesion development in the murine model. (+info)
Diagnosis of treponemal co-infection in HIV-infected West Africans.
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