Effect of Treponema hyodysenteriae infection on mucosal mast cells and T cells in the murine cecum

Abstract

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 < 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/W' 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.

Susceptibility of inbred mouse strains to infection with Serpula (Treponema) hyodysenteriae

“…Mouse strains are identified for both panels by the inset in panel B. (14) 85 (13) 100 (19) 100 (20) 93 (14) 86 (7) 57 7C3H/HeJ 86 (7) 71(7) 64 (14) 38 (14) 13 (8) NDc ND C57BL/6J 29 (7) 71 (7) 0 (6) 0 (6) ND ND ND DBA/1J 100 (6) 86 (7) 14 729 (7) ND ND ND BALB/cByJ 0 (8) 0 (8) 0 (8) 0 (8) ND ND ND a The percentage of mice in each challenge group that were culture positive for S. hyodysenteriae B204 at the time the mice were killed. For C3H/HeN mice infected with 1 x 104 organisms, seven of the mice were killed at 10 days p.i.…”

“…Potential virulence determinants of S. hyodysenteriae include an endotoxinlike moiety (21,22) and a P-hemolysin (18,31). In vivo models (other than pigs) used to examine the virulence of S. hyodysenteriae have included guinea pigs (14), mice (12,13,20,35), and chicks (36). Because of availability of reagents and the ability to adoptively transfer cells, we have utilized inbred mice as a model to study the pathogenesis of S. hyodysenteriae.…”

[beta]-hemolysin and the pathogenesis of Serpulina hyodysenteriae infection

“…Lymphocytes collected from swine infected with S. hyodysenteriae were shown to be capable of undergoing blastogenesis in vitro following exposure to 5. hyodysenteriae antigens, and some infected animals were capable of developing delayed type hypersensitivity reactions following intradermal injection of serpulinal antigen (73). Mucosal mast cell deficient mice were utilized to demonstrate the lack of a role for mucosal mast cells in lesion development in mice infected with S. hyodysenteriae (122). Most recently, examination of surface molecule expression and cytokine profiles of lymph node and lamina proprial lymphocytes from mice infected with S. hyodysenteriae on either a short or long term basis indicated that T-lyraphocytes from infected mice secreted more interferon-gamma, especially in response to Bacteroides vulgatus antigens, as well as to S. hyodysenteriae antigens, early in infection (43).…”