Intestinal changes associated with expression of immunity to challenge with Eimeria vermiformis

Abstract

To provide more information on the mechanisms involved in the immune inhibition of eimeria infections, NIH mice were adoptively immunized against infection with Eimeria vermiformis by the transfer of mesenteric lymph node cells from primed animals and homologously challenged. Subsequent changes in the architecture and cellular composition of the intestine were compared with those observed in similarly challenged susceptible control mice and correlated with the development of the parasite in the two groups. Actively immunized mice were also examined. In adoptively immunized mice, the development of E. vermiformis was inhibited within 3 days of administering the challenge inoculum. Concurrent changes in the intestine included lymphocytic infiltration, crypt hyperplasia, flattening of the crypt epithelium, and a reduction in the number of Paneth cells. Hyperplasia of goblet and pyroninophilic cells in response to challenge, although accelerated and enhanced in adoptively immunized hosts, occurred after the inhibition of the parasites, and mastocytosis was not observed in these animals, findings which suggest that the activities of goblet, pyroninophilic, and mast cells were not instrumental in reducing the numbers of parasites. The intestines of immunized mice contained fewer intraepithelial lymphocytes at the time of inhibition of the parasites than did those of the controls. The * Corresponding author.

Avian coccidiosis: changes in intestinal lymphocyte populations associated with the development of immunity to Eimeria maxima

“…(Lillehoj 1989) and it is possible that the increase in their numbers, evident here towards the end of the primary infection, contributed towards its control. In studies on eimeria-infected animals that involved enumeration, either of conventionally stained i-IEL in situ (Rose & Hesketh 1982, Rose, Millard & Hesketh 1992, or those recoverable from the intestine (Findly, Roberts & Hayday 1993), there was a biphasic increase in numbers, separated at the height of infection by subnormal values. Where the phenotype of these i-IEL was examined, Findly et al (1993) found the changes in TCRI' cells mirrored those seen in the total population.…”

“…They include both antibody production and the development of an array of cell-mediated responses, the latter being the more important for protection (Wakelin & Rose 1990, Lillehoj 1991. A cellular response in the gut is a prominent feature of coccidiosis (Fernando 1982, Barber 1993 and attempts have been made to correlate it with immunity (Rose & Hesketh 1982, Rose, Millard & Hesketh 1992. Now that chicken lymphocyte markers are available, it is possible to investigate fluctuations in the sub-sets of some of these cells during the course of infection in the target host (Lillehoj & Bacon 1991, Lillehoj 1994).…”

Fas ligand- mediated killing by intestinal intraepithelial lymphocytes. Participation in intestinal graft-versus-host disease.

“…However, the biological significance of IEL cytotoxicity is unclear. The localization of IEL to areas constantly exposed to high microbiological content suggests that they may play a role in host defense; however, evidence supporting this hypothesis has not been conclusive (12)(13)(14).…”

Young Woman With Epigastric Pain

“…Capsule endoscopy gave us a unique glimpse of the tapeworm, made viewing part of its life cycle possible, and helped us to make a correct diagnosis, followed by specific successful treatment. The increased intraepithelial lymphocytes with preserved villi seen in this case, which provoked the screening of the entire small bowel in search of pathology, might represent a mucosal cell‐mediated immune response 3 …”

“…The increased intraepithelial lymphocytes with preserved villi seen in this case, which provoked the screening of the entire small bowel in search of pathology, might represent a mucosal cell-mediated immune response. 3 Oren Atia, Eva Niv and Fireman Zvi Department of Gastroenterology, Hillel Yaffe Medical Center, Hadera, Israel…”