The effect of oral recombinant interleukin (rIL) treatment on the course of Campylobacterjejuni infection and the development of mucosal immunity in mice was investigated. rIL-2, rIL-5, and rIL-6 were administered to mice at 24 and 6 h before infection and at 0, 24, and 48 h after infection with C. jejuni HC, and the subsequent development of an immune response and intestinal colonization resistance were determined. In this model, orally administered cytokines retained their biological activities with no apparent side effects. Following infection, initial bacterial counts in fecal samples collected from cytokine-treated and untreated mice were similar. However, within 48 h of infection a greater than 3-log-unit reduction in the number of C. jejuni shed in the feces was found for rIL-6-treated animals. Colonization levels were similarly reduced in rIL-5-treated mice, although the rate of clearance was somewhat slower. In contrast, rIL-2 treatment had no significant effect on colonization levels compared with that in controls. Oral rIL-6 treatment was also associated with enhanced intestinal and systemic Campylobacter-specific immunoglobulin A responses compared with those observed in either rIL-5-or rIL-2-treated animals. Upon rechallenge, initial colonization in all cytokine-treated groups was approximately 2 log units lower than that in controls. However, local infection was controlled only in rIL-2-treated mice over time. rIL-5 and rL-O6 treatment had only a marginal effect on colonization resistance following rechallenge. On the basis of these results, it appears that rIL-2 and rIL-5 or rIL-6 may function to modulate the induction and/or expression of anti-C. jejuni immunity through different mechanisms.

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SYNOPSIS Fine structure of gametocytes and oocyst formation of Sarcocystis sp. from Quiscalus quiscula Linnaeus grown in cultured embryonic bovine kidney cells was studied. Microgametocytes measured up to ∼5 μm diameter. During nuclear division of the microgametocyte, dense plaques were found adjacent to the nucleus just beneath the pellicle; occasionally microtubules were present within these plaques. These microtubules subsequently formed 2 basal bodies with a bundle of 4 microtubules between them. Microgametocytes also contained numerous mitochondria, micropores, granules, vacuoles, and free ribosomes. Each microgamete was covered by a single membrane and consisted of 2 basal bodies, 2 flagella, a bundle of 4 microtubules, a perforatorium, a mitochondrion, and a long dense nucleus which extended anteriorly and posteriorly beyond the mitochondrion. The bundle of 4 microtubules is thought to be the rudiment of a 3rd flagellum. Macrogametes were covered by a double membrane pellicle, and contained a large nucleus (∼2.5 μm), vacuoles, and a dilated nuclear envelope connected with the rough endoplasmic reticulum (ER). In young macrogametes (∼4 μm), the ER was arranged in concentric rows in the cortical region, and several sizes of dense granules were found in the cytoplasm. However, in later stages (∼8 μm) the ER was irregularly arranged and was dilated with numerous cisternae; only large dark granules remained and a few scattered polysaccharide granules were found. No Golgi apparatus or micropores were observed. After the disappearance of dark granules 5 concentric membranes appeared. Four of these fused to form an oocyst wall composed of a dense outer layer (∼66 nm thick) and a thin inner layer (∼7 nm). The 5th or innermost membrane surrounded the cytoplasmic mass which was covered by a 2‐layered pellicle and contained a nucleus, small amounts of ER, large vacuoles, and mitochondria. The sexual stages described greatly resemble those of Eimeria and Toxoplasma.

Respiratory deficient (res-) mutants of E.