XXXX antigens facilitate experimental @entity384 : prevention with @entity4580 .

@entity55 @entity384 @entity406 @entity95 @entity4580 @entity21334 @entity12374 @entity1028 @entity165 @entity9693
OBJECTIVE: The purpose of this study was to investigate whether @entity55 (live, antigens, or polysaccharide) cause @entity1028 in a susceptible animal host with appropriate drug reversal. METHODS: At laparotomy, preparations of @entity21334 (live, @entity406 -inactivated, and heat-inactivated) in @entity12374 were applied to the adventitial surface of the abdominal aorta of @entity95 fed a @entity165 -enriched diet. Aortic diameter was measured with ultrasonography. After 3 weeks, immunohistochemistry was used to detect aortic @entity21334 and macrophages. Presence of @entity21334 DNA also was assessed. RESULTS: At high doses (5 x 10(7) organisms) periaortic application of both live and @entity406 -inactivated preparations resulted in doubling of aortic diameter after 3 weeks, from 2.0 +/- 0.5 mm to 4.3 +/- 1.3 mm (P <.02). @entity21334 DNA and antigens, together with a heavy macrophage infiltrate, were detected in the dilated aorta. In contrast, periaortic application of heat-inactivated preparations resulted in minimal macrophage influx and @entity384 . Treatment of @entity95 with @entity4580 or @entity9693 for 10 days after laparotomy abolished the effects of @entity406 -inactivated @entity21334 on @entity384 . @entity4580 reduced the number of macrophages in the aortic wall more effectively than @entity9693 . CONCLUSION: Because membrane antigenicity is retained in @entity406 -inactivated but not heat-inactivated organisms, in this experimental model, chlamydial membrane antigens (rather than live organisms) appear to cause the @entity384 and associated macrophage recruitment. @entity4580 is likely to reverse these effects with an antiinflammatory mechanism.
