Treponeme-associated foot disease has been described in cattle with digital dermatitis and sheep with contagious ovine digital dermatitis. In this study, severe foot lesions in dairy goats associated with digital dermatitis treponemes (i.e. Treponema medium, Treponema phagedenis and Treponema pedis) were characterized macroscopically, radiographically and histologically. The main macroscopic foot lesion was of extensive solar ulceration with or without exophytic papilliform hyperkeratosis. Radiographically, the distal phalanx and distal sesamoid bones were severely damaged and remodelled. Histologically, the lesion was categorized as a chronic lymphoplasmacytic, suppurative and ulcerative pododermatitis. Immunohistochemistry identified the spirochaetal microorganisms located extracellularly in the superficial horn. Study limitations mean that the treponeme bacteria could not be considered the sole or causal agents in the cases described.
Peritoneal macrophages from Mesocestoides corti-infected mice showed a marked and progressive loss of ability to act as accessory cells for syngeneic Con A-stimulated mesenteric lymph node lymphocytes. The same effect on the macrophages could be induced by intraperitoneal injection of M. corti culture supernatant, despite a concurrent increase in numbers of peritoneal adhesive macrophages. The findings are used to compare and contrast the known immunomodulatory effects of M. corti and taeniid metacestodes, the latter differing chiefly in their potential for modifying T-cell as well as macrophage behaviour.
Summary :Taenia multiceps secretions modify accessory cell activity in macrophages. The present experiments were designed to elucidate the cellular mechanisms involved. W hile normal, murine peritoneal macrophages amplified mitogen-activated T-cell proliferation, macrophages modified by exposure to parasite secretions inhibited this proliferation. The modified behaviour w as shown by glutaraldehyde-fixed as well as living macrophages, and modification w as inducible by FPLC fraction 2 4 of coenurus fluid and w as associated with an expanded population of la -macrophages. Secretory products of parasite-activated macrophages also inhibited T-cell proliferation, and secretion was prevented by indomethacin. The measurement of modified accessory activity w as not influenced by the concentration of tritiated thymidine in lymphocyte proliferation assays. Consequently there is no evidence that the reported events are affected by macrophage-derived, cold thymidine secretion. It is concluded that T. multiceps is able to manipulate macrophage accessory function by mechanisms which involve altered histocompatibility antigen expression and the secretion of prostaglandin.
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E x p o s u r e t o s o l u b l e f a c t o r s f r o m T aen ia m ulti ceps im p a ir s t h e a c c e s s o r y f u n c t i o n o f m a c r o p h a g e s in p r e s e n t i n g m i t o g e n i c s ig n a ls t o ly m p h o c y t e s ( R a k h a e t a l ., 1 9 9 1 a ). T h e p a r a s i t e c o m p o n e n t s w h i c h m e d i a t e t h is m o d i f i c a t i o n c a n b e s e p a r a t e d c h r o m a t o g r a p h i c a l l y f r o m o t h e r im m u n o log ic a ll y a c t i v e c o m p o n e n t s o f T. multiceps, s u c h a s t h e T -c e l l m i t o g e n i c f a c t o r . T h e m a c r o p h a g e m o d if y in g f r a c t i o n o f T. m ulticeps h a s b e e n s h o w n t o im p a ir t h er o s e t t e f o r m in g r e s p o n s e o f m u r in e ly m p h -n o d e c e lls t o s h e e p e r y t h r o c y t e s ( R a k h a et al., 1 9 9 1 b), b u t t h e s a m e f r a c t i o n is a l s o a n a n t ig e n w h i c h i n d u c e s a n t i b o d y r e s p o n s e in t h e n a t u r a l o v i n e i n f e c t i o n ( R a k h a is a p o t e n t ia l m e a n s f o r t h e p a r a s it e t o r e g u la t e t h e h o s t 's p r im a r y a n d s e c o n d a r y r e s p o n s e t o a n t ig e n , it a p p e a r s im p o r t a n t t o id e n t if y c h a n g e s in m a c r o p h a g e m e m b r a n e s t r u c t u r e o r s e c r e t o r y b e h a v i o u r w h i c h a r e c h a r a c t e r i s t i c o f t h e m o d if ie d s t a t e . T h e p r e s e n t r e p o r t d e s c r i b e s i n c r e a s e d f r e q u e n c y o f l a -c e l l s in m o d if ie d m u r in e m a c r o p h a g e p o p u la t io n s , a n d t h e s e c r e t i o n , b y a n i n d o m e t h a c i n -s e n s i t i v e m e c h a n i s m , o f a s o l u b l e s u p p r e s s o r o f l y m p h o p r o lif e r a t iv e r e s p o n s e t o T -c e l l m it o g e n s .
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