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. 1993 Dec;77(4):395-404.
doi: 10.1006/expr.1993.1099.

Brugia pahangi: effects of protective resistance on lymphatic lesions and granulomatous inflammation in infected jirds (Meriones unguiculatus)

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Brugia pahangi: effects of protective resistance on lymphatic lesions and granulomatous inflammation in infected jirds (Meriones unguiculatus)

T A Petit et al. Exp Parasitol. 1993 Dec.

Abstract

Effects of protective resistance on lymphatic lesions and granulomatous inflammation in infected jirds (Meriones unguiculatus). Experimental Parasitology 77, 395-404. The hypothesis that protective immune responses play a role in the induction of filarial-associated lymphatic lesions was tested in jirds immunized twice with 75 Brugia pahangi radiation-attenuated third-stage larvae. Lymphatic lesions and granulomatous reactivity were compared in immunized, infected, and naive jirds at both acute and chronic periods following challenge with 100 third-stage larvae. Challenge worm burdens were reduced in immunized jirds at both infection periods. The ratio of lymph thrombi to lymphatic worms, an indicator of lymphatic lesion severity, was significantly greater in immunized jirds than in nonimmunized-challenged jirds during acute but not chronic infections. Parasite-specific-granulomatous hypersensitivity was assessed by measurements of granuloma areas around B. pahangi-soluble adult worm antigen-coated sepharose beads embolized in the lungs prior to necropsy. Marked granulomatous inflammatory responses seen during the acute period in both immunized-challenged and nonimmunized-challenged jirds were significantly reduced in similar jirds during chronic periods. Jirds with existing B. pahangi infections were not resistant to homologous challenge infection and had fewer lymphatic lesions and reduced granulomatous inflammatory responses to soluble adult worm antigen compared to previously naive jirds at acute periods postchallenge. These data suggest that protective immune responses increase the severity of filariae-induced lymphatic inflammation. The subsequent modulation of these lesions is probably associated with parasites that survived the protective immune response.

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