In-Vitro Delayed Hypersensitivity Granuloma Formation In Mice Vaccinated With Ultra-Violet Attenuated Cercariae Of Schistosoma Mansoni.

1Maklad S; 2Aly FT; 2Riad M; 3Phillips SM and 1El-Sheikh N.

1Microbiology Department, Faculty of Medicine for Girls, Al Azhar University; 2Biochemistry Department, Faculty of Science, Ain Shams University and 3Allergy and Immunology Division, University of Pennsylvania, USA.

Vaccination of C57BL/6 mice with attenuated larvae of Schistosoma mansoni stimulates a high level of protective immunity against challenge infection with normal parasites. The effector mechanism is dependent upon a cell mediated delayed- type hypersensitivity (CM-DTH) response and the major site of challenge elimination appears to be the lung. The aim of the present study was to analyze the CM-DTH responses in this model at two weeks after vaccination and infection, a time that coincide with the migration of the schistosome out of the lung and at eight weeks after infection when the production of eggs and granuloma formation are maximal. An in vitro granuloma formation (IVGF) assay that utilizes polyacrylamide beads coated with soluble egg antigen (SEA) and cultured with spleen cells from C57 BL/ 6 mice vaccinated with ultra-violet (UV) attenuated cercariae of S. mansoni was performed. Naive (N1 and N2), vaccinated once (V1), vaccinated twice (V2), vaccinated/challenged (VC) and naive/challenged (NC) mice groups were assessed. The protection level induced by vaccination ranged from 52 % to 70.7 %. The granuloma index (G.I.) (mean) was 1.23 and 1.86 for V1 and for V2 respectively as compared to 1.17 and 1.31 in N1 and N2 mice groups, respectively (p< 0.001). Although significant increase in G.I was found among both VC and NC mice groups at two weeks post challenge infection, NC mice mounted higher (4.95) IVGF reaction at the time of in-vivo egg deposition as compared to VC (4.37) mice groups, (P< 0.002). It is concluded that the UV-attenuated cercariae vaccine induces significant CM-DTH responses during the pulmonary phase of schistosome migration and that this protective immunity decreases the granulomatogenic potentials of schistosome antigens during the egg-deposition phase of infection.