Immunological reactivity of jird (meriones unguiculatus) to infection of brugla pahangi

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Date
1993
Authors
Panasoponkul, Chotechuang
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Abstract
Filariasis is a chronic parasitic infection which is considerable public health and socioeconomic importance in many tropical and subtropical countries and remains a major health problem in many areas of the world. The present study was undertaken to elucidate the various immunoregulatory mechanisms elicited by different doses of subcutaneous infection with B. pahangi in jirds (Meriones unguiculatus) We found that jirds infected with B. pahangi showed microfilaraemia at about 8-10 weeks postinfection. The microfilarial densities was dependent on the number of infective larvae inoculated and times post-infection, but it was not dependent on the number of adult worms recovered from the infected jirds. The average worm recovery were 36, 28.4, 27.07 and 22.53% in jirds infected with 5, 25, 75 and 25 x 3 infective larvae respectively and this was not significantly different. The majority of !he adult worms in every group of the infected jirds were found in the lymphatics of spermatic cords. The rest of the worms were distributed in heart and lungs and other lymphatics. No worms were found in the lymphatics of cervical and axillary. The average length of both male and female adult worms recovered from all the infected jirds also did not show any significant difference. This means that the inoculation of up to 75 infective larvae did not cause any crowding effect or resistance to the parasite growth and microfilariae production. Peripheral blood eosinophilia was observed in all infected jirds. There were two distinct peaks during the course of infection, one occurred at 2-3 weeks post-infection and the other occurred at 7-10 weeks post-infection. The number of eosinophils appeared to be directly proportional to the number of infective larvae inoculated and were never below the values of control jirds throughout the period of 16 weeks post-infection. The number of eosinophils in microfilaraemic jirds were higher than in amicrofilaraemic jirds but they were not dependent on the total number of circulating microfilariae. Analysis of the other llaematological parameters showed no significant changes. All the jirds infected with B. pahangi expressed some degree of non-specific humoral immunosuppression throughout the period of 16 weeks post-infection when compared to the uninfected control group.The suppression was time dependent, it is higher in the early weeks of infection and dropped gradually with the evolution of the infection. It was also found that plastic . adherent cells were responsible for the number of PFC reaction and non-adherent cell fraction from infected jirds seemed to be able to induce suppression in control cell population. When in vitro blastogenic assays were performed, we . found that non-specific cellular immunosuppression occurred in both spleen and lymph node cells of infected jirds but it was more prominent in the spleen cells. The suppression was not dependent on the quantum of the . infections but dependent on the timesĀ· post-infection; the maximum suppression occurred at about the time of patency. However, the specific cellular immunosuppression occurred only in the spleen cells of jirds infected with 25 and 75 infective larvae while lymph node cells from all the infected jirds exhibited significant responses to all the antigens. There was no significant difference in the responses among the three antigens. The results showed that both antigen specific and non-specific regulatory activities were correlated with the presence of circulating microfilariae and that specific suppression was only anatomically restricted to the spleen. When co-cultivation were performed in blastogenic assay, we found that spleen cells from the infected jirds were able to suppress the PHA and Con A responsiveness of normal spleen cells and that these infected spleen cells were also able to suppress all the antigens responsiveness of lymph node cells from the infected jirds. In contrast, lymph node cells from the infected jirds were unable to suppress both PHA and Con A responsiveness of normal lymph node cells. Further characterize the spleen cells responsible for the suppression, showed that depletion of plastic adherent spleen cells from the infected jirds restored the blastogenic response to PHA and Con A. These plastic adherent spleen cells were able to suppress PHA and Con A responses of the infected non-adherent spleen cells and normal lymph node cells. However, depletion of plastic adherent spleen cells frorn the infected jirds did not restore the blastogenic responses to all the antigens, but these plastic adherent spleen cells were able to suppress all the three antigen responses of the infected lymph node cells. The lgG antibody could be first detected in sorne infected jirds at one week post infection, with the highest titer at about the tirne of patency. The high titers of the antibody persisted throughout the period of 16 weeks post-infection in all groups of the infected jirds. The levels of lgG antibody in jirds infected with B. pahangi were dependent on times of post-infection and the quantum of the larvae inoculation. There were no signfiicant difference among the three antigens, but adult worm antigen was recommended for the ELISA technique due to its high specificity, sensitivity and consistency in the detection of specific antifilarial lgG antibody
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Meriones unguiculatus , Brugla pahangi
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