Trypanosoma musculi: Tracking parasites and circulating lymphoid cells in host mice

Citation
Jw. Albright et al., Trypanosoma musculi: Tracking parasites and circulating lymphoid cells in host mice, EXP PARASIT, 91(2), 1999, pp. 185-195
Citations number
42
Categorie Soggetti
Microbiology
Journal title
EXPERIMENTAL PARASITOLOGY
ISSN journal
00144894 → ACNP
Volume
91
Issue
2
Year of publication
1999
Pages
185 - 195
Database
ISI
SICI code
0014-4894(199902)91:2<185:TMTPAC>2.0.ZU;2-X
Abstract
Two aspects of host-parasite relationships that seem worthy of more attenti on are: (a) the distribution of parasites among host organs in the early co urse of infection, and (b) the dynamics of host lymphocyte tissue localizat ion and recirculation during the course of infection. We have employed the derivatized aminostyrylpyridinium dye, [I-125] I 2P-Di-6-ASP, to provide a relatively stable tag on both a parasite, Trypanosoma musculi, and on host mouse splenocytes, enriched B and T lymphocytes, and natural killer cells. The organ distribution of the parasites, splenocytes, and lymphocytes in re cipient, host mice was tracked. Radiolabeled T. musculi localized primarily in the liver with lesser numbers in spleen, lungs, and kidneys. Per unit w et weight, the spleen accumulated parasites most efficiently. When T. muscu li were inoculated intraperitoneally, most of them remained in the peritone al space and the numbers that gained access to liver, lungs, and spleen wer e significantly smaller than in mice inoculated intravenously. The acquisit ion of parasites by the spleen (and lungs) of mice with an existing T. musc uli infection was markedly inhibited. This was true also of syngeneic splen ocytes and lymphocytes. In addition, lymphocytes from infected mice were si gnificantly less likely to take residence in the spleens of normal recipien t mice and were especially unlikely to localize in the spleens of infected recipients. These and other findings suggested that the inability of circul ating lymphocytes to gain access to lymphoid tissues in infected mice, coup led with the poor ability of those tissues to sequester parasite antigens, could account for the known prolonged delay in the development of curative antibody response characteristic of ir: musculi-infected mice. It is likely that the marked disruption of lymphoid tissue histoarchitecture that is ty pical of T. musculi infection contributes significantly to the failure of t he tissues to sequester parasites and lymphocytes. Because lymphoid tissue disruption is seen in many parasitic infections, the findings reported here may have fairly broad relevance. In any case, the procedure described here for labeling parasites and lymphocytes should be of general utility for tr acking their disposition in vivo. (C) 1999 Academic Press.