Trypanosoma musculi: tracking parasites and circulating lymphoid cells in host mice.
Two aspects of host-parasite relationships that seem worthy of more attention are: (a) the distribution of parasites among host organs in the early course of infection, and (b) the dynamics of host lymphocyte tissue localization and recirculation during the course of infection. We have employed the derivatized aminostyrylpyridinium dye, [125I] 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 recipient, host mice was tracked. Radiolabeled T. musculi localized primarily in the liver with lesser numbers in spleen, lungs, and kidneys. Per unit wet weight, the spleen accumulated parasites most efficiently. When T. musculi were inoculated intraperitoneally, most of them remained in the peritoneal space and the numbers that gained access to liver, lungs, and spleen were significantly smaller than in mice inoculated intravenously. The acquisition of parasites by the spleen (and lungs) of mice with an existing T. musculi infection was markedly inhibited. This was true also of syngeneic splenocytes and lymphocytes. In addition, lymphocytes from infected mice were significantly less likely to take residence in the spleens of normal recipient mice and were especially unlikely to localize in the spleens of infected recipients. These and other findings suggested that the inability of circulating lymphocytes to gain access to lymphoid tissues in infected mice, coupled 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 T. musculi-infected mice. It is likely that the marked disruption of lymphoid tissue histoarchitecture that is typical of T. musculi infection contributes significantly to the failure of the 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 tracking their disposition in vivo.
Albright
J W
JW
Department of Microbiology and Immunology, George Washington University School of Medicine, Washington, DC 20037, USA.
Mease
R C
RC
Lambert
C
C
Albright
J F
JF
D000631:Aminopyridines; D000818:Animals; D004396:Coloring Agents; D006790:Host-Parasite Interactions; D007422:Intestines / Q000469:parasitology; D007457:Iodine Radioisotopes; D007668:Kidney / Q000469:parasitology; D007694:Killer Cells, Natural / Q000469:parasitology; D008099:Liver / Q000469:parasitology; D008168:Lung / Q000469:parasitology; D008214:Lymphocytes / Q000469:parasitology; D008221:Lymphoid Tissue / Q000166:cytology / Q000469:parasitology*; D051379:Mice; D008809:Mice, Inbred C3H; D016513:Mice, SCID; D010537:Peritoneum / Q000469:parasitology; D012588:Scintillation Counting; D013154:Spleen / Q000469:parasitology; D014345:Trypanosoma / Q000502:physiology*; D014352:Trypanosomiasis / Q000276:immunology / Q000469:parasitology*