Increased release of glucuronoxylomannan antigen and induced phenotypic changes in Trichosporon asahii by repeated passage in mice.
Clinically important fungi such as Candida albicans and Cryptococcus neoformans are known to undergo phenotypic changes after repeated subculture or passages in vivo. However, there are no reports describing this phenomenon in Trichosporon species. This study investigated whether in-vivo passages of environmental isolates of Trichosporon asahii in mice changes their phenotype; three environmental isolates and 14 clinical isolates (from deep-seated infections) were used. The shape of the colony and cell type were observed, and the titre of glucuronoxylomannan (GXM) antigen and concentration of (1-->3)-beta-D-glucan were measured for each isolate. Changes in these features were also examined after three passages of the environmental isolates in mice. The shape of colonies and cell types were clearly different in environmental and clinical isolates. Furthermore, the clinical isolates released significantly higher levels of GXM antigen than environmental isolates (titre: log2 9.4 SD 0.7 versus log2 5.4 SD 1.4). The phenotype of passaged isolates was significantly different from the original environmental isolates with respect to the morphology of colonies and cell type and GXM release (titre: log2 10.0 SD 0.7 versus log2 5.4 SD 1.4). These results suggest that the phenotypic changes in T. asahii occur as a result of in-vivo passages. This process may allow a proportion of the fungal population to escape eradication by the host immune system, as GXM antigen is considered to protect the fungi against phagocytosis by polymorphonuclear leucocytes and monocytes in vivo.
Karashima
Reiko
R
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
Yamakami
Yuriko
Y
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
Yamagata
Eiji
E
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
Tokimatsu
Issei
I
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
Hiramatsu
Kazufumi
K
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
Nasu
Masaru
M
Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.
D000818:Animals; D000946:Antigens, Fungal / Q000276:immunology / Q000378:metabolism*; D005936:Glucans / Q000378:metabolism; D006801:Humans; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010641:Phenotype; D011134:Polysaccharides / Q000276:immunology / Q000378:metabolism*; D012692:Serial Passage; D014250:Trichosporon / Q000166:cytology / Q000254:growth & development / Q000276:immunology*
D000946:Antigens, Fungal; D005936:Glucans; D011134:Polysaccharides; C033671:epiglucan; C027478:glucuronoxylomannan