Translocation of microbes and changes of immunocytes in the gut of rapid‐ and slow‐progressor Chinese rhesus macaques infected with SIVmac239
Summary Human/simian immunodeficiency virus (HIV/SIV) infection can cause severe depletion of CD4+ T cells in both plasma and mucosa; it also results in damage to the gut mucosa barrier, which makes the condition more conducive to microbial translocation. In this study, we used SIV‐infected Chinese...
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Published in | Immunology Vol. 147; no. 4; pp. 443 - 452 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Wiley Subscription Services, Inc
01.04.2016
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Summary
Human/simian immunodeficiency virus (HIV/SIV) infection can cause severe depletion of CD4+ T cells in both plasma and mucosa; it also results in damage to the gut mucosa barrier, which makes the condition more conducive to microbial translocation. In this study, we used SIV‐infected Chinese rhesus macaques to quantify the extent of microbial translocation and the function of immune cells in the entire gastrointestinal tract and to compare their differences between rapid and slow progressors. The results showed that in the slow progressors, microbial products translocated considerably and deeply into the lamina propria of the gut; the tissue macrophages had no significant differences compared with the rapid progressors, but there was a slightly higher percentage of mucosal CD8+ T cells and a large amount of extracellular microbial products in the lamina propria of the intestinal mucosa of the slow progressors. The data suggested that although microbial translocation increased markedly, the mucosal macrophages and CD8+ T cells were insufficient to clear the infiltrated microbes in the slow progressors. Also, therapies aimed at suppressing the translocation of microbial products in the mucosa could help to delay the progression of SIV disease. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0019-2805 1365-2567 |
DOI: | 10.1111/imm.12574 |