期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 185, 期 6, 页码 1649-1665出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2015.01.033
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资金
- NIH/National Institute of Neurological Disorders and Stroke [NS040237, NS063897, NS082116]
- NIH Nonhuman Primate Reagent Resource grants [RR016001, AI040101]
Macrophage recruitment to the central nervous system (CNS) during AIDS pathogenesis is poorly understood. We measured the accumulation of brain perivascular (CD163(+)) and inflammatory (MAC387(+)) macrophages in SIV-infected monkeys. Monocyte progenitors were 5-bromo-2'-deoxyuridine (BrdU) labeled in bone marrow, and CNS macrophages were labeled serially with fluorescent dextrans injected into the cisterna magna. MAC387(+) macrophages accumulated in the meninges and choroid plexus in early inflammation and in the perivascular space and SIV encephalitis (SIVE) Lesions late. CD163(+) macrophages accumulated in the perivascular space and SIVE Lesions with late inflammation. Most of the BrdU(+) cells were MAC387; however, CD163(+)BrdU(+) macrophages were present in the meninges and choroid plexus with AIDS. Most (81.6% +/- 1.8%) of macrophages in SIVE Lesions were present in the CNS before SIVE Lesion formation. There was a 2.9-fold increase in SIVp28(+) macrophages entering the CNS late compared with those entering early (P < 0.05). The rate of CD163(+) macrophage recruitment to the CNS inversely correlated with time to death (P < 0.03) and increased with SIVE. In SIVE animals, soluble CD163 correlated with CD163(+) macrophage recruitment (P = 0.02). Most perivascular macrophages that comprise SIVE lesions and multinucleated giant cells are present in the CNS early, before SIVE Lesions are formed. Most SIV-infected macrophages traffic to the CNS terminally with AIDS.
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