PMID- 21852898
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211020
IS  - 1179-1497 (Print)
IS  - 1179-1497 (Electronic)
IS  - 1179-1497 (Linking)
VI  - 3
DP  - 2011 May 1
TI  - Expression of mannose binding lectin in HIV-1-infected brain: implications for 
      HIV-related neuronal damage and neuroAIDS.
PG  - 41-52
AB  - Mannose binding lectin (MBL) activates complement pathway that leads to pathogen 
      opsonization and phagocytosis. MBL deficiency is linked to HIV transmission and 
      disease progression. We sought to determine the role of MBL in HIV encephalitis 
      (HIVE) by evaluating its presence and distribution in the HIV-1-infected brain 
      and by assessing its association with monocyte chemoattractant protein-1 (MCP-1) 
      expression. This retrospective study utilized archived post-mortem brain tissues 
      obtained from 35 individuals enrolled in a longitudinal study as part of the 
      California NeuroAIDS Tissue Network. MBL, MCP-1 and brain cell markers in 
      post-mortem brain tissues with or without HIVE were evaluated using 
      immunocytochemistry, immunofluorescence, confocal microscopy, and western blots. 
      MBL was expressed in neurons, astrocytes, microglia, and oligodendrocytes of the 
      frontal cortex of the HIV-1-infected brain. Overall, there were 30% to 40% more 
      MBL-positive brain cells in HIVE vs non-HIVE cases (P = 0.01, paired t-test). 
      Specifically, there was an increased MBL expression in the neuronal axons of HIVE 
      cases. Also, western blots showed 3- to 4-fold higher levels of 78 kD MBL trimers 
      in HIVE vs non-HIVE cases. This MBL-HIVE link was further confirmed by MBL 
      associated higher MCP-1 expression in HIVE vs non-HIVE cases. HIV negative 
      healthy individuals and normal or the gp120 transgenic mice did not show any 
      differential MBL expression. Increased MBL expression in the major brain cell 
      types, specifically in the neuronal axons of HIVE brain, and MBL associated 
      higher MCP-1 expression in HIVE suggest that MBL could cause neuroinflammation 
      and neuronal injury through MBL complement activation pathway.
FAU - Singh, Kumud K
AU  - Singh KK
AD  - Department of Pediatrics, University of California San Diego, La Jolla, CA, USA.
FAU - Nathamu, Satyanarayana
AU  - Nathamu S
FAU - Adame, Anthony
AU  - Adame A
FAU - Alire, Tara U
AU  - Alire TU
FAU - Dumaop, Wilmar
AU  - Dumaop W
FAU - Gouaux, Ben
AU  - Gouaux B
FAU - Moore, David J
AU  - Moore DJ
FAU - Masliah, Eliezer
AU  - Masliah E
CN  - and HIV Neurobehavioral Research Center Group
LA  - eng
GR  - P30 NS047101/NS/NINDS NIH HHS/United States
GR  - R24 MH059745/MH/NIMH NIH HHS/United States
GR  - R01 MH062962/MH/NIMH NIH HHS/United States
GR  - R01 MH085608-02/MH/NIMH NIH HHS/United States
GR  - U01 MH083506/MH/NIMH NIH HHS/United States
GR  - R01 MH085608/MH/NIMH NIH HHS/United States
GR  - P30 MH062512/MH/NIMH NIH HHS/United States
GR  - U01 MH083545/MH/NIMH NIH HHS/United States
PT  - Journal Article
PL  - New Zealand
TA  - Neurobehav HIV Med
JT  - Neurobehavioral HIV medicine
JID - 101530425
PMC - PMC3156486
MID - NIHMS307238
COIS- Disclosure The authors disclose no conflicts of interest.
EDAT- 2011/08/20 06:00
MHDA- 2011/08/20 06:01
PMCR- 2011/08/16
CRDT- 2011/08/20 06:00
PHST- 2011/08/20 06:00 [entrez]
PHST- 2011/08/20 06:00 [pubmed]
PHST- 2011/08/20 06:01 [medline]
PHST- 2011/08/16 00:00 [pmc-release]
AID - 10.2147/NBHIV.S19969 [doi]
PST - ppublish
SO  - Neurobehav HIV Med. 2011 May 1;3:41-52. doi: 10.2147/NBHIV.S19969.