PMID- 11086093
OWN - NLM
STAT- MEDLINE
DCOM- 20010111
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 165
IP  - 11
DP  - 2000 Dec 1
TI  - Mu-opioid induction of monocyte chemoattractant protein-1, RANTES, and 
      IFN-gamma-inducible protein-10 expression in human peripheral blood mononuclear 
      cells.
PG  - 6519-24
AB  - Strong evidence for the direct modulation of the immune system by opioids is well 
      documented. Mu-opioids have been shown to alter the release of cytokines 
      important for both host defense and the inflammatory response. Proinflammatory 
      chemokines monocyte chemoattractant protein-1 (MCP-1), RANTES, and 
      IFN-gamma-inducible protein-10 (IP-10) play crucial roles in cell-mediated immune 
      responses, proinflammatory reactions, and viral infections. In this report, we 
      show that [D-Ala(2),N:-Me-Phe(4),Gly-ol(5)]enkephalin (DAMGO), a 
      mu-opioid-selective agonist, augments the expression in human PBMCs of MCP-1, 
      RANTES, and IP-10 at both the mRNA and protein levels. Because of the proposed 
      relationship between opioid abuse and HIV-1 infection, we also examined the 
      impact of DAMGO on chemokine expression in HIV-infected cells. Our results show 
      that DAMGO administration induces a significant increase in RANTES and IP-10 
      expression, while MCP-1 protein levels remain unaffected in PBMCs infected with 
      the HIV-1 strain. In contrast, we show a dichotomous effect of DAMGO treatment on 
      IP-10 protein levels expressed by T- and M-tropic HIV-infected PBMCs. The 
      differential modulation of chemokine expression in T- and M-tropic HIV-1-infected 
      PBMCs by opioids supports a detrimental role for opioids during HIV-1 infection. 
      Modulation of chemokine expression may enhance trafficking of potential 
      noninfected target cells to the site of active infection, thus directly 
      contributing to HIV-1 replication and disease progression to AIDS.
FAU - Wetzel, M A
AU  - Wetzel MA
AD  - Department of Microbiology, Center for Substance Abuse Research and Fels 
      Institute for Cancer Research and Molecular Biology, Temple University School of 
      Medicine, Philadelphia, PA 19140, USA.
FAU - Steele, A D
AU  - Steele AD
FAU - Eisenstein, T K
AU  - Eisenstein TK
FAU - Adler, M W
AU  - Adler MW
FAU - Henderson, E E
AU  - Henderson EE
FAU - Rogers, T J
AU  - Rogers TJ
LA  - eng
GR  - DA-06650/DA/NIDA NIH HHS/United States
GR  - DA-11130/DA/NIDA NIH HHS/United States
GR  - DA-12113/DA/NIDA NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Peptides)
RN  - 0 (Phytohemagglutinins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Opioid, mu)
RN  - 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-)
RN  - 69344-77-0 (connective tissue-activating peptide)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/blood/genetics
MH  - Chemokine CCL5/*biosynthesis/blood/genetics
MH  - Chemokine CXCL10
MH  - Chemokines, CXC/*biosynthesis/blood/genetics
MH  - Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology
MH  - Humans
MH  - Interferon-gamma/physiology
MH  - Leukocytes, Mononuclear/drug effects/*immunology/*metabolism
MH  - Lymphocyte Activation/drug effects/immunology
MH  - Peptides/pharmacology
MH  - Phytohemagglutinins/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Opioid, mu/agonists/antagonists & inhibitors/blood/*physiology
MH  - Up-Regulation/drug effects/genetics/immunology
EDAT- 2000/11/22 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/11/22 11:00
PHST- 2000/11/22 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/11/22 11:00 [entrez]
AID - 10.4049/jimmunol.165.11.6519 [doi]
PST - ppublish
SO  - J Immunol. 2000 Dec 1;165(11):6519-24. doi: 10.4049/jimmunol.165.11.6519.