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International Immunology Advance Access originally published online on August 17, 2006
International Immunology 2006 18(10):1443-1451; doi:10.1093/intimm/dxl078
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© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Host chemokine (C-C motif) ligand-2 (CCL2) is differentially regulated in HIV type 1 (HIV-1)-infected individuals

Abdul Wahid Ansari1,2, Nupur Bhatnagar2, Oliver Dittrich-Breiholz3, Michael Kracht3, Reinhold E. Schmidt2 and Hans Heiken2

1 MD/PhD Program, Hannover Medical School, Carl-Neuberg-Street 1, D-30625 Hannover, Germany
2 Department of Clinical Immunology, Hannover Medical School, Carl-Neuberg-Street 1, D-30625 Hannover, Germany
3 Institute of Molecular Pharmacology, Hannover Medical School, Carl-Neuberg-Street 1, D-30625 Hannover, Germany

Correspondence to: H. Heiken; E-mail: heiken.hans{at}mh-hannover.de and A. W. Ansari; E-mail: ansari.wahid{at}mh-hannover.de

Several cytokines and chemokines including chemokine (C-C motif) ligand-2 (CCL2) are induced in HIV-1 infection. However, the impact of HIV-1 viremia on CCL2 regulation is largely unknown. We utilized a DNA oligonucleotide microarray covering 110 inflammatory genes. Five genes were induced by at least 2-fold in PBMCs of HIV-1 viremic (>100.000 RNA copies ml–1) as compared with aviremic (<50 RNA copies ml–1) individuals. These genes were CCL2, CXC chemokine ligand-10, IFN-{gamma}, GTP-cyclohydrolase-1 and C-C chemokine receptor-1. In addition to microarray data verification by real-time PCR, analysis of independent patient samples revealed a similar expression pattern. CCL2 was the most strongly regulated gene at mRNA level and its serum concentration was significantly elevated in viremic compared with aviremic and HIV-1 seronegative controls, indicating a positive correlation between viremia and CCL2. Flow cytometric studies demonstrated a higher percentage of CCL2-expressing CD14+ monocytes in viremic compared with aviremic individuals. These results suggest a highly restricted modulation of host inflammatory gene response by HIV. Genes up-regulated in the viremic state, in particular CCL2, presumably serve as potential enhancing factors in HIV-1 replication, represented by high viral load in HIV-1 viremic patients. Inhibition of increased CCL2 production could provide a new therapeutic intervention in HIV-1 infection.

Keywords: CCL2, HIV-1 viremia, inflammatory genes, microarray

Transmitting editor: S. Koyasu


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