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Inhibition of HIV‐1 or bacterial activation of macrophages by products of HIV‐1‐resistant human cells
Author(s) -
Li Guanhua,
Aaron Sagiv,
Kazmierczak Katarzyna,
Lesner Adam,
Li Yuchang,
Ivanova Anna,
Bentsman Galina,
Potash Mary Jane,
Simm Malgorzata
Publication year - 2007
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/sj.icb.7100092
Subject(s) - biology , lipopolysaccharide , tumor necrosis factor alpha , virus , macrophage , bacteria , microbiology and biotechnology , cell culture , pathogenesis , transcription factor , dna , gene , immunology , in vitro , biochemistry , genetics
We have recently described the molecular basis of HIV‐1 resistance factor (HRF)‐mediated anti‐viral activity in primary and transformed CD4 T cells. HRF(+) cell culture supernatants or partially purified HRF were found to incapacitate the formation of the NF‐ κ B/DNA complex, which is indispensable for long terminal promoter‐driven transcription of virus genes. In this study, we tested whether HRF might have much broader activity against other organisms whose pathogenesis is linked to NF‐ κ B activation. Specifically, we tested the effects of HRF on the NF‐ κ B‐mediated responses of primary macrophages to HIV‐1 or several bacterial antigens. We found that exposure to HRF inhibited HIV‐1 expression in macrophages and also induced the production of HRF‐like activity by macrophages, which prevented replication of virus in HIV‐1‐infected peripheral blood lymphocytes cultured in the adjacent compartment. We investigated the mechanism of this inhibition and found that HRF impeded NF‐ κ B/DNA binding in macrophages induced by either HIV‐1 or lipopolysaccharide from several bacteria species, resulting in impaired tumor necrosis factor‐alpha responses to these organisms.