Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Abstract

Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms.We demonstrate that (1) macrophages exposed to bacterial cell wall components such as lipopolysaccharide (

Opposite Effects of IL-10 on the Ability of Dendritic Cells and Macrophages to Replicate Primary CXCR4-Dependent HIV-1 Strains

“…However, laboratory-adapted X4 HIV-1 strains such as IIIB appear to be blocked during postentry steps in M⌽s (26). Interestingly, exposure to bacterial products renders M⌽s highly susceptible to X4 HIV-1 strains in vitro (27). Similarly, it has been reported that maturation of DCs is associated with up-regulation of CXCR4 expression and a higher susceptibility of DC to infection with X4 HIV-1 strains (28,29).…”

Transcriptional Mechanisms Regulating Alveolar Epithelial Cell-specific CCL5 Secretion in Pulmonary Tuberculosis

“…Constructs containing sitespecific mutations were the very generous gift of Professor Hiroyuki Moriuchi, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. These constructs contained mutations of the -B1 (Ϫ44), -B2 (Ϫ30), NF-IL-6 (Ϫ92), TRE1/2 (Ϫ345), TRE3/4 (Ϫ327), TRE1/2/3/4, and CD28RE/ B2/ B1 (Ϫ579, Ϫ44, Ϫ30) sites as described previously (27). Constructs had been inserted into the firefly luciferase expression plasmid PGL2-basic.…”

“…Transcriptional regulation of the CCL5 gene is critical in T lymphocytes (1,2,26,27). The CCL5 promoter contains response elements for the transcriptional activators NF B, AP-1, and NF-IL-6 (26,27) and for late acting factors restricted to T cells (28).…”

“…Transcriptional regulation of the CCL5 gene is critical in T lymphocytes (1,2,26,27). The CCL5 promoter contains response elements for the transcriptional activators NF B, AP-1, and NF-IL-6 (26,27) and for late acting factors restricted to T cells (28). NF B comprises a family of Relrelated proteins retained in the cytoplasm bound to the inhib-itor I B␣ and is a pivotal regulator of proinflammatory responses (29).…”

“…RSV-induced CCL5 gene expression in lung epithelium is associated with the nuclear translocation of NF-IL-6 (33). However, little data exists on the functional role of NF-IL-6 or AP-1 in cytokine-induced CCL5 gene activation, although NF B may be required (16,27,35).…”