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C-C chemokines released by lipopolysaccharide (LPS)-stimulated human macrophages suppress HIV-1 infection in both macrophages and T cells.

Verani A, Scarlatti G, Comar M, Tresoldi E, Polo S, Giacca M, Lusso P, Siccardi AG, Vercelli D - J. Exp. Med. (1997)

Bottom Line: A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS.Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages.Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Technological Research, San Raffaele Scientific Institute, Milan, Italy.

ABSTRACT
Human immunodeficiency virus-1 (HIV-1) expression in monocyte-derived macrophages (MDM) infected in vitro is known to be inhibited by lipopolysaccharide (LPS). However, the mechanisms are incompletely understood. We show here that HIV-1 suppression is mediated by soluble factors released by MDM stimulated with physiologically significant concentrations of LPS. LPS-conditioned supernatants from MDM inhibited HIV-1 replication in both MDM and T cells. Depletion of C-C chemokines (RANTES, MIP-1 alpha, and MIP-1 beta) neutralized the ability of LPS-conditioned supernatants to inhibit HIV-1 replication in MDM. A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS. Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages. Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

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LPS-induced inhibition of HIV-1 expression in MDM cultures is dependent on the time of addition of LPS. MDM were infected  with HIV-1Ba-L (500 pg/ml), and stimulated with LPS (1 μg/ml) at different times from the initiation of the culture. Culture supernatants were  harvested daily, and tested for p24 Ag secretion by ELISA. The data represent the mean of two separate experiments.
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Figure 2: LPS-induced inhibition of HIV-1 expression in MDM cultures is dependent on the time of addition of LPS. MDM were infected with HIV-1Ba-L (500 pg/ml), and stimulated with LPS (1 μg/ml) at different times from the initiation of the culture. Culture supernatants were harvested daily, and tested for p24 Ag secretion by ELISA. The data represent the mean of two separate experiments.

Mentions: LPS-induced inhibition of HIV-1 replication was dependent on the time of addition of LPS to the culture. Fig. 2 shows that HIV-1 expression was completely blocked when LPS was added at the time of infection or 1 d later, but was progressively less affected when LPS was added 2 or 3 d after infection with HIV-1. Notably, viral replication was completely inhibited by pretreating MDM with LPS for 48 h before infection. However, the inhibitory effect of LPS pretreatment was abolished if the cells were subsequently washed before virus addition (data not shown). These data suggest that LPS interferes with early events in HIV-1 infection.


C-C chemokines released by lipopolysaccharide (LPS)-stimulated human macrophages suppress HIV-1 infection in both macrophages and T cells.

Verani A, Scarlatti G, Comar M, Tresoldi E, Polo S, Giacca M, Lusso P, Siccardi AG, Vercelli D - J. Exp. Med. (1997)

LPS-induced inhibition of HIV-1 expression in MDM cultures is dependent on the time of addition of LPS. MDM were infected  with HIV-1Ba-L (500 pg/ml), and stimulated with LPS (1 μg/ml) at different times from the initiation of the culture. Culture supernatants were  harvested daily, and tested for p24 Ag secretion by ELISA. The data represent the mean of two separate experiments.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196157&req=5

Figure 2: LPS-induced inhibition of HIV-1 expression in MDM cultures is dependent on the time of addition of LPS. MDM were infected with HIV-1Ba-L (500 pg/ml), and stimulated with LPS (1 μg/ml) at different times from the initiation of the culture. Culture supernatants were harvested daily, and tested for p24 Ag secretion by ELISA. The data represent the mean of two separate experiments.
Mentions: LPS-induced inhibition of HIV-1 replication was dependent on the time of addition of LPS to the culture. Fig. 2 shows that HIV-1 expression was completely blocked when LPS was added at the time of infection or 1 d later, but was progressively less affected when LPS was added 2 or 3 d after infection with HIV-1. Notably, viral replication was completely inhibited by pretreating MDM with LPS for 48 h before infection. However, the inhibitory effect of LPS pretreatment was abolished if the cells were subsequently washed before virus addition (data not shown). These data suggest that LPS interferes with early events in HIV-1 infection.

Bottom Line: A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS.Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages.Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Technological Research, San Raffaele Scientific Institute, Milan, Italy.

ABSTRACT
Human immunodeficiency virus-1 (HIV-1) expression in monocyte-derived macrophages (MDM) infected in vitro is known to be inhibited by lipopolysaccharide (LPS). However, the mechanisms are incompletely understood. We show here that HIV-1 suppression is mediated by soluble factors released by MDM stimulated with physiologically significant concentrations of LPS. LPS-conditioned supernatants from MDM inhibited HIV-1 replication in both MDM and T cells. Depletion of C-C chemokines (RANTES, MIP-1 alpha, and MIP-1 beta) neutralized the ability of LPS-conditioned supernatants to inhibit HIV-1 replication in MDM. A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS. Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages. Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

Show MeSH
Related in: MedlinePlus