Expression of CCR5 Is Increased in Human Monocyte-Derived Macrophages and Alveolar Macrophages in the Course of in Vivo and in Vitro Mycobacterium tuberculosis Infection

Fraziano, Maurizio; Cappelli, Giulia; Santucci, Marilina B.; Mariani, Francesca; Amicosante, Massimo; Casarini, M; Giosuè, S; Bisetti, A; Colizzi, Vittorio

doi:10.1089/088922299310575

Cited by 58 publications

(48 citation statements)

References 28 publications

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“…For instance, morphine has been shown to modulate the expression of other cellular proteins that may induce CCR5 expression. Specifically, morphine reportedly modulates the cellular activation of NFB and TNF-␣ in macrophages (27) and interleukin-2 in lymphocytes (28); activation of NFB, TNF-␣, and interleukin-2 has been found to up-regulate CCR5 expression (10,29). Alternatively, morphine may up-regulate CCR5 by inhibiting chemokine synthesis and thus chemotaxis.…”

Section: Infection Of Cem X174 Cells With Sivmac239 or Srv-methodsmentioning

confidence: 99%

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Miyagi¹,

Chuang²,

Doi³

et al. 2000

Journal of Biological Chemistry

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All HIV-1 strains studied to date use CCR5, CXCR4, or both receptors to enter cells. Simian immunodeficiency virus (SIV) infection of non-human primates has served as a useful model for understanding AIDS pathogenesis in humans. Research on several genetically divergent SIV isolates has revealed that SIV uses CCR5, and not CXCR4, for entry. CEM x174, a human lymphoid cell line, has been routinely used to cultivate and maintain various SIV strains. However, questions have arisen about how CEM x174, which reportedly was unable to express detectable amounts of CCR5 transcripts, efficiently supports the growth of SIV. In searching for an answer, we resorted to a sensitive competitive reverse transcriptase-polymerase chain reaction procedure in an attempt to detect as well as quantify the amount of CCR5 expression. Here we present our findings, which indicate that CEM x174 indeed expresses CCR5 and that the amount of CCR5 is increased in cells pretreated with morphine. These results correlate well with our previous observations that morphine treatment causes CEM x174 cells to be more susceptible to SIV infection. Similar morphine effect was not observed on CEM x174 cells infected with simian retroviruses, which do not depend on CCR5 for entry. These findings suggest a plausible mechanism whereby opiate drug users render themselves more susceptible to HIV infection, thereby explaining the vast prevalence of HIV infection among endemic drug use populations.

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Section: Infection Of Cem X174 Cells With Sivmac239 or Srv-methodsmentioning

confidence: 99%

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Miyagi¹,

Chuang²,

Doi³

et al. 2000

Journal of Biological Chemistry

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“…Nonactivated AM are not equipped with effector mechanisms sufficient to clear the microbial invader. Ag-specific T cells are attracted to the site of disease by the action of locally released chemokines (12)(13)(14)(15)(16)(17)(18). Consequently, T cells secrete macrophageactivating cytokines (e.g., TNF and IFN-␥) (15) or directly lyse infected cells and contribute to the containment of mycobacterial infection (19).…”

Section: Induction Of Tnf In Human Alveolar Macrophages As a Potentiamentioning

confidence: 99%

Induction of TNF in Human Alveolar Macrophages As a Potential Evasion Mechanism of VirulentMycobacterium tuberculosis

Engele

Stössel

Castiglione

et al. 2002

The Journal of Immunology

123

100

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The ability of macrophages to release cytokines is crucial to the host response to intracellular infection. In particular, macrophage-derived TNF plays an important role in the host response to infection with the intracellular pathogen Mycobacterium tuberculosis. In mice, TNF is indispensable for the formation of tuberculous granulomas, which serve to demarcate the virulent bacterium. TNF is also implicated in many of the immunopathological features of tuberculosis. To investigate the role of TNF in the local immune response, we infected human alveolar macrophages with virulent and attenuated mycobacteria. Infection with virulent strains induced the secretion of significantly higher levels of bioactive TNF than attenuated strains correlating with their ability to multiply intracellularly. Treatment of infected macrophages with neutralizing anti-TNF Abs reduced the growth rate of intracellular bacteria, whereas bacterial replication was augmented by addition of exogenous TNF. Infected and uninfected macrophages contributed to cytokine production as determined by double-staining of M. tuberculosis and intracellular TNF. The induction of TNF by human alveolar macrophages at the site of infection permits the multiplication of intracellular bacteria and may therefore present an evasion mechanism of human pathogens.

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“…10 In this context, cell activation and apoptosis can be induced by MTB infection depending upon the MOI used. 3,13,14 In fact, previously reported results showed that low levels of MTB 13 or BCG 15 prevent monocyte apoptosis whereas high amounts of the virulent strain of MTB H37Rv can induce apoptosis. 2,3 It is plausible, therefore, to hypothesize that the presence of a threshold signal, represented by the amount of mycobacteria and possibly by the amount of cell wall associated 19-kDa lipoprotein, determines whether the cell will live or die.…”

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confidence: 99%