Abstract
Patients infected with human immunodeficiency virus (HIV) frequently have increased production of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), and these cytokines may in turn contribute to the disease pathogenesis. It has been hypothesized that secretion of these cytokines by HIV-exposed mononuclear cells or HIV-infected monocyte/macrophages (M/Ms) is the principal source of their overproduction in HIV-infected patients, and the present study was undertaken to explore this issue. We observed that in the absence of endotoxin or cytokines, M/Ms productively infected by HIV do not produce detectable IL-6 or TNF-α. However, granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances HIV replication in M/Ms and is frequently used to propagate monocytotropic strains of HIV, can induce the relatively long-term production of IL-6 (up to 47 U/ml) and TNF-α (up to 47 pg/ml) by M/Ms, even in the absence of HIV. Also, HIV induced production of a relatively small (≤9 U/ml) quantity of IL-6 in M/Ms stimulated with macrophage-colony stimulating factor (M-CSF). Finally, while highly concentrated HIV induced production of both cytokines by either M/Ms or peripheral blood mononuclear cells (PBMCs), this production was almost completely eliminated when rare was taken to avoid contamination of HIV by endotoxin. These data suggest that the excess IL-6 and TNF-α in H-infected patients does not simply result from their production by HIV-infected M/Ms and that alternative mechanisms are involved in this process.
| Original language | English |
|---|---|
| Pages (from-to) | 829-839 |
| Number of pages | 11 |
| Journal | AIDS Research and Human Retroviruses |
| Volume | 13 |
| Issue number | 10 |
| Publication status | Published - Jul 1 1997 |
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ASJC Scopus subject areas
- Immunology
- Virology
Cite this
Effects of human immunodeficiency virus and colony-stimulating factors on the production of interleukin 6 and tumor necrosis factor a by monocyte/macrophages. / Foli, A.; Saville, M. W.; May, L. T.; Webb, D. S A; Yarchoan, R.
In: AIDS Research and Human Retroviruses, Vol. 13, No. 10, 01.07.1997, p. 829-839.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of human immunodeficiency virus and colony-stimulating factors on the production of interleukin 6 and tumor necrosis factor a by monocyte/macrophages
AU - Foli, A.
AU - Saville, M. W.
AU - May, L. T.
AU - Webb, D. S A
AU - Yarchoan, R.
PY - 1997/7/1
Y1 - 1997/7/1
N2 - Patients infected with human immunodeficiency virus (HIV) frequently have increased production of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), and these cytokines may in turn contribute to the disease pathogenesis. It has been hypothesized that secretion of these cytokines by HIV-exposed mononuclear cells or HIV-infected monocyte/macrophages (M/Ms) is the principal source of their overproduction in HIV-infected patients, and the present study was undertaken to explore this issue. We observed that in the absence of endotoxin or cytokines, M/Ms productively infected by HIV do not produce detectable IL-6 or TNF-α. However, granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances HIV replication in M/Ms and is frequently used to propagate monocytotropic strains of HIV, can induce the relatively long-term production of IL-6 (up to 47 U/ml) and TNF-α (up to 47 pg/ml) by M/Ms, even in the absence of HIV. Also, HIV induced production of a relatively small (≤9 U/ml) quantity of IL-6 in M/Ms stimulated with macrophage-colony stimulating factor (M-CSF). Finally, while highly concentrated HIV induced production of both cytokines by either M/Ms or peripheral blood mononuclear cells (PBMCs), this production was almost completely eliminated when rare was taken to avoid contamination of HIV by endotoxin. These data suggest that the excess IL-6 and TNF-α in H-infected patients does not simply result from their production by HIV-infected M/Ms and that alternative mechanisms are involved in this process.
AB - Patients infected with human immunodeficiency virus (HIV) frequently have increased production of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), and these cytokines may in turn contribute to the disease pathogenesis. It has been hypothesized that secretion of these cytokines by HIV-exposed mononuclear cells or HIV-infected monocyte/macrophages (M/Ms) is the principal source of their overproduction in HIV-infected patients, and the present study was undertaken to explore this issue. We observed that in the absence of endotoxin or cytokines, M/Ms productively infected by HIV do not produce detectable IL-6 or TNF-α. However, granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances HIV replication in M/Ms and is frequently used to propagate monocytotropic strains of HIV, can induce the relatively long-term production of IL-6 (up to 47 U/ml) and TNF-α (up to 47 pg/ml) by M/Ms, even in the absence of HIV. Also, HIV induced production of a relatively small (≤9 U/ml) quantity of IL-6 in M/Ms stimulated with macrophage-colony stimulating factor (M-CSF). Finally, while highly concentrated HIV induced production of both cytokines by either M/Ms or peripheral blood mononuclear cells (PBMCs), this production was almost completely eliminated when rare was taken to avoid contamination of HIV by endotoxin. These data suggest that the excess IL-6 and TNF-α in H-infected patients does not simply result from their production by HIV-infected M/Ms and that alternative mechanisms are involved in this process.
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M3 - Article
C2 - 9197377
AN - SCOPUS:0030969553
VL - 13
SP - 829
EP - 839
JO - AIDS Research and Human Retroviruses
JF - AIDS Research and Human Retroviruses
SN - 0889-2229
IS - 10
ER -