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Journal of Virology, September 1998, p. 7642-7647, Vol. 72, No. 9
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Cytokine Regulation of Human Immunodeficiency Virus
Type 1 Entry and Replication in Human Monocytes/Macrophages through
Modulation of CCR5 Expression
Jinhai
Wang,
Gregory
Roderiquez,
Tamás
Oravecz, and
Michael A.
Norcross*
Division of Hematologic Products, Center for
Biologics Evaluation and Research, Food and Drug Administration,
National Institutes of Health, Bethesda, Maryland 20892
Received 10 February 1998/Accepted 15 May 1998
 |
ABSTRACT |
Human macrophages express chemokine receptors that act as
coreceptors for human immunodeficiency virus type 1 (HIV-1) and are
major targets for HIV-1 infection in vivo. The effects of cytokines on
HIV-1 infection of macrophages and on the expression of CCR5, the
principal coreceptor for macrophage-tropic viruses, have now been
investigated. Expression of CCR5 on the surface of freshly isolated
human monocytes was virtually undetectable by flow cytometry with the
monoclonal antibody 5C7. However, after culture of monocytes for
48 h in serum-free medium, approximately 30% of the resulting
macrophages expressed CCR5 and the cells were susceptible to infection
by macrophage-tropic HIV-1. Addition of either macrophage
colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) to the cultures markedly increased both the extent of HIV-1 entry and replication as well as surface expression of CCR5. In contrast, addition of the T-helper 2 (Th2) cell-derived cytokine interleukin-4 (IL-4) or IL-13 prevented the
expression of CCR5 induced by culture in medium alone, and IL-4
inhibited virus entry, replication, and cytopathicity under these
conditions. IL-4 or IL-13 also prevented the stimulatory effects of
M-CSF or GM-CSF on CCR5 expression as well as HIV-1 entry and
replication. In addition, IL-4 reversed the increase in CCR5 expression
induced by pretreatment of cells with M-CSF. Although IL-10 also
inhibits HIV-1 replication in macrophages, it did not suppress surface
CCR5 expression induced by colony-stimulating factors. These results
indicate that the cytokine environment determines the susceptibility of
macrophages to HIV-1 infection by various mechanisms, one of which is
the regulation of HIV-1 coreceptor expression.
| |
TEXT |
Macrophages and CD4+ T
lymphocytes are the major targets of infection by human
immunodeficiency virus type 1 (HIV-1) in vivo (28, 43, 45,
60). The entry of virus into these cells is mediated by
interaction of the virus envelope with both CD4 and chemokine
receptors. The receptor for stromal cell-derived factor-1
(5), CXC chemokine receptor 4 (CXCR4), has been identified as the coreceptor for T-cell-tropic strains of HIV-1 (21),
whereas the CC chemokine receptor CCR5 (48, 52) and, to a
lesser extent, CCR3 (29) and CCR2b mediate the binding and
entry of macrophage-tropic and dual-tropic primary isolates of HIV-1
(1, 9, 14, 18, 19). The envelope proteins (gp120) of
T-cell-tropic and macrophage-tropic viruses have been shown to interact
with CXCR4 (32) and CCR5 (59, 61), respectively,
in a CD4-dependent manner.
The level of expression of specific chemokine receptors on the cell
surface correlates with the susceptibility of cells to HIV-1 infection.
Both CXCR4 and CCR5 are differentially expressed and regulated in human
T lymphocytes (6). CXCR4 is expressed predominantly on naive
T lymphocytes (CD26low CD45RA+
CD45RO
), whereas CCR5 is expressed on activated or memory
T cells (CD26high CD45RAlow
CD45RO+) (6, 62). The expression of CXCR4 and
CCR5 on T cells is up-regulated by exposure to interleukin-2 (IL-2) and
phytohemagglutinin (6, 59), whereas CCR5
expression is down-regulated by CD28 costimulation (7).
Although lipopolysaccharide rapidly inhibits the expression of CCR2 in
human monocytes (55), the regulation of CCR5 expression on
monocytes/macrophages and its relation to viral entry have not been
characterized.
Cytokines are major host factors in the pathogenesis of HIV-1 infection
(20). Patterns of cytokine expression have been linked to a
proposed polarization into T-helper 1 (Th1) (cell mediated) or Th2
(humoral) immune responses. Th1 cells are characterized by secretion of
IL-2 and gamma interferon, whereas Th2 cells are characterized by
secretion of IL-4, IL-5, IL-10, and IL-13. HIV-1 infection affects
patterns of cytokine production (24, 34), and cytokines
modify the production of HIV-1 from macrophages (31) and T
cells (20). Both tumor necrosis factor alpha and IL-1
enhance HIV-1 production through NF-
B-mediated transactivation of
the viral long terminal repeat (44). Macrophage
colony-stimulating factor (M-CSF) increases the production of HIV-1
(31, 35), while granulocyte-macrophage colony-stimulating
factor (GM-CSF) either enhances (31) or in some cases
suppresses (17, 35) virus infection. Other cytokines such as
the Th2 cytokines IL-4, IL-10, and IL-13 inhibit HIV-1 infection in
human primary macrophages (15, 30, 36, 37, 40, 53), and IL-4
blocks virus replication in peripheral blood cultures (46),
although the mechanism of inhibition has not been determined.
We have now investigated the roles of growth factors and cytokines in
HIV-1 entry and replication, as well as in modulation of the expression
of the monocytotropic virus coreceptor CCR5, in human primary
macrophages.
Effects of M-CSF, GM-CSF, and IL-4 on HIV-1 entry and replication
in macrophages.
To evaluate further the effects of M-CSF, GM-CSF,
and IL-4 on virus replication and entry, we incubated each cytokine at
a concentration of 20 ng/ml with monocytes in serum-free cultures before and during infection with HIV-1 BaL. Similar to previous results obtained with serum-containing cultures (30),
GM-CSF and M-CSF each increased the production of HIV-1 p24 antigen in our serum-free culture system (Fig. 1A).
In contrast to the stimulatory effects of M-CSF and GM-CSF, IL-4 (20 ng/ml) almost completely inhibited p24 antigen release (Fig. 1A) and
eliminated HIV-1-induced syncytium formation and cytopathicity (data
not shown).
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FIG. 1.
Effects of M-CSF, GM-CSF, and IL-4 on HIV-1 replication
and entry. Monocytes were isolated by elutriation (26),
cultured for 48 h in macrophage-SFM in the absence or presence of
M-CSF (20 ng/ml), GM-CSF (20 ng/ml), or IL-4 (20 ng/ml), and then
subjected to infection with HIV-1 BaL (2.34 × 107
cell-free virus) (23). (A) At the indicated times after
infection, culture supernatants were harvested from cells incubated in
the absence or presence of M-CSF, GM-CSF, or IL-4 and were then assayed
for p24 antigen by enzyme-linked immunosorbent assay (Coulter, Miami,
Fla.). Data are means ± standard deviations of triplicates from a
representative experiment. (B) Four hours after infection, lysates were
prepared from cells incubated in medium alone or in medium containing
the indicated cytokine and were analyzed by semiquantitative PCR for
proviral DNA. A control lysate was prepared from cell line 8E5
(22), which contains one copy of the HIV-1 genome per cell.
PCR was performed with the gag-specific primers SK38 (5'-ATA
ATC CAC CTA TCC CAG TAG GAG AAA T-3') and SK39 (5'-TTT GGT CCT TGT CTT
ATG TCC AGA ATG C-3'), 10 µl of lysate, and Taq polymerase
for 30 cycles. The PCR products were detected by hybridization with
excess SK19 probe (5'-ATC CTG GGA TTA AAT AAA ATA GTA AGA ATG TAT AGC
CCT AC-3') end labeled with [ -32P]ATP. Indicated copy
numbers (1,000, 100, 10) of control HIV-1 DNA were used as positive
controls. Medium, uninfected parallel macrophages treated with medium
only. GAG, HIV-1 prototypic gag gene segment amplified by
SK18 and SK19 primers.
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To determine whether the effects of these cytokines on viral
replication and cell fusion reflected an action at the early
steps of
virus entry, we subjected proviral DNA to semiquantitative
PCR
amplification 4 h after infection. Both M-CSF and GM-CSF
increased,
whereas IL-4 reduced, the amount of viral DNA synthesized at
this
early time point (Fig.
1B). Thus, these cytokines appear to affect
HIV-1 infection in human macrophages at an early step of virus
entry.
Relation of the effects of cytokines on virus replication to those
on expression of CCR5.
The entry of macrophage-tropic HIV-1 into
cells depends on the cell surface expression of CD4 and CCR5, although
some virus strains can also use CCR2b and CCR3. CCR3 mRNA is not
present in either freshly isolated monocytes or cultured macrophages, whereas CCR2b is expressed in fresh monocytes but not in macrophages (42, 55). Therefore, to study the effect of cytokines on
HIV-1 coreceptor expression, we focused on the cell surface abundance of CCR5 on monocytes and macrophages.
Cell surface expression of CCR5 in monocytes and macrophages was
measured by flow cytometry with the monoclonal antibody 5C7.
Less than
1% of fresh monocytes expressed CCR5 (Fig.
2A), which
is consistent with previously
published flow cytometry data (
62)
and reverse
transcription-PCR results (
17,
42,
62) indicating
very low
to absent CCR5 expression in resting monocytes. After
culture in
macrophage-serum-free medium (SFM) for 2 days, 29%
of the cells
expressed CCR5. Addition of M-CSF or GM-CSF to the
culture increased
the number of cells expressing CCR5 to 72 or
86%, respectively. In
contrast, IL-4 completely prevented the
increase in CCR5 expression
induced by incubation of cells in
medium alone (Fig.
2B). In the
same cultures, the expression of
CD4 was not affected by IL-4
treatment. These results indicated
that the expression of CCR5 is
related to the entry and replication
of monocytotropic virus in
macrophages cultured in the studied
cytokine environments.
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FIG. 2.
Regulation of CCR5 expression by M-CSF, GM-CSF, and
IL-4. (A) Freshly isolated monocytes were maintained at 4°C in medium
(Med) or cultured at 37°C for 48 h in macrophage-SFM alone or in
the presence of M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) as indicated.
Surface expression of CCR5 was then examined by flow cytometric
analysis with monoclonal antibody 5C7 to CCR5 (62) using a
FACSortflow cytometer (Becton Dickinson, Sunnyvale, Calif.); analysis
was also performed with a mouse isotype-matched immunoglobulin G2a
(IgG2a) control antibody (top). (B) Cells were cultured for 48 h
at 37°C in medium alone or in the presence of IL-4 (20 ng/ml), after
which surface expression of CCR5 and CD4 (Leu-3a) was assessed by flow
cytometry; mouse IgG2a was used as an isotype-matched control
antibody.
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Effects of IL-4 and IL-13 on M-CSF-induced enhancement of
HIV-1 infection.
To investigate the interaction of positive and
negative effects of different cytokines on HIV-1 infection of
macrophages, we next examined the impact of IL-4 and IL-13 on
M-CSF-induced enhancement of HIV-1 entry and replication. IL-13 was
chosen because it exhibits a subset of the activities of the
structurally related IL-4 (64) and it inhibits HIV-1
infection of primary macrophages (36, 37). Seven days after
infection of M-CSF-treated macrophages with macrophage tropic
viruses HIV-1 BaL, HXB2-168.1, or HXB2-168.3, p24 antigen production in
cells cultured in the presence of IL-4 (20 ng/ml) or IL-13 (20 ng/ml) was 0 to 30% of that of cells incubated with M-CSF alone
(Fig. 3A). To determine whether the
reduced infection in macrophages treated with IL-4 or
IL-13 was related to early entry events, we examined proviral
DNA synthesis by semiquantitative PCR. Four hours after exposure
to HIV-1 BaL in the presence of M-CSF, the amount of proviral DNA in
IL-4- or IL-13-treated macrophages was markedly less than that in
macrophages cultured with M-CSF alone (Fig. 3B).
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FIG. 3.
Inhibition of M-CSF enhancement of HIV-1 entry and
replication by IL-4 and IL-13. (A) Monocytes were cultured for 48 h in macrophage-SFM containing M-CSF (20 ng/ml) in the absence
or presence of IL-4 (20 ng/ml) or IL-13 (20 ng/ml) and were then
subjected to infection with HIV-1 BaL, HXB2-168.1, or
HXB2-168.3 isolates (13). Seven days after
infection, culture supernatants were harvested and assayed for p24
antigen by enzyme-linked immunosorbent assay. Data are expressed as
percentages of p24 production for cells cultured with M-CSF alone and
are means ± standard deviations of triplicates from a
representative experiment. (B) Four hours after HIV-1 BaL infection of
cells treated as described for panel A, cell lysates were prepared and
analyzed for proviral DNA by semiquantitative PCR. Indicated copy
numbers (500, 50, 5) of control HIV-1 DNA were used as positive
controls. No virus, uninfected parallel macrophages treated with medium
only as negative control. Gag, HIV-1 prototypic gag gene
segment amplified by SK18 and SK19 primers and detected by
[-32P]ATP-end-labeled SK19 hybridization; Free Probe,
SK19 end labeled with [-32P]ATP.
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Effects of IL-4 and IL-13 on CCR5 expression induced by M-CSF or
GM-CSF.
We next examined the effects of IL-4 and IL-13 on
the M-CSF- and GM-CSF-induced increases in CCR5 expression on
macrophages. IL-4 and IL-13 prevented not only the increase in CCR5
expression normally apparent during culture in medium alone for
48 h but also the up-regulation of CCR5 expression by M-CSF and
GM-CSF (Fig. 4). Titration experiments
showed that a concentration of 2 ng/ml was sufficient for IL-4 to
inhibit completely the M-CSF-induced increase in CCR5 expression (data
not shown).
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FIG. 4.
Effects of IL-4 and IL-13 on up-regulation of CCR5
expression by M-CSF and GM-CSF. Monocytes were cultured for 48 h
in macrophage-SFM in the presence of the indicated combinations of
cytokines. Surface expression of CCR5 was then examined by flow
cytometry; mouse IgG2a was used as an isotype-matched control antibody
(upper). Fluorescence intensity is presented on a logarithmic scale.
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Effect of IL-10 on CCR5 expression.
IL-10, like IL-4 and
IL-13, is a Th2 cytokine that is produced by monocytes and inhibits
HIV-1 infection of macrophages (8, 30, 37, 53). We therefore
examined the effect of IL-10 on CCR5 expression. In contrast to IL-4
and IL-13, IL-10 (30 ng/ml) did not downmodulate CCR5 expression on
macrophages incubated in the absence or presence of M-CSF or GM-CSF
(Fig. 4) and actually increased CCR5 expression in the presence of
M-CSF. IL-10 was active on these cells as shown by suppression of
HLA-DR expression (data not shown). These results are consistent with a
previous study showing that IL-10 does not affect viral entry in human primary macrophages (30).
Effect of IL-4 on cells already expressing CCR5 in response to
M-CSF.
Given that IL-4 prevented the M-CSF-induced increase in
CCR5 expression in macrophages, we next investigated the effect of IL-4
in cells in which coreceptor expression had already been induced by
M-CSF. Monocytes were incubated with M-CSF for 1 day and then in the
additional presence of IL-4 for 2 days (Fig.
5). CCR5 expression was then evaluated by
flow cytometry and compared with that of cells cultured continuously
with M-CSF alone or with M-CSF plus IL-4. CCR5 expression was increased
after exposure of cells to M-CSF for 1 day, and this increase was
prevented by addition of IL-4 at the beginning of the culture. The
M-CSF-induced increase in CCR5 expression was also completely reversed
after addition of IL-4 at the end of day 1.
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FIG. 5.
Reversal of the M-CSF-induced increase in CCR5
expression in monocytes by IL-4. Monocytes were cultured for 1 day in
the presence of M-CSF and then for an additional 2 days with M-CSF
alone (top) or with M-CSF plus IL-4 (middle). Alternatively, cells were
cultured in the presence of M-CSF and IL-4 for 3 days (bottom). Cell
surface expression of CCR5 was examined by flow cytometry with antibody
5C7 (filled histogram) at the indicated times; mouse IgG2a (open
histogram) was used as an isotype-matched control antibody.
Fluorescence intensity is presented on a logarithmic scale.
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We have determined the effects of several cytokines on the expression
of CCR5 as well as on HIV-1 entry and replication in
human primary
macrophages. Our results indicate that cytokines
affect early steps in
viral entry through modulation of CCR5 expression.
Our demonstration of the lack of expression of CCR5, the primary
coreceptor for monocytotropic viruses, on freshly isolated
monocytes
may partially explain the absence of infected peripheral
blood
monocytes in the circulation of HIV-1-positive individuals
and the
resistance of freshly isolated blood monocytes to HIV-1
infection
(
50,
54). Transcripts encoding other chemokine receptors,
including CCR3, a coreceptor for HIV-1 in microglial cells
(
27),
are not detectable by reverse transcription-PCR in
freshly isolated
blood monocytes (
42,
55). Although CCR2b
mRNA is detectable
in fresh monocytes by such analysis (
42,
55), this coreceptor
may not function to mediate HIV-1 infection
in monocytes and it
is not targeted by the virus isolates used in the
present study.
The abundance of CCR2b mRNA also decreases markedly
during the
maturation of monocytes into macrophages (
42).
After culture in SFM for 48 h, 29% of monocytes expressed CCR5
and the cells became infectable by macrophage-tropic HIV-1.
Thus, our
results indicate that monocyte differentiation into
macrophages, such
as that which occurs during migration of monocytes
into tissues, is
accompanied by the expression of CCR5 and the
development of
susceptibility to infection by macrophage-tropic
HIV-1. Similar results
were reported recently by Di Marzio et
al. (
17). Our data
are consistent with CCR5 being the primary
coreceptor for infection by
monocytotropic virus, as was indicated
previously in a report that
cells isolated from individuals with
a mutation in the CCR5 gene were
resistant to monocytotropic virus
infection (
12,
47). We
have also observed a high level of
expression of CXCR4 on
monocytes/macrophages, and this expression
was increased by culture
(for up to 2 weeks) but the cells were
not susceptible to infection by
T-cell-line-tropic virus, as determined
by p24 production. Whether the
expressed CXCR4 receptors are defective
in mediating virus entry or
whether other cell surface molecules
such as heparan sulfate
(
51) are also required remains to be
determined.
GM-CSF and M-CSF enhanced viral entry and replication in human primary
macrophages and markedly increased expression of CCR5.
GM-CSF is
secreted by monocytes in response to stimulation with
gp120 from
certain strains of HIV-1 (
10), and M-CSF has been
shown to
be secreted after virus infection in vitro (
25). However,
a
progressive impairment in the ability of CD4
+ T cells to
secrete GM-CSF has been described for HIV-1-infected
individuals
(
4,
49), and this impairment may in turn limit
coreceptor
expression in vivo. Other groups have reported that
GM-CSF inhibits HIV
replication in macrophages at an undefined
dose (
35) and
suppresses expression of a marker gene carried
by an HIV envelope
pseudotyped virus at a high dose of recombinant
GM-CSF but not at lower
doses of the cytokine (
17). Differences
in experimental
systems, including culture conditions and dose
of GM-CSF used to
activate cells, may account for these divergent
results.
IL-4 or IL-13 not only prevented the expression of CCR5 and inhibited
HIV-1 infection in monocytes/macrophages cultured in
medium alone, but
they also blocked the increase in CCR5 expression
induced by GM-CSF or
M-CSF as well as M-CSF stimulation of HIV-1
entry. Although the Th2
cytokine IL-10 has previously been shown
to inhibit HIV replication
(
8,
30,
37,
53), a recent
report showed that IL-10 increased
HIV-1 replication and enhanced
CCR5 expression (
57). We
found that IL-10 did not downmodulate
or stimulate CCR5 expression in
macrophages directly but instead
slightly enhanced CCR5 surface
expression when added together
with M-CSF (see Fig.
4).
The receptors for IL-4 and IL-13 share the IL-4 receptor
chain
(CD124) (
2,
41). Both IL-4 and IL-13 induce the tyrosine
phosphorylation of the kinase JAK1 and 4PS, a 170-kDa protein
associated with phosphatidylinositol 3-kinase, and they induce
expression of the LSK tyrosine kinase in human monocytes
(
39)
and STAT6 (IL-4 STAT) in human colon carcinoma cell
lines (
38).
It is possible that both IL-4 and IL-13 may
regulate CCR5 expression
by a common pathway and at the transcription
level.
It is possible that IL-4 and IL-13 suppress CCR5 expression on
macrophages as a result of ligand-induced endocytosis. The
chemokines
stromal cell-derived factor-1
and RANTES (regulated
on activation,
normal T expressed and secreted) induce rapid endocytosis
of their
specific receptors (
3). However, in our culture system,
neither IL-4 nor IL-13 induced the release of the CCR5 ligands
RANTES,
MIP-1
, and MIP-1
from human monocytes/macrophages in
the absence
or presence of M-CSF (unpublished data). In fact,
both IL-4 and IL-13
inhibit lipopolysaccharide-induced MIP-1
secretion (
16)
and
Staphylococcus aureus-induced MIP-1
production.
Increased expression of IL-4 in HIV-1-seropositive individuals has been
detected (
33,
46). The abundance of IL-13 has
also been
shown to be greater than that of IL-4 in peripheral
blood mononuclear
cells and lymph nodes of such individuals (
63).
It is not
clear whether the T-helper phenotype shifts from Th1
to Th2 or from Th1
to Th0 in HIV-1-infected individuals (
34).
However,
both Th2 and Th0 T cells, as well as CD8
+ cells,
produce IL-4 and IL-13 (
33,
58). CD8
+ T cells
also produce RANTES, MIP-1
, and MIP-1
, all of which
are
capable of blocking CCR5-mediated entry of macrophage-tropic
virus into
CD4
+ T cells (
11).
The regulation of the expression of CCR5 by IL-4 and IL-13, the
blocking of virus coreceptors by chemokines, and the production
of
as-yet-unidentified suppressor factors are likely important
host
determinants in the control of HIV-1 infection. The combination
of IL-4
and IL-13 with CCR5 antagonists (
56) may prove
therapeutically
beneficial for HIV-1-infected individuals. In this
regard, treatment
of patients with Kaposi's sarcoma with IL-4 has been
associated
with moderate decreases in HIV viral load
(
35a).
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ACKNOWLEDGMENTS |
We thank V. Calvert for the preparation of human primary monocytes.
Monoclonal antibody 5C7 was obtained through the AIDS Research and
Reference Reagent Program of the Division of AIDS, National Institute
of Allergy and Infectious Diseases, NIH.
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Division of
Hematologic Products, Center for Biologics Evaluation and Research,
Food and Drug Administration, NIH, Building 29B, Room 4E12, HFM-541, Bethesda, MD 20892. Phone: (301) 827-0793. Fax: (301) 827-0998. E-mail:
miken{at}helix.nih.gov.
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