© 2000 American Heart Association, Inc.
Cellular Biology |
Postanoxic T Lymphocyte–Endothelial Cell Interactions Induce Tumor Necrosis Factor-
Production and Neutrophil Adhesion
Role of Very Late Antigen-4/Vascular Cell Adhesion Molecule-1
From the Department of Molecular and Cellular Physiology (S.K., D.N.G., T.Y.A.) and Center of Excellence in Arthritis and Rheumatism (R.E.W.), Louisiana State University Health Sciences Center, Shreveport, La, and First Department of Internal Medicine (T.Y.), Kyoto Prefectural University of Medicine, Kyoto, Japan.
Correspondence to Tak Yee Aw, PhD, Department of Molecular and Cellular Physiology, LSU Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130-3932. E-mail taw{at}lsumc.edu
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Abstract |
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Abstract—The objective of this study was to define the influence of postanoxic T-lymphocyte–endothelial cell interactions on anoxia-reoxygenation (A/R)–induced neutrophil–endothelial cell adhesion and cell adhesion molecule (CAM) expression on human umbilical vein endothelial cells (HUVECs). HUVEC monolayers were exposed to 60 minutes of anoxia, followed by 24 hours of reoxygenation, wherein freshly isolated human T lymphocytes were added at 6 hours during reoxygenation. After an additional 18 hours of incubation (ie, total of 24 hours of reoxygenation), the T-cell/endothelial cell (TC/EC) coculture media were collected and added to naive HUVEC monolayers incubated with neutrophils. Although the A/R-conditioned media per se had no effect on neutrophil adhesion, the media from TC/EC cocultures significantly increased the adhesion response. This enhanced adhesive interaction was associated with significant increases in tumor necrosis factor-
(TNF-) and interleukin-8 (IL-8) levels in the
TC/EC coculture media and was accompanied by a pronounced increase in
endothelial E-selectin expression. Treatment of the
TC/EC coculture media with anti–TNF- or anti-IL-8 antibodies
reduced the media-induced neutrophil adhesion response. The enhanced
neutrophil adhesion and the elevated medium levels of TNF-, but not
IL-8, were markedly reduced by inserts that prevented direct TC/EC
contact and by monoclonal antibodies directed against vascular cell
adhesion molecule-1 (VCAM-1) or very late antigen-4 (VLA-4).
Collectively, these findings show that VLA-4–/VCAM-1–mediated
interactions between T lymphocytes and postanoxic
endothelial cells stimulates TNF-
production, which in turn elicits endothelial
cell adhesion molecule expression and a corresponding increase in
neutrophil adhesion.
Key Words: anoxia/reoxygenation • E-selectin • neutrophil–endothelial cell adhesion • T lymphocytes • tumor necrosis-
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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It is well appreciated that the inflammatory response elicited by anoxia-reoxygenation (A/R) is associated with enhanced neutrophil adhesion to endothelial cells. We and others have used a simple in vitro model wherein endothelial cell monolayers are exposed to A/R to mimic the microvascular dysfunction that is elicited by ischemia-reperfusion (I/R) in vivo. Most analyses of leukocyte recruitment in postischemic tissues have focused on neutrophils, which appear to be the ultimate circulating cell that mediates I/R-induced microvascular dysfunction.1 2 However, there is growing evidence that T lymphocytes also contribute to the pathogenesis of I/R injury.3 4 5 Zwacka et al6 have demonstrated a role for CD4+ T cells in mediating the neutrophil infiltration associated with hepatic I/R in vivo. To promote neutrophil adhesion to endothelial cells, T lymphocytes may rely on different mechanisms, some of which are dependent on soluble factors derived from endothelial cells, and others of which require direct contact of T lymphocytes to endothelial cells. We recently demonstrated that T lymphocytes are rapidly activated by H2O2 produced by postanoxic endothelial cells.7 The activated T cells release tumor necrosis factor-
(TNF-), which in turn increases expression of
endothelial E-selectin that mediates
neutrophil–endothelial cell adhesion.7 In
other studies, direct contact between stimulated T lymphocytes and
endothelial cells has been shown to induce expression
of cell adhesion molecules (CAMs) and
cytokines,8 9 but the mechanisms underlying the
induction of these inflammatory molecules have not been defined.
Very late antigen-4 (VLA-4), a major adhesion receptor expressed by T
lymphocytes, mediates T-cell adhesion in the microvasculature via an
interaction with vascular CAM-1 (VCAM-1) on activated
endothelial cells.10 11 12 13 14 Damle and
Aruffo15 have demonstrated that VCAM-1 sustains the
activation of T lymphocytes by mediating the binding to
antigen-responsive VLA-4+ T lymphocytes. Direct
evidence implicating VLA-4/VCAM-1 interactions in T-lymphocyte
activation is provided by studies demonstrating that binding of T
lymphocytes to VCAM-1 on endothelial cells induces a
72-kDa gelatinase in T lymphocytes.16 We previously
demonstrated that the adhesion of T lymphocytes to postanoxic
endothelial cells is mediated by VLA-4/VCAM-1 and
lymphocyte function–associated antigen-1 (LFA-1)/intercellular
adhesion molecule-1 (ICAM-1) interactions that are induced, at least
partially, by interleukin-8 (IL-8).17 We also observed
that the H2O2 generated by
A/R-exposed human umbilical vein endothelial cells
(HUVECs) activates T lymphocytes to produce
TNF-.7 Because the A/R-induced enhancement of
H2O2 only occurs within the
initial few minutes after
reoxygenation,18 19 the enhanced
neutrophil adhesion observed at 4 hours after
reoxygenation is not likely to be mediated by
H2O2-stimulated T
lymphocytes. However, VCAM-1 expression is elevated on postanoxic
endothelial cells, with peak expression occurring
between 6 and 10 hours after
reoxygenation.17 Collectively, these
findings raise the interesting possibility that at 4 hours after
reoxygenation, VLA-4/VCAM-1 interactions induce
T-lymphocyte activation, which increases expression of
endothelial CAMs. Recent studies suggest that ligation
of the VLA-4 integrin on freshly isolated human T lymphocytes with
VCAM-1, when coimmobilized with anti-CD3 monoclonal
antibody (mAb), increased the induction of transcription factors and
cytokines that are related to TNF-
stimulation.20 These findings led us to hypothesize
that A/R-exposed HUVECs exhibit VLA-4–/VCAM-1–mediated T
cell–endothelial cell adhesive interactions that
stimulate TNF- production by T cells, which causes a further
enhancement of endothelial CAM expression.
The objectives of this study were to (1) determine whether T
lymphocytes influence the intensity of
neutrophil–endothelial cell adhesion and
endothelial CAM expression induced by exposing HUVEC
monolayers to A/R, (2) determine whether the postanoxic T
lymphocyte–endothelial cell interactions promote
release of TNF- from T cells and enhance A/R-induced
neutrophil–endothelial cell adhesion, and (3) define
the mechanisms that underlie the enhanced TNF- release from T cells
that are cocultured with postanoxic endothelial
cells.
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Materials and Methods |
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The Materials and Methods section in its entirety is available online at http://www.circresaha.org.
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Results |
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Media from normoxia- and A/R-conditioned HUVECs and from normoxia- and A/R-conditioned HUVECs cocultured with freshly isolated peripheral T lymphocytes were collected after 24 hours of reoxygenation. Figure 1A
illustrates the neutrophil adhesion (at 4 hours) to naive monolayers
that were incubated with each medium. Without T cells, 24-hour
A/R-conditioned medium did not enhance neutrophil adhesion, as
compared with normoxia-conditioned medium. Moreover, medium conditioned
by T cells alone (without endothelial cells) did not
affect neutrophil adhesion to HUVECs exposed to normoxia or A/R (data
not shown). In contrast, medium from the coculture of T cells with
A/R-exposed HUVECs (TC/EC), but not with normoxia-exposed HUVECs,
caused a significant increase in neutrophil adhesion. Because we have
previously demonstrated an involvement of IL-8 in
leukocyte-endothelial cell adhesion after
A/R17 and a role for T cell–derived TNF- in
neutrophil–endothelial cell interaction in a coculture
system of T lymphocytes with A/R-exposed HUVECs,7 TNF-
and IL-8 levels were quantified in the media of A/R-conditioned HUVECs
incubated with or without T lymphocytes. The results (Figure 1B)
show that TNF- concentrations in A/R-conditioned media were
unchanged from normoxia-conditioned media but were significantly
elevated in TC/EC coculture media. IL-8 levels in A/R-conditioned media
were 5-fold higher than control and were further increased (20-fold)
when cocultured with T lymphocytes (Figure 1C). To define the
potential contributions of soluble TNF- and IL-8 (derived from TC/EC
coculture) to neutrophil–endothelial cell adhesion,
naive HUVEC monolayers were incubated in the coculture medium in the
presence of mAbs directed against TNF- or IL-8. Figure 2 demonstrates that anti–TNF-
completely blocked the ability of the TC/EC medium to induce neutrophil
adhesion to naive HUVECs, whereas a partial attenuation of this
response was obtained with anti–IL-8. A/R-conditioned medium in the
absence or presence of the respective mAbs but without T cells did not
influence the adhesion response.
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Figure 3 summarizes the effects of mAbs
directed against different endothelial CAMs on
neutrophil adhesion to HUVECs incubated with TC/EC coculture medium.
The increase in neutrophil adhesion induced by coculture medium was
significantly and dose-dependently reduced by
anti–E-selectin–specific antibody, implicating a role for E-selectin
in the adhesion response. Anti–ICAM-1 at 20 µg/mL tended to
attenuate the adhesion response, whereas anti–P-selectin had no effect
at any concentration. To further define the endothelial
CAMs that were responsible for the enhanced adhesion response, we
quantified the surface expression of these glycoproteins.
The results are summarized in the
Table. Medium from A/R-exposed HUVECs
with or without T cells did not affect endothelial
P-selectin expression. Expression of E-selectin in
endothelial cells incubated with 24-hour medium from
A/R-exposed HUVECs was not significantly different from control;
however, expression was elevated 12-fold when cells were incubated with
24-hour TC/EC coculture medium. Unlike E- and P-selectin, surface
expression of ICAM-1 was high in control HUVECs and in cells incubated
with the medium from A/R-exposed HUVECs. Endothelial
ICAM-1 expression was increased significantly, albeit to a small
extent, in the presence of TC/EC coculture medium. Notably, although
both E-selectin and ICAM-1 were significantly increased by TC/EC
coculture medium, the magnitude of E-selectin upregulation (12-fold)
was substantially greater than for ICAM-1 (1.3-fold). These results,
together with the blocking effect of anti–E-selectin (see Figure 3), suggest that an increase in endothelial
E-selectin expression accounts for the increased
neutrophil–endothelial cell adhesion induced by TC/EC
coculture medium. Our finding also implicates TNF- or IL-8 as a
candidate molecule that mediates this increased E-selectin
expression.
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To determine whether E-selectin expression is mediated by TNF-
and/or IL-8 derived from TC/EC coculture, we quantified surface
expression of E-selectin on HUVECs incubated with the coculture medium
in the presence of anti–TNF- or anti–IL-8. The results (Figure 4A) show that the increased E-selectin
expression caused by coculture medium was significantly attenuated by
the mAb directed against TNF-, but not IL-8. Incubations with the
respective mAbs per se without T lymphocytes had no effect on
E-selectin expression. We also directly tested the effect of TNF-
and IL-8 on E-selectin expression using similar concentrations of the
cytokines that were found in the 24-hour TC/EC coculture
medium. Figure 4B shows that TNF- dose-dependently increased
E-selectin expression. Notably, 5 pg/mL TNF- induced
endothelial E-selectin expression to the same degree as
that induced by the coculture medium (see Table
), supporting our
contention that soluble TNF- in the TC/EC coculture medium promoted
the observed neutrophil–endothelial cell interaction.
IL-8 alone (20–320 ng/mL) did not induce E-selectin expression (data
not shown), nor did IL-8 (20 ng/mL) enhance TNF-–induced E-selectin
expression (Figure 4B), consistent with a lack of
participation of this chemokine in T cell–mediated
endothelial E-selectin expression.
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To determine whether the neutrophil–endothelial cell
adhesion induced by 24-hour TC/EC coculture was dependent on direct
contact between T cells and endothelial cells, T
lymphocytes were separated from HUVEC monolayers grown in 24-well
plates by 0.4 µm Millipore filters in culture inserts. The
results (Figure 5A) show that
medium obtained from coincubation of T lymphocytes and HUVECs in
separate chambers did not elicit a neutrophil adhesion response.
Furthermore, coculture medium–induced E-selectin expression was also
absent when T cells and endothelial cells were
separated in different chambers (Figure 5B). These data
demonstrate that direct contact between T lymphocytes and HUVECs is
essential for the neutrophil–endothelial cell
interaction induced by the coculture medium. In our present study,
T lymphocytes were added into A/R-exposed HUVECs at 6 hours after
reoxygenation. We previously found that direct
interaction of postanoxic endothelial cells with T
lymphocytes at 6 hours after reoxygenation is mediated
by VLA-4/VCAM-1 and LFA-1/ICAM-1 interactions.17
Therefore, we assessed the role of these interactions in the
inflammatory responses induced by TC/EC coculture. The results (Figure 5A) show that coculture medium–induced adhesion response was
inhibited by the mAbs directed against VCAM-1 and VLA-4, whereas
neither anti–ICAM-1 nor anti–LFA-1 was effective, indicating that
VLA-4/VCAM-1 interaction is necessary to elicit the coculture
medium–mediated neutrophil adhesion response. Accordingly, E-selectin
expression in A/R-exposed monolayers induced by TC/EC interaction was
similarly blocked by anti–VCAM-1 and anti–VLA-4 (Figure 5B).
The presence of the respective mAbs per se without T cells were without
effect on E-selectin expression (Figure 5B). Figure 6 illustrates the results of TNF- and
IL-8 production in the coculture medium in the presence of mAbs
directed against the VCAM-1/VLA-4 or ICAM-1/LFA-1 receptor-ligand pair.
The results show that TNF- levels in the coculture media were
significantly attenuated in the presence of anti–VCAM-1 or
anti–VLA-4, but not anti–ICAM-1 or anti–LFA-1 (Figure 6A).
Furthermore, TNF- levels in media were not elevated when T cells
were separated from endothelial cells in culture
inserts. These results indicate that direct cell contact of T
lymphocytes with HUVECs via VLA-4/VCAM-1 ligation is critical for
TNF- production induced by coculture of the 2 cell
populations. None of the antibodies tested nor use of culture inserts
influenced the elevation of IL-8 levels induced by 24-hour TC/EC
coculture (Figure 6B), suggesting that IL-8 production
is not dependent on direct TC/EC interaction in the coculture system.
We further found that production of TNF- and IL-8,
expression of endothelial E-selectin, and neutrophil
adhesion induced by coculture medium were all unaffected by
pretreatment with catalase (data not shown), suggesting that
H2O2 was not the mediator
of this 24-hour T lymphocyte–endothelial cell
response. To validate that anti–VCAM-1 or anti–VLA-4 per se did not
affect the adhesion response mediated by TNF- subsequent to TC/EC
interaction, TNF-–induced neutrophil adhesion was examined directly
in the absence or presence of anti–VCAM-1 or anti–VLA-4. The results
(Figure 7) show that the neutrophil
adhesion response elicited by TNF- at low (such as that measured
after TC/EC coincubation, 10 pg/mL) or high concentrations (10 ng/mL)
was unaffected by addition of anti–VCAM-1 or anti–VLA-4, thus
negating a direct effect of the mAbs on the adhesion response.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The current study provides evidence that VLA-4–/VCAM-1–mediated adhesive interactions (at 6 hours) between T lymphocytes and A/R-exposed endothelial cells promote the adhesion of neutrophils to these postanoxic endothelial cells. Moreover, direct contact of T cells with endothelial cells is a prerequisite for TNF-
production that leads to
upregulation of endothelial E-selectin expression and
enhancement of neutrophil–endothelial cell adhesion.
Several lines of evidence support these conclusions, as follows: (1)
TC/EC coculture enhanced TNF- production and promoted
neutrophil adhesion; (2) increased neutrophil adhesivity induced by
TC/EC coculture medium was due to TNF-–mediated expression of
endothelial E-selectin; (3) TNF- release, E-selectin
expression, and neutrophil adhesion normally elicited by TC/EC
coculture media were abrogated by preventing direct contact of T
lymphocytes with HUVECs; and (4) immunoneutralization of VLA-4, or
its endothelial ligand VCAM-1, prevented the TC/EC
medium-induced inflammatory responses.
Although the role of T lymphocytes as cellular mediators of
neutrophil-dependent inflammatory responses is well appreciated, the
mechanisms used by T cells to mediate these neutrophil adhesion
responses remain poorly understood. We recently demonstrated that T
lymphocytes are activated by
H2O2 produced by postanoxic
endothelial cells in the early phase of
reoxygenation and that the activated T cells
release TNF-, which increases E-selectin expression and promotes
neutrophil–endothelial cell adhesion.7
Because the A/R-induced enhancement of
H2O2 occurs within the
initial few minutes after reoxygenation, the enhanced
neutrophil adhesion observed during the late phase (24 hours) of
reoxygenation (current study) is not likely to be
mediated by H2O2-stimulated
T lymphocytes. Indeed, we found that catalase was without effect on
TNF- and IL-8 release and on neutrophil adhesion when added to HUVEC
monolayers immediately before addition of T cells. Our current results
are consistent with a major role for T cell–derived TNF- in
mediating the TC/EC medium–induced neutrophil adhesivity to
endothelial cells at 24 hours after
reoxygenation. Moreover, the data show that the
adhesive interactions between T lymphocytes and postanoxic
endothelial cells is a prerequisite for the enhanced
production of TNF-.
We recently demonstrated that unstimulated T lymphocytes adhere to
A/R-exposed HUVECs by VLA-4/VCAM-1 and LFA-1/ICAM-1
ligation.17 It is notable that, although both of these
interactions participate in mediating TC/EC adhesion,17
only the VLA-4/VCAM-1 ligation appears to be a prerequisite for TNF-
production (current study). The reason for this interesting
difference is unclear; one possibility may be that VCAM-1 occupancy is
directly linked to a specific signaling pathway for TNF- expression.
The nature of such a pathway has yet to be identified. Regardless of
mechanism, our finding is consistent with evidence in the
literature that supports a direct association between TNF-
production and VCAM-1/VLA-4 interaction. For example, ligation
of VLA-4 integrin has been shown to induce transcription factor
activation that enhances cytokine production by T
cells.15 16 22 In our study, mAbs directed against VLA-4
or VCAM-1 significantly attenuated the enhanced production of
TNF- and neutrophil adhesion elicited by TC/EC medium. This
observation, coupled with reports in the literature,16 22
strongly suggests that VLA-4–mediated binding of T lymphocytes to
VCAM-1 on A/R-exposed HUVEC surface induces a late phase (24 hours) of
neutrophil adhesion that is dependent on TNF-. This conclusion is
supported by studies of Udagawa et al,20 who demonstrated
that ligation of the VLA-4 integrin on freshly isolated human T
lymphocytes with VCAM-1, when coimmobilized with anti-CD3
mAb, enhanced transcription factor induction and TNF-
production. Additional evidence comes from studies that show
that integrins trigger a number of intracellular signaling events in T
cells.23 24 25
Activation of naive T lymphocytes requires recognition of foreign
antigens bound to a self–major histocompatibility complex (MHC)
molecule together with costimulatory signals by an
antigen-presenting cell. However, Pober et al26 have
reported that HUVEC monolayers do not express MHC molecules. This
suggests that activation of unstimulated T cells after binding to
A/R-exposed HUVECs may occur via an antigen-independent pathway.
Alternatively, self-antigens may be modified by reactive oxygen species
generated during A/R such that HUVEC monolayers appear foreign to T
lymphocytes. These possibilities are supported by 2 previous studies;
Bacon et al27 documented an antigen-independent activation
mechanism for T lymphocytes, and Niemelä et al28
demonstrated protein modifications resulting from oxidation associated
with inflammatory processes. Although our results implicate T
lymphocytes as the major source of TNF-, we cannot exclude the
possible involvement of A/R-exposed HUVECs as a contributor to TNF-
release into the coculture media. Because ligation of VCAM-1 or ICAM-1
to their ligands has been shown to induce transcription of
cytokines,29 30 adhesion molecules can function
not only as adhesive substrates, but also as transducers of signals for
enhanced cytokine production. Therefore, further
studies are warranted to delineate the quantitative contribution of T
lymphocytes and/or endothelial cells to the elevated
TNF- concentrations detected in the coculture media during T
cell–endothelial cell adhesion.
An interesting and potentially important observation is the
participation of IL-8 in the enhanced
neutrophil–endothelial cell adhesion induced by TC/EC
coculture medium. We previously found that A/R per se induces
endothelial cell IL-8 production and that IL-8
derived from A/R-exposed HUVECs induces T cell adhesion to
endothelial cells.17 Our current results
show that 24 hours of TC/EC coculture increases IL-8
production, which promotes neutrophil adhesion to HUVECs.
Interestingly, unlike TNF-, IL-8 production is not dependent
on direct cell-to-cell-contact between T lymphocytes and HUVECs. This
finding, together with previous reports that IL-8 induces its own
production in T lymphocytes,31 32 suggests that
postanoxic HUVECs produce IL-8, which in turn upregulates IL-8
production by T lymphocytes. IL-8 has been shown to bind to the
endothelial cell surface, where it can act as a
chemoattractant and activator of
neutrophils.33 34 It is also conceivable that IL-8 may
promote neutrophil–endothelial cell adhesion by
increasing the expression of endothelial CAMs. However,
we found that IL-8 per se does not induce the expression of E-selectin,
nor does it enhance E-selectin expression mediated by TNF-. Taken
together, these results suggest that the IL-8 derived from TC/EC
coculture most likely plays a direct role in the activation of
neutrophils.
In conclusion, the present study demonstrates that direct adhesive
interactions between VLA-4 on T lymphocytes and VCAM-1 on A/R-exposed
endothelial cells results in an exaggerated, late-phase
neutrophil adhesion response that is mediated by TNF-–stimulated
E-selectin expression on endothelial cells. A role for
T lymphocyte–derived IL-8 in the activation of neutrophils is also
supported. These results may provide a molecular basis for
understanding the modulatory influence of T lymphocytes in the late
stages of ischemia/reperfusion–induced microvascular
dysfunction.
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Acknowledgments |
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This study was supported by NIH Grant P01-DK43785.
Received February 16, 2000; accepted April 28, 2000.
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