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1b-Adrenergic Receptors1
Center for Experimental Pathology, Istituto Cantonale di Patologia, Locarno, Switzerland
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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2-adrenergic antagonist
yohimbine and inhibited by local treatment with the specific
1-adrenergic antagonist prazosin (PRA). Consistently, NE
enhances spontaneous emigration of DC from ear skin explants, and PRA
inhibits this effect. In addition, local treatment with PRA during
sensitization with FITC inhibits the contact hypersensitivity response
6 days later. In vitro, bone marrow-derived immature, but not
CD40-stimulated mature DC migrate in response to NE, and this effect is
neutralized by PRA. NE seems to exert both a chemotactic and
chemokinetic activity on immature DC. Coherently, immature, but not
mature DC, express mRNA coding for the 1b-adrenergic
receptor subtype. Inactivation of this adrenergic receptor by the
specific and irreversible antagonist chloroethylclonidine hinders the
migration of injected DC from the footpad to regional lymph nodes.
Thus, besides regulating lymph flow, the sympathetic innervation of
lymphatic vessels may participate in directing DC migration from the
site of inflammation to regional lymph nodes. Alternatively, the
chemokinetic activity of NE may enhance the ability of DC to sample
local Ags, and hence increase the number of DC migrating to the
draining lymph nodes. This finding might improve our understanding of
the biological basis of skin diseases and allergic reactions, and opens
new pharmacological possibilities to modulate the immune
response. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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2 (2A,
2B, 2C), and three
1 (1a,
1b, 1d) receptor
subtypes. The 1-ARs are present in several
tissues, including brain, heart, blood vessels, liver, kidney,
prostate, and spleen, where they mediate a variety of physiological
effects such as cardiac inotropy and chronotropy, vasocontraction,
glycogenolysis, and the contractions of the urinary tract
(8). On the other hand, the interaction between
sympathetic nerves and cells of the immune system has been demonstrated
in terms of distribution of tyrosine hydroxylase-positive fibers in
lymphoid organs, expression of ARs on cells of the immune system, and
immunomodulatory effects of the main sympathetic neurotransmitter NE
(9, 10, 11). We reported that catecholamines can also exert
important hemopoietic effects via 1-ARs
expressed in bone marrow progenitor cells (12, 13, 14, 15, 16).
Relevant to the present study, NE has been shown to stimulate lymphoid
cell mobilization via ß-ARs (17). |
Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Female 2- to 3-mo-old C57BL/6 or C3H/He inbred mice were purchased from Charles River Breeding Laboratories (Calco, Italy) and maintained in our animal room under a standard 12-h photoperiod, at 21 ± 1°C, with food and water ad libitum for at least 10 days before the experiments.
DC cultures
Bone marrow-derived DC were generated according to a recently described method with minor modifications (18). Briefly, bone marrow cells were collected from the long bones; suspended (2 x 106 cells/ml) in RPMI 1640, 25 mM HEPES, 10% FCS, 50 µM 2-ME, 2 mM L-glutamine, 100 IU/ml penicillin, 100 µg/ml streptomycin, and 20 ng/ml GM-CSF (PeproTech, Rocky Hill, NJ); and incubated in 100-mm-diameter bacteriological petri dishes. At day 3, 10 ml of complete culture medium was added to the plates. At days 6 and 8, half of the culture supernatant was collected and centrifuged, and the cell pellet was resuspended in 10 ml of complete culture medium and given back to the original plate. At day 10, cells were collected, layered onto a metrizamide gradient (14.5 g in 100 ml of RPMI 1640 culture medium), and centrifuged for 10 min at 600 x g. Then the low-density cell fraction was depleted from lymphocytes and GR-1+ cells using a mixture of mAbs and rabbit complement for 60 min at 37°C. The mAbs used were anti-CD4, TIB 207 GK1.5; anti-CD8, TIB 2109 2.43; and anti-B220, TIB 146 RAB-BA1/61 (American Type Culture Collection, Manassas, VA). GR-1 mAb was purchased from PharMingen (Basel, Switzerland). After depletion, cells were washed and analyzed by flow cytometry. Cells showing a typical dendritic morphology were always >90%, whereas the DC marker CD11c was invariably found on >95% of the cells. High expression of major histocompatibility class II Ags and of the costimulatory molecule CD86 (B7-2), typical of mature DC, was expressed by 25–30% of the cells. In general, cell yield and degree of maturation agreed with the reported method (18).
Flow cytometry
DC were washed and 5 x 105 cells/sample were incubated for 30 min at 4°C with saturating concentrations of PE- or FITC-conjugated mAbs. After further washings, the cells were analyzed with single or two-color immunofluorescence by flow cytometry (FACScan; Becton Dickinson, Mountain View, CA). Ten thousand cells were analyzed per sample with the gate set around the cluster of large cells. Negative controls included cells incubated with FITC- or PE-labeled isotype-matched, unrelated mAb.
In vivo migration of epidermal Langerhans cells
Mice were painted on the shaved back with 50 µl of 1% FITC (Sigma, St. Louis, MO) dissolved in a 50:50 (v/v) acetone-dibutylphtalate mixture. Twenty-four hours after painting with FITC in the presence or absence of 10 µM prazosin (PRA; Sigma) or 10 µM propranolol (Sigma), the mice were killed and single-cell suspensions were prepared from inguinal, axillary, and brachial lymph nodes. Other groups of mice were injected i.p. with yohimbine (5 mg/kg body weight; Sigma) or phosphate saline just after FITC painting. Lymph nodes were incubated in collagenase A (0.5 mg/ml; Boehringer Mannheim, Rot Kreuz, Switzerland) and DNase I (40 µg/ml; Perkin-Elmer, Rot Kreuz, Switzerland)) for 10 min at 37°C. Afterward, the tissue was teased and cells were filtered through a 70-µm cell strainer (Falcon; Becton Dickinson). Cells were washed and layered onto a metrizamide gradient (14.5 g in 100 ml RPMI 1640 culture medium) and centrifuged for 10 min at 600 x g. Cells at the interface were collected, washed, and labeled with PE-conjugated anti-CD86 (PharMingen) mAb and analyzed by flow cytometry. Cells labeled with both FITC and PE were quantitated as migrated Langerhans cells.
Skin organ culture
Ears from mice were rinsed with 70% ethanol and air dried for 10 min. Ear skin was split in dorsa and ventral halves, and the dorsal halves were cultured in a 24-well tissue culture plate in 2 ml of RPMI 1640, 10% FCS, 2 mM glutamine, 100 U/ml penicillin, and 100 µg/ml streptomycin. Adrenergic agents were added at the beginning of the culture. After 24 h, the ear halves were removed and free cells were collected, centrifuged, and counted in trypan blue. DC were identified morphologically as large veiled cells.
Assay for contact hypersensitivity (CHS) to FITC
Mice were sensitized by painting 400 ml of 0.5% FITC with or without the adrenergic antagonists (PRA, 10 µM; propranolol, 10 µM) on the shaved trunk, and 6 days later were challenged by applying 20 µl of 0.5% FITC on the dorsal and ventral sides of the right ear. As a control, the left ear was painted with an identical amount of vehicle (acetone-dibutylphtalate, 1:1). The CHS response was determined by measuring the degree of ear swelling of the FITC-painted ear compared with that of the vehicle-treated contralateral ear at 24 h after challenge using a digital micrometer (Mitutoyo, Kawasaki, Japan). The results were expressed as net ear swelling, which was calculated by subtracting the thickness of the vehicle-treated ear from the thickness of the FITC-challenged ear.
In vitro migration
Cell migration was evaluated in vitro using a chemotaxis chamber technique. A total of 27 µl of a chemoattractant solution containing NE (Sigma), isoproterenol (Sigma), the chemokines 6Ckine and RANTES (R&D Systems, Abingdon, U.K.), or control medium RPMI 1640 and 1% FCS were added to the lower wells of a chemotactic chamber (Neuroprobe, Gaithersburg, MD). A polycarbonate filter (5-µm pore size; Neuroprobe) was layered onto the wells and covered with a silicon gasket and a top plate. A total of 50 µl of cell suspension (1.5 x 106 cells/ml) was seeded in the upper chamber. In certain experiments, NE or PRA was added in the upper wells along with DC. The chamber was incubated at 37°C for 90 min. At the end of the incubation, filters were removed and stained with Diff-Quick (Dade Behring, Düdingen, Switzerland), and high-power fields (x100) were counted. Results are expressed as the mean number of migrated cells in 10 fields.
CD40-induced maturation
For CD40 cross-linking, DC were incubated in ice for 10 min in phosphate saline plus 10% mouse serum for 20 min with hamster anti-mouse CD40 mAb (5 µg/ml; PharMingen) and then overnight at 37°C with goat anti-hamster Abs (Pierce, Rockford, IL) in IMEM plus 10% FCS. Morphometric and flow cytometry analysis showed that >95% of CD40-stimulated cells were mature DC.
RT-PCR
Total RNA isolated from 5 x 106
cells was reverse transcribed using 400 U of SuperScript RT (Life
Technologies, Basel, Switzerland) and 40 U of RNase inhibitor
(Perkin-Elmer, Rot Kreuz, Switzerland) in 50 mM Tris-HCl (pH 8.3), 75
mM KCl, 3 mM MgCl2, 10 µM dithyotretol, 60 µM
random hexamers, 4.3 µM polyT(16, 17, 18), and 500 µM of each
deoxynucleotide were added, and the mix was incubated for 1 h at
37°C. cDNA amplification was performed in 50 mM KCl, 10 mM Tris (pH
8.6), 1.5 mM MgCl2, 250 µM deoxynucleotides,
0.5 µM primers (Genset, Paris, France), and 2.5 U of AmpliTaq
polymerase (Perkin-Elmer). Forty cycles of PCR were performed according
to the following steps: 94°C, 4 min (once); 94°C, 2 min; 46°C, 1
min; and 72°C, 2 min. At the end, the reaction mixture was kept for
10 min at 72°C and finally chilled in ice until analysis. For
selection of the primers, we referred to the National Center for
Biotechnology Information database. The primers sequence is reported,
as follows: 1a, upstream,
5'-CCTGGTTATGTACTGTCGAGTCTAC-3', and downstream,
5'-TATGATAGGGTTGATGCAACTATTT-3'; 1b, upstream,
5'-CCAACCAACTACTTCATTGTCA-3', and downstream, 5'-
GCCAACATAAGATGAACATTCC-3'; and 1d,
upstream, 5'- CTTCTCTTCCGTATGCTCCTTCTA-3', and downstream, 5'-
GGGTTCACACAGCTATTGA AGTAG-3'.
The RNA quality was controlled by amplifying hypoxanthine-guanine phosphoribosyltransferase mRNA using the following oligonucleotides as primers: upstream, 5'-GATTATGGACAGGACTGAAAG-3' and downstream, 5'- CGAGAGGTCCTTTTCACCAGC-3'.
In vivo migration of passively transferred DC
I-Ab DC were incubated with chloroethylclonidine (10 µM; Sigma) for 30 min at 37°C or with culture medium alone. After washing, 5 x 105 cells in 50 µl were then injected s.c. into the hind footpads of I-Ak mice. Forty-eight hours after injection, the mice were killed, and the popliteal and inguinal lymph nodes were removed. Single-cell suspensions of lymph node cells were centrifuged on a metrizamide gradient, and the low-density DC fraction was harvested. Flow cytometry analysis was performed to detect I-Ab-positive cells.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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We studied whether NE participates in determining the emigration
pathway of skin DC such as epidermal Langerhans cells. We used the
fluorescent molecule FITC as an Ag to induce migration of Langerhans
cells to regional lymph nodes. Mice were painted with FITC on the back
after shaving, and the effect of adrenergic agents was evaluated in
terms of the number of cells positive for both FITC and CD86 (B7-2)
found 24 h later in the draining lymph nodes. The results obtained
show that topical application of the
1-adrenergic antagonist PRA, but not the
ß-adrenergic antagonist propranolol inhibited migration of Langerhans
cells to the draining lymph nodes (Fig. 1
). In addition, the i.p. injection of
yohimbine, an 2-adrenergic antagonist that
increases the noradrenergic tone, resulted in a significant increase of
migrated Langerhans cells. Altogether these results suggest that NE is
involved in skin DC migration via 1-ARs.
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A strong stimulation of DC emigration from dorsal halves of ear
skin was noted when NE was added in the culture medium. On average, a
3-fold increase of migrated DC was found in the presence of NE, and a
4-fold increase was found using the chemokine 6Ckine as positive
control (Table I). As expected, the
1-AR antagonist PRA inhibited the NE effect
(Table I). These results confirmed that NE can mobilize skin DC via
1-ARs.
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To investigate whether the adrenergic inhibition of skin DC
migration in vivo results in an altered development of DC-dependent
immune response, we measured the CHS response to FITC after
sensitization in presence of either PRA or propranolol. Fig. 2 shows that PRA, but not propranolol
treatment during sensitization inhibited the CHS response expressed as
net ear swelling after FITC challenge 6 days later. This indicated that
the PRA-induced inhibition of DC migration resulted in a reduced
sensitization to FITC.
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To study in greater detail the possibility that NE is involved in
DC migration, we set up experiments in a chemotaxis microchamber using
NE or the synthetic ß-adrenergic agonist isoproterenol as
chemoattractants. Fig. 3 shows that NE,
but not isoproterenol, is indeed a powerful chemoattractant for bone
marrow-derived DC. The DC generated from bone marrow cultures were
heterogeneous for their expression of MHC class II and B7-2, i.e., for
their degree of maturation. With this cell population containing
immature DC, NE 10-6 M (319.3 ng/ml) exerted a
chemotactic activity that was intermediate in comparison with those
exerted by RANTES (100 ng/ml) and the secondary lymphoid tissue
chemokine 6Ckine (120 ng/ml), which has been recently suggested to play
a role in migration and homing of mature DC
(19). Consistently, 6Ckine was highly chemotactic, with DC brought to maturation by CD40 stimulation, while NE apparently did not attract mature DC (Fig. 3). In line with the results obtained in vivo and with the lack of effect of isoproterenol, PRA neutralized the chemotactic effect of NE (Fig.>
3).
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). When seeded in the upper chamber
together with the cells, NE prevented spontaneous (control) migration,
but not the chemotactic activity of RANTES (Fig. 4). However, although
less than toward a NE gradient (NE in lower wells only), DC also
migrated in a constant NE concentration (10-6 M
NE both in the upper and lower wells; Fig. 4). These results indicate
that NE is both a chemoattractant and a chemokinetic factor for
immature, but not for mature DC.
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1-ARs in DC
The PRA sensitivity of DC migration and the lack of effect of
ß-adrenergic agents both in vivo and in vitro imply the participation
of 1-ARs. This type of AR has been indeed
reported to mediate the effect of catecholamines on lymphatic vessels
(20). However, our studies suggest that DC may likewise
express 1-ARs. To elucidate this point, we
investigated the presence of mRNA coding for the three
1-AR subtypes (a, b, and d) in bone
marrow-derived DC before and after CD40 stimulation. RT-PCR analysis
revealed the expression of the 1b-AR mRNA in
bone marrow-derived DC. Apparently, the other two
1-AR subtypes were not expressed (Fig. 5). The 1b-AR
mRNA expression was, however, almost undetectable in DC stimulated by
anti-CD40 Abs (Fig. 5). This is most likely the reason that NE does
not attract mature CD40-stimulated DC (Fig. 3
). Presumably, the
1b-AR is expressed in an immature fraction of
bone marrow-derived DC. This would agree also with the in vivo effect
of PRA on epidermal Langerhans cells (Fig. 1) that are considered
immature DC (21).
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To further investigate the role of DC
1b-AR in vivo, we performed experiments in
which bone marrow-derived I-Ab-positive (C57BL/6)
DC were preincubated with the irreversible and selective
1b-AR antagonist chloroethylclonidine and then
injected into the hind footpads of I-Ak (C3H/He)
mice. Forty-eight hours after injection, the number of
I-Ab-positive DC that migrated to the popliteal
and inguinal lymph nodes were evaluated by flow cytometry. Table II shows that incubation of bone
marrow-derived DC with chloroethylclonidine impairs their migration
from the footpad to regional lymph nodes.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1b-ARs expressed in DC drive at least part of
their emigration pathway to regional lymph nodes. In vivo, the effect
of PRA and yohimbine suggests that endogenous NE indeed plays a role in
DC migration. PRA and propranolol were administered topically to
possibly target Langerhans cells or other epidermal structures, whereas
yohimbine was injected i.p. because its well-known sympathomimetic
activity depends on blockade of both peripheral and central presynaptic
2-ARs. In addition, NE greatly stimulated skin
DC emigration in organ cultures, and the NE effect was neutralized by
PRA. This indicates that the effect of PRA and yohimbine in vivo (Fig. 1) was not dependent on an altered FITC labeling of DC. Finally,
preincubation of DC with the irreversible
1b-AR antagonist chloroethylclonidine resulted
in impaired migration when DC were adoptively transferred. It should be
noted that after the chloroethylclonidine exposure, DC were viable and
retained the ability to migrate in vitro against RANTES, but not
against NE (data not shown). Therefore, the impaired migration of these
DC in vivo was probably due to the irreversible inactivation of the
1b-AR, and this confirmed a role for NE in DC
migration in vivo. Most interesting, the inhibition of DC migration
induced by PRA was followed by an impaired DC-dependent immune
response, as shown in the CHS experiments (Fig. 2). Probably the
impaired DC migration resulted in a reduced Ag presentation and T cell
activation.
In vitro, NE exerted a powerful chemoattractant/chemokinetic effect on
bone marrow-derived immature DC via their
1b-AR. The fact that CD40-stimulated mature DC
show a very low expression of the 1b-AR may
explain why NE did not act on these cells and suggests that, unlike
6Ckine (5), NE is not involved in the homing of mature DC
in lymph nodes. 6Ckine is, in fact, strongly expressed in the high
endothelial venules of lymph nodes and has been shown to mediate both
chemotaxis and adhesion of mature, but not immature DC
(5).
Possibly, the rich sympathetic innervation of lymphatic smooth muscle
(7) creates a NE gradient able to recruit immature DC from
nonlymphoid tissues. Nerve fibers are in fact present in the tunica
externa and media of afferent lymphatic vessels. Thus, the sympathetic
innervation of lymphatic vessels would have the dual role of
stimulating smooth muscle contraction, which in turn promotes lymph
flow, and of recruiting DC. Nevertheless, an alternative physiological
interpretation of the results obtained may also be proposed. Since NE
appears to be also chemokinetic (Fig. 4) and DC seem to lose their
sensitivity to NE during maturation, it might be that under condition
of enhanced sympathetic activity (stress, anxiety, cold exposure),
increased DC chemokinesis enhances the ability of DC to sample local
Ags. This would result in an increased number of maturing DC that can
be attracted by relevant chemokines such as 6Ckine and reach the
draining lymph nodes. In any case, NE might interact with the
chemoattractant activity of chemokines that are expressed at sites of
inflammation to activate Ag uptake (22). This, however,
does not seem to apply for RANTES (Fig. 3). A better understanding of
the role of NE in DC migration requires more detailed studies on the
interaction between the 1b-AR, antigenic activation, and locally
produced inflammatory cytokines and chemokines (4).
In conclusion, we show that immature DC express
1b-ARs that participate in cell mobilization
and migration to regional lymph nodes. This finding should be
considered in studies concerning skin diseases, allergy, and autoimmune
disorders. As far as it concerns skin diseases, psoriasis and atopic
dermatitis may worsen with anxiety (23), a behavioral
condition that can be mimicked pharmacologically by yohimbine, which is
known to augment catecholamine release. The fact that yohimbine
accelerates skin DC migration might be relevant in our understanding of
these elusive yet widespread skin diseases. In addition, our finding
might open new pharmacological possibilities for modulating the immune
response.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Georges J. M. Maestroni, Center for Experimental Pathology, Istituto Cantonale di Patologia, P.O. Box 6601 Locarno 1, Switzerland.
3 Abbreviations used in this paper: DC, dendritic cell; AR, adrenergic receptor; PRA, prazosin; CHS, contact hypersensitivity; NE, norepinephrine.
Received for publication June 27, 2000. Accepted for publication September 13, 2000.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1-Adrenergic receptor subtypes: molecular structure, function, and signaling. Circ. Res. 78:737.-1 adrenergic receptors on bone marrow cells. Exp. Hematol. 22:314.
1- and 2-adrenoreceptors. Am. J. Physiol. 263:H473.This article has been cited by other articles:
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