|
Hua Xie,
Shao-Heng He, Allergy and Inflammation Research Institute,
Shantou University Medical College, Shantou 515031, Guangdong
Province, China
Supported by the Li Ka Shing Foundation, Hong Kong, China,
No. C0200001; the Planned Science and Technology Project of
Guangdong Province, China, No. 2003B31502
Correspondence to: Professor Shao-Heng He, Allergy and
Inflammation Research Institute, Shantou University Medical College,
22 Xin-Ling Road, Shantou 515031, Guangdong Province, China.
shoahenghe@hotmail.com
Telephone: +86-754-8900405
Fax: +86-754-8900192
Received: 2004-04-30
Accepted: 2004-07-15
Abstract
Mast cell has a long history of being recognized as an important
mediator-secreting cell in allergic diseases, and has been
discovered to be involved in IBD in last two decades. Histamine is a
major mediator in allergic diseases, and has multiple effects that
are mediated by specific surface receptors on target cells. Four
types of histamine receptors have now been recognized
pharmacologically and the first three are located in the gut. The
ability of histamine receptor antagonists to inhibit mast cell
degranulation suggests that they might be developed as a group of
mast cell stabilizers. Recently, a series of experiments with
dispersed colon mast cells suggested that there should be at least
two pathways in man for mast cells to amplify their own activation-degranulation
signals in an autocrine or paracrine manner. In a word, histamine is
an important mediator in allergic diseases and IBD, its antagonists
may be developed as a group of mast cell stabilizers to treat these
diseases.
© 2005 The WJG Press and Elsevier Inc. All rights reserved.
Key words: Allergic diseases; Immunoglobulin
Xie H, He SH. Roles of histamine and its receptors in allergic and
inflammatory bowel diseases. World J Gastroenterol
2005; 11(19): 2851-2857
http://www.wjgnet.com/1007-9327/11/2851.asp
INTRODUCTION
Allergic diseases including allergic asthma, allergic rhinitis,
food allergy, drug allergy, and allergic atopic eczema/dermatitis
syndrome, etc. are
a group of common disorders which are regarded to be mediated by
immunoglobulin (Ig) E. People at all ages in countries throughout
the world suffer from these diseases. The prevalence of allergy has
shown an increase in the last few years. At present it affects about
30-40% of world population and has become one of the three key
diseases in the 21st
century.
Since last two decades, inflammation has been
known as the main pathophysiological characteristics of allergy.
Mast cells are major participants of allergic reactions, and their
activation may be all that is sufficient and necessary for the rapid
development of microvascular leakage and tissue edema in sensitized
subjects exposed to allergen. Mast cell is a key source of potent
mediators of allergic inflammation including histamine, neutral
proteinases, proteoglycans, prostaglandin D2,
leukotriene C4 and
certain cytokines[1].
Among them, histamine is the first mediator implicated in the
pathophysiological changes of asthma when it was found to mimic
several features of the disease, and James received the Nobel Prize
for medicine in 1988 for his outstanding achievements in histamine
research. Recently, some novel findings concerning histamine, mast
cell and allergy or IBD have been reported and are summarized
herein.
THE ROLES OF MAST CELLS IN ALLERGIC
DISEASES
Mast cell has a long history of being recognized as an important
mediator-secreting cell in allergic diseases. It has a high capacity
to release an array of both preformed and newly generated mediators
in response to environmental stimuli, especially allergen exposure.
Cross linkage of IgE bound to high affinity receptors on mast cells
not only results in the rapid release of autacoid mediators, but
also the sustained synthesis and release of cytokines, chemokines
and growth factors.
Mature mast cells are ubiquitous in human tissues and can thus
participate in the processes of inflammation at different sites.
Systemic anaphylaxis, a life-threatening disease, involves mast cell
activation in multiple organs. In bronchial asthma, a disease
characterized by widespread but potentially reversible bronchial
obstruction, there are increased numbers of mast cells and a greater
degree of continuous mast cell degranulation in bronchoalveolar
lavage fluid from asthmatics compared with normal controls.
Increased mast cell numbers and evidence for continuous
degranulation of mast cells have been observed also in nasal lavage
fluid and the nasal epithelium of the patients with allergic
rhinitis.
Recent population surveys have estimated rates of
prevalence of perceived food hypersensitivity of 12-20% in adults
though this rate varied largely across different countries (e.g.
Spain, 4.6%; Australia, 19.1%) despite a common standardized
methodology[2].
Intestinal mast cells, as well as eosinophils, have been shown to be
involved in the pathogenesis of food-allergy-related enteropathy.
Adverse drug reactions are common, but only 6-10%
are immunologically mediated[3].
Although allergic drug reactions are just one type of adverse
reactions to medications, they are clinically very important because
of the morbidity and mortality they cause. Allergic drug reactions
may result in anaphylaxis, urticaria, bronchospasm and angioedema.
During these reactions, allergic drugs cause direct histamine
release from mast cells.
THE ROLES OF HISTAMINE IN ALLERGIC
DISEASE
Since its discovery in 1911, histamine has been recognized as a
major mediator in allergic diseases. Histamine is a primary amine
synthesized from histidine in the Golgi apparatus, from where it is
transported to the granule for storage in ionic association with the
acidic residues of the glycosaminoglycans side chains of heparin and
with proteinases. The histamine content of mast cells dispersed from
human lung and skin is similar at 2-5 pg/cell, and the histamine
stored ranges from 10 to 12 µg/g in both tissues. Following mast
cell activation, histamine is rapidly dissociated from the granule
matrix by exchange with sodium ions in the extracellular
environment. Proteoglycans comprise the major supporting matrix of
the mast cell granule with the sulfate groups binding to histamine,
proteinases and acid hydrolases. As only mast cells and basophils
contain histamine in man (apart from histaminergic nerve), and there
are few basophils in human tissues, histamine can be used as a
marker of mast cell degranulation.
The allergic process is believed to consist of
two phases: early and late. The early phase reaction is mainly
induced by histamine released from mast cells. Histamine is a potent
vasoactive agent, bronchial smooth muscle constrictor, and stimulant
of nociceptive itch nerves. In addition to its known effects on
glands, vessels and sensory nerves, recent data have provided
further evidence of histamine’s proinflammatory actions[4].
Histamine binding specific cell receptors produces clinical allergic
symptoms. This mediator also activates neutrophils and eosinophils
as well as being a chemoattractant for these cells[5].
Histamine increases IL-8 level and evokes leukocyte rolling on
endothelial cells. Thus histamine participates in both early and
late-phase allergic responses.
ROLES OF HISTAMINE IN PATHOGENESIS OF IBD
Using segmental jejunal perfusion system with a two-balloon,
six-channel small tube, Knutson and colleagues found that the
histamine secretion rate was increased in patients with Crohn’s
disease compared with normal controls, and the secretion of
histamine was related to disease activity, indicating strongly that
degranulation of mast cells was involved in active Crohn’s disease[6].
The highly elevated mucosal histamine levels were also observed in
allergic enteropathy and ulcerative colitis[7].
Moreover, enhanced histamine metabolism was found in collagenous
colitis and food allergy[8],
and increased level of N-methylhistamine, a stable metabolite
of the mast cell mediator histamine, was detected in the urine of
patients with active Crohn’s disease or ulcerative colitis[9,10].
Since increased level of N-methylhistamine was significantly
correlated to clinical disease activity, the above findings further
strongly suggest the active involvement of histamine in the
pathogenesis of these diseases.
Interestingly, mast cells originated from the
resected colon of active Crohn’s disease or ulcerative colitis
were able to release more histamine than those from normal colon
when being stimulated with an antigen, colon-derived murine
epithelial cell-associated compounds[11].
Similarly, cultured colorectal endoscopic samples from patients with
IBD secreted more histamine towards substance P alone or substance P
with anti-IgE than the samples from normal control subjects under
the same stimulation[12].
In a guinea pig model of intestinal inflammation induced by cow’s
milk proteins and trinitrobenzene sulfonic acid, both IgE titers and
histamine levels were higher than normal control animals[13].
As a proinflammatory mediator, histamine is
selectively located in the granules of human mast cells and
basophils and released from these cells upon degranulation. To date,
a total of three histamine receptors H1,
H2 and H3
have been discovered in
human gut[14,15].
It proves that there are some specific targets that histamine can
work on in intestinal tract. Histamine was found to cause a
transient concentration-dependent increase in short-circuit current,
a measure of total ion transport across the epithelial tissue in the
gut[16]. This
could be due to that histamine interacts with H1
receptors to increase the secretion of Na and Cl ions from
epithelium[17].
The finding that H1-receptor
antagonist pyrilamine was able to inhibit anti-IgE induced histamine
release and ion transport[18]
suggested further that histamine is a crucial mediator responsible
for diarrhea in IBD and food allergy. The ability of SR140333, a
potent NK1
antagonist in reducing mucosal ion transport, was most likely due to
its inhibitory actions on histamine release from colon mast cells[19].
HISTAMINE RECEPTORS
Histamine has multiple effects that are mediated by specific surface
receptors on target cells. Four types of histamine receptors have
now been recognized pharmacologically. Histamine receptors were
first differentiated into H1
and H2 by Ash
and Schild in 1966, when it was found that some responses to
histamine were blocked by low doses of mepyramine (pyrilamine),
whereas others were insensitive.
A third histamine receptor subtype, termed H3,
was cloned in 1999 by Lovenberg and
co-workers[20]
and the fourth histamine receptor subtype, termed H4,
was first reported in 2000 by Oda and co-workers[21].
H1
receptors
H1 receptors
have been cloned from cows, rats, guinea pigs and humans. The
published sequences suggest that there are surprisingly large
differences among species. H1
receptors mediate most of the effects of histamine that are relevant
to asthma. The cardinal features of asthma include smooth muscle
spasm, mucosal edema, inflammation and mucous secretion. It has been
demonstrated that at least two of these features, bronchospasm and
mucosal edema, can be caused by H1-receptor
stimulation. Northern analysis has demonstrated that there is a high
level of expression of H1
receptor messenger ribonucleic acid in lung.
Ocular allergy presents unsolved mysteries in
molecular and cellular mechanisms, the recent understanding of the
key role of the T helper type 2 cytokines, adhesion molecules and
chemokines may provide future avenues for pharmacological targeting
of releasable inflammatory mediators. More potent topical mast cell
stabilizers and H1
receptor antagonists have become commercially available for the
management of the prevalent and benign forms of allergic
conjunctivitis[22].
Immunostimulatory DNA sequences present an innovative and promising
route for the treatment of ocular allergy, but clinical studies are
needed to demonstrate their efficacy in humans.
Bphs controls Bordetella pertussis toxin (PTX)-induced
vasoactive amine sensitization elicited by histamine (VAASH) and has
an established role in autoimmunity. Ma and co-workers[23]
reported that congenic mapping links Bphs to the histamine H1
receptor gene (Hrh1/H1R)
and that H1R differs at
three amino acid residues in VAASH-susceptible and -resistant mice.
Hrh1-/- mice are protected from VAASH, which can be restored by
genetic complementation with a susceptible Bphs/Hrh1 allele, and
experimental allergic encephalomyelitis and autoimmune orchitis due
to immune deviation. Thus, natural alleles of Hrh1 control both the
autoimmune T cells and vascular responses regulated by histamine
after PTX sensitization.
H2
receptors
H2 receptors
have been cloned from dogs and humans. Although H2
receptors are present in the airway, their clinical relevance is
unclear, because H2
receptor antagonists have few measurable effects on airway function.
Histamine stimulates an increase in cyclic AMP levels in lung
fragments that is blocked by H2
receptor antagonists, indicating that H2
receptors are positively coupled to adenylyl cyclase in lung.
Atopic diseases such as allergic rhinitis and
asthma are characterized by increases in Th2 cells and serum IgE
antibodies. The binding of allergens to IgE on mast cells triggers
the release of several mediators, of which histamine is the most
prevalent. Mazzoni and co-workers reported that histamine, together
with a maturation signal, acts directly upon immature dendritic
cells (DCs), which express H1
and H2,
two active histamine receptors. Histamine, acting upon the H2
receptor for a short period of time, increased IL-10 production and
reduced IL-12 secretion. As a result, histamine-matured DCs
polarized naive CD4(+) T cells toward a Th2 phenotype, as compared
with DCs that had matured in the absence of histamine. The Th2 cells
favor IgE production, leading to increased histamine secretion by
mast cells, thus creating a positive feedback loop that could
contribute to the severity of atopic diseases[24].
H3
receptors
The identification of H3
receptor cDNA allowed several groups to reveal the complexity of the
histamine-mediated systems. Comparison of the cDNA with available
genome databases revealed that the gene encoding H3
receptor is located on chromosome 20 and contains at least two
introns. In rats, H3
receptors consist of at least three functional isoforms, referred to
as H3A, H3B
and H3C,
which vary in the length of their third intracellular loop (I3) (136
104 and 88 amino acids respectively). In humans, H3
receptor isoforms have been cloned, including one with an
80-amino-acid deletion of I3. Moreover, another isoform has been
identified, in which the 80-amino-acid deletion is accompanied by an
additional 8 amino acids at the C-terminal tail. Using reverse
transcription polymerase chain reaction, the human isoforms have
been found to be differentially expressed in various brain areas.
The 80-amino-acid sequence located at the C-terminal portion of I3
plays an essential role in H3
agonist-mediated signal transduction. The existence of multiple H3
isoforms with different signal transduction capabilities suggests
that H3-mediated
biological functions might be tightly regulated through alternative
splicing mechanisms. Otherwise, histamine H3
receptor activation inhibits neurogenic sympathetic vasoconstriction
in porcine nasal mucosa, suggesting that histamine H3
receptors may play a role in the regulation of vascular tone and
nasal patency in allergic nasal congestive disease[25].
H4 receptors
The discovery of the histamine H4
receptor adds a new chapter to the histamine story. The H4
receptor is a G protein-coupled receptor and is most closely related
to the H3
receptor, sharing 58% identity in the transmembrane regions. The
gene encoding the H4
receptor was discovered initially in a search of the GenBank
databases as sequence fragments retrieved in a partially sequenced
human genomic contig mapped to chromosome 18[26].
About the histamine-binding site of H4
receptor, Shin reported that Asp94 (3.32) in transmembrane region
(TM) 3 and Glu182 (5.46) in TM5 are critically involved in histamine
binding. Asp94 probably serves as a counter-anion to the cationic
amino group of histamine, whereas Glu182 (5.46) interacts with the
N(tau) nitrogen atom of the histamine imidazole ring via an ion
pair. These results resemble those for the analogous residues in the
H1 histamine
receptor but contrast with findings regarding the H2
histamine receptor. It indicates that although histamine seems to
bind to the H4
receptor in a fashion similar to that predicted for the other
histamine receptor subtypes, there are also important differences
that can probably be exploited for the discovery of novel H4-selective
compounds[27].
H4 receptor
exhibits a very restricted localization, expression is primarily
found in intestinal tissue, spleen, thymus and immune active cells,
such as T cells, mast cells, neutrophils and eosinophils. It
suggests an important role for the H4
receptor in the regulation of immune function and offers novel
therapeutic potentials for histamine receptor ligands in allergic
and inflammatory diseases[28].
THE EFFECTS OF HISTAMINE RECEPTOR
ANTAGONISTS ON HISTAMINE RELEASE
FROM MAST CELLS
Today, according to action on different receptors, the histamine
receptor agonists (Table 1) and antagonists (Table 2) are classified
into four subtypes, respectively.
Among H1 receptor
antagonists, the first generation antihistamines have considerable
sedative effects caused by their ability to cross the blood-brain
barrier. The second generation of antihistamines to emerge in the
market is devoid of these sedative effects. The third generation
antihistamines, metabolites of the earlier drugs, have demonstrated
no cardiac effects of the parent drugs and are at least potent[29].
Table 1 Agonists of
histamine receptors
| Receptor
subtype |
Agonists |
| H1 |
Dimethylhistaprodifen[30],
methylhistaprodifen[30],
histaprodifen[30,31],
histamine-trifluoromethyl- toluidine[32],
2-thiazolylethylamine[33],
2-(3- trifluoromethylphenyl) histamine[34],
2-phenylhistamines[31],
2-pyridylethylamine[35] |
| H2 |
Dimaprit[30,34] |
| H3 |
Imetit[32],
alpha-methylhistamine[33,34] |
| H4 |
Clobenpropit[32],
imetit[32] |
Table 2 Antagonists
of histamine receptors
| Receptor
subtype |
Antagonists |
| H1 |
First-generation |
| |
Azatadine,
clemastine, chlorpheniramine |
| |
(chlorphenamine
maleate), diphenhydramine, |
| |
dexchlorpheniramine,
hydroxyzine, mepyramine (pyrilamine), promethazine,
terfenadine (teldane), |
| |
triprolidine[35–37] |
| |
Second-generation |
| |
Acrivastine[37,38],
astemizole (hismanal)[38], |
| |
azelastine[38],
cetirizine (virilx, zirtek, zyrtec)[39–41], |
| |
chlorpheniramine[42,43],
desloratadine[44,45],
ebastine[37,44], |
| |
emedastine[37],
epinastine[41,46],
homochlorcyclizine[47], |
| |
ketotifen[41,48]
levocabastine[46],
loratadine (claritin, |
| |
clarityne)[41,44,49],
olopatadine[41,50],
mequitazine[47], |
| |
mizolastine[47],
pseudoephedrine[51,52],
rupatadine[53,54], |
| |
tripelennamine
(pyribenzamin)[55] |
| |
Third-generation |
| |
Fexofenadine[37,44,56],
levocetirizine[37,39] |
| H2 |
First-generation |
| |
Cimetidine[57],
metiamide[58] |
| |
Second-generation |
| |
Ranitidine
(1979)[59],
omeprazole (1982)[60] |
| |
Third-generation |
| |
Famotidine[61],
ebrotidine[62],
lafutidine[63,64], |
| |
niperotidine[60],
nizatidine[60],
potentidine[65], |
| |
roxatidine[60],
zolantidine[58] |
| H3 |
A-304121[66],
A-317920[66],
4-(aminoalkoxy) |
| |
benzylamines[67],
ciproxifan[66],
clobenpropit[68], |
| |
D-alanine-piperazine-amides[69],
imidazopyridine[70], |
| |
indole[70],
indolizine[70],
4’-[(NR1R2-1-yl)]-propoxy- |
| |
biaryl-4-carboxamides[70],
pyrazolopyridine[71], |
| |
1-(4-(phenoxymethyl)benzyl)
piperidines[72],
SCH |
| |
79687[73],
thioperamide[68,74], |
| H4 |
JNJ
7777120[75,76],
thioperamide[77] |
Among them, H1
receptor antagonists loratadine and terfenadine were able to inhibit
IgE-induced histamine release from human mast cells[78],
which may at least partially explain their potent antiallergic
activity[79].
However, the extent of H1
receptor antagonists binding to mast cells is quite
different. Wescott et al., reported tripelennamine >
pyrilamine > diphenhydramine in binding H1
receptor[80].
Fexofenadine, an effective H1
antihistamine, is the active metabolite of terfenadine, but they had
different effects on histamine and tryptase release from mast cells.
Terfenadine inhibited release of histamine and tryptase from
mast cells during the early allergic response, whereas fexofenadine
did not[81].
In combination with H1
antihistamines, H2
antihistamines famotidine, ranitidine or cimetidine suppressed
effectively the chronic swelling. It is deduced that simultaneous
blockage of both histamine H1
and H2
receptors may be necessary for sufficient inhibition of the
microvascular permeability increase in some kinds of anaphylactic
reactions, and that histamine, mainly interacting with H2
receptors, may play an important role in activation of a certain
phase of chronic inflammation where mast cell degranulation is
involved[82].
Metiamide, one H2
receptor antagonist, can reduce the histamine release from secreting
mast cells in mast-cell mediated angiogenesis[83].
H3
antagonists, thioperamide and clobenpropit combined with H1
antihistamine loratadine, not the H2
antagonist ranitidine, reduced nasal congestion[84]
in mast cell-deficient mice, indicating that its action was not
associated with mast cell degranulation[85].
THE HYPOTHESIS OF SELF-AMPLIFICATION MECHANISM OF MAST CELL
DEGRANULATION
Tryptase has been proved to be a unique marker of mast cell
degranulation in vitro as it is more selective than histamine
to mast cells. Inhibitors of tryptase[86,87]
and chymase[88]
have been discovered to possess the ability to inhibit histamine or
tryptase release from human skin, tonsil, synovial[89]
and colon mast cells[90],
suggesting that they are likely to be developed as a novel class of
mast cell stabilizers. Recently, a series of experiments with
dispersed colon mast cells suggested that there should be at least
two pathways in man for mast cells to amplify their own activation-degranulation
signals in an autocrine or paracrine manner, which may partially
explain the phenomena that when a sensitized individual contacts
allergen only once the local allergic response in the involved
tissue or organ may last for days or weeks. These findings included
that both anti-IgE and calcium ionophore were able to induce
significant release of tryptase and histamine from colon mast cells,
histamine is a potent activator of human colon mast cells and the
agonists of PAR-2 and trypsin are potent secretagogues of human
colon mast cells. Since tryptase was reported to be able to activate
human mast cells[86]
and H1
receptor antagonists terfenadine and cetirizine[78]
were capable of inhibiting mast cell activation, the hypothesis of
mast cell degranulation self-amplification mechanisms is that mast
cell secretagogues induce mast cell degranulation, and release of
histamine, which then stimulates the adjacent mast cells or
positively feedbacks to further stimulate its host mast cells
through H1
receptors, whereas released tryptase acts similarly to histamine,
but through its receptor PAR-2 on mast cells.
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