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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 415 records · Page 23Linked to original sources
PubMed1998

Conservative management of post-operative peritoneal cysts associated with endometriosis.

OBJECTIVE: To describe the usefulness of fine-needle aspiration cytology and drainage, followed by long-acting GnRH-agonist therapy in the management of post-operative peritoneal cysts with endometriosis. METHODS: In six women who were diagnosed as having post-operative peritoneal cysts with endometriosis, fine-needle aspiration cytology and drainage was performed. Thereafter, four patients were treated with long-acting GnRH-agonists for 6 months. Two patients refused the treatment. RESULTS: In all patients fine-needle aspiration yielded specimens which consisted of a population of mesothelial cells. The mean follow-up time was 4 years (range 3.5-5). The four patients treated with long-acting GnRH-agonists show no evidence of recurrence. In two patients who had no additional treatment, the recurrence of the cyst was noted 2 months and 5 months after the drainage. CONCLUSION: Combination of fine-needle aspiration cytology and drainage and subsequent long-acting GnRH-agonist therapy can be a useful conservative management of post-operative peritoneal cysts associated with endometriosis.

Adult↗
PubMed1998

Administration of fructose 1,6-diphosphate during early reperfusion significantly improves recovery of contractile function in the postischemic heart.

OBJECTIVES: Fructose-1,6-diphosphate is a glycolytic intermediate that has been shown experimentally to cross the cell membrane and lead to increased glycolytic flux. Because glycolysis is an important energy source for myocardium during early reperfusion, we sought to determine the effects of fructose-1,6-diphosphate on recovery of postischemic contractile function. METHODS: Langendorff-perfused rabbit hearts were infused with fructose-1,6-diphosphate (5 and 10 mmol/L, n = 5 per group) in a nonischemic model. In a second group of hearts subjected to 35 minutes of ischemia at 37 degrees C followed by reperfusion (n = 6 per group), a 5 mmol/L concentration of fructose-1,6-diphosphate was infused during the first 30 minutes of reperfusion. We measured contractile function, glucose uptake, lactate production, and adenosine triphosphate and phosphocreatine levels by phosphorus 31-nuclear magnetic resonance spectroscopy. RESULTS: In the nonischemic hearts, fructose-1,6-diphosphate resulted in a dose-dependent increase in glucose uptake, adenosine triphosphate, phosphocreatine, and inorganic phosphate levels. During the infusion of fructose-1,6-diphosphate, developed pressure and extracellular calcium levels decreased. Developed pressure was restored to near control values by normalizing extracellular calcium. In the ischemia/reperfusion model, after 60 minutes of reperfusion the hearts that received fructose-1,6-diphosphate during the first 30 minutes of reperfusion had higher developed pressures (83 +/- 2 vs 70 +/- 4 mm Hg, p < 0.05), lower diastolic pressures (7 +/- 1 vs 12 +/- 2 mm Hg, p < 0.05), and higher phosphocreatine levels than control untreated hearts. Glucose uptake was also greater after ischemia in the hearts treated with fructose-1,6-diphosphate. CONCLUSIONS: We conclude that fructose-1,6-diphosphate, when given during early reperfusion, significantly improves recovery of both diastolic and systolic function in association with increased glucose uptake and higher phosphocreatine levels during reperfusion.

Adenosine Triphosphate↗
PubMed1998

Effects of pituitary adenylate cyclase activating polypeptide-27 on alkaline secretory and mucosal ulcerogenic responses in rat duodenum.

Effects of pituitary adenylate cyclase activating polypeptide (PACAP) on duodenal mucosal HCO3- secretion and ulcerogenic responses induced by mepirizole in anesthetized rats were examined and compared with those of vasoactive intestinal polypeptide (VIP). Animals were given mepirizole (200 mg/kg, s.c.) for induction of duodenal ulcers, and gastric acid and duodenal HCO3- secretions were measured with or without pretreatment of PACAP-27 or VIP. Mepirizole increased acid secretion and induced hemorrhagic lesions in the proximal duodenum within 6 h. Intravenous bolus injection or infusion of PACAP-27 (4 and 8 nmol/kg or 8 nmol/kg/h) increased duodenal HCO3- secretion even in the presence of mepirizole, without effect on acid secretion, and significantly reduced the severity of duodenal lesions caused by mepirizole. In contrast, VIP (8 nmol/kg, i.v.) given by bolus injection significantly decreased acid secretion induced by mepirizole, in addition to stimulation of HCO3- secretion, and prevented duodenal lesions in response to mepirizole. These results suggest that PACAP-27 increases duodenal HCO3- secretion and this action may be important in maintaining the duodenal mucosal integrity against acid, and VIP affords duodenal protection by both increasing duodenal HCO3- secretion and decreasing acid secretion. The reason for the different effects of PACAP and VIP on acid secretion is unknown.

Animals↗
PubMed1998

Stimulation of duodenal bicarbonate secretion by carbenoxolone in rats: a comparative study with prostaglandin E2.

1. The effects of carbenoxolone on duodenal HCO3- secretion were examined in anesthetized rats and compared with those of prostaglandin E2 (PGE2). 2. After 18-hr fasting, the duodenal loop (1.7 cm) that was made between the pyloric ring and the area just proximal to the outlet of the common bile duct was perfused with saline (pH 4.5), the pH of perfusate and the transmucosal potential difference (PD) were continuously monitored and HCO3- output was determined by titration with 10 mM HCl. 3. Under these conditions, duodenal pH, PD, and HCO3- secretion were increased in response to PGE2 (0.3 and 1.0 mg/kg) given intravenously as a single injection. Carbenoxolone (0.1-1.0 mg/kg, intravenously) also caused an increase in duodenal pH and HCO3- output in a dose-dependent manner, with a concomitant rise in PD; at 1 mg/kg, the magnitude of HCO3- output was almost equivalent to that induced by PGE2 at 0.3 mg/kg. 4. Prior administration of indomethacin, a cyclooxygenase inhibitor (5 mg/kg, subcutaneously), did not affect the HCO3- stimulatory action of carbenoxolone or PGE2. 5. Duodenal HCO3- secretion was also increased by intravenous injection of dibutylyl adenosine 3',5'-cyclic monophosphate (dbcAMP) but not by isobutylmethyl xanthine (IBMX; 10 mg/kg), an inhibitor of phosphodiesterase, but the former action was significantly potentiated in the presence of IBMX. Likewise, the pretreatment of IBMX significantly enhanced the HCO3- stimulatory action of PGE2 but had no effect on the HCO3- response induced by carbenoxolone. 6. These results suggest that carbenoxolone stimulates duodenal HCO3- secretion in rats, similar to PGE2 and this mechanism does not involve endogenous prostaglandins and is not associated with the intracellular accumulation of cAMP.

Animals↗
PubMed1998

Total synthesis of 25-hydroxy-16,23E-diene vitamin D3 and 1 alpha,25-dihydroxy-16,23E-diene vitamin D3: separation of genomic and nongenomic vitamin D activities.

Separation of genomic and nongenomic vitamin D activities was achieved by structural modification of 1,25-dihydroxy vitamin D3 by introduction of 16 and 23E double bonds. The modified compound 3, lacking a 1 alpha-hydroxy group, exhibits only nongenomic activity. Its 1 alpha-hydroxy relative 4 expresses fully both genomic and non-genomic activities. A total synthesis of analogues 3 and 4 is described.

Animals↗
PubMed1998

Effect of cilazapril on ventricular remodeling assessed by Doppler-echocardiographic assessment and cardiac gene expression.

The purpose of this study is to determine whether the administration of the ACE inhibitor cilazapril can lessen the adverse effects of ventricular remodeling, including systolic and diastolic dysfunction, modulation of fetal gene expression, increase of collagen genes, and depression of the sarcoplasmic reticulum (SR) Ca2+ ATPase gene in a myocardial infarcted (MI) rat model. At 1 day after MI, the animals were randomly assigned to cilazapril treatment or no treatment. We performed Doppler-echocardiographic examinations and measured cardiac mRNA in rats at 1 month and 3 months after MI (each group n = 8). The weights of the right (RV) and left ventricles (LV) in 1- and 3-month MI rats were significantly larger than those of the control rats. Cilazapril significantly prevented the increase. The MI rats showed systolic dysfunction, as evidenced by decreased fractional shortening (control, 34 +/- 3% vs. MI, 17 +/- 3%; P < 0.01) and ejection fraction measured by the modified Simpson's method (control, 61 +/- 2% vs. MI, 36 +/- 3%; P < 0.01) in rats at 1 month after operation. MI rats showed diastolic dysfunction, defined as increased peak early filling velocity, increased deceleration rate of the early filling wave, decreased late filling velocity, and an increase in the ratio of early filling to late filling velocity. Cilazapril significantly prevented systolic and diastolic dysfunction in rats after MI. The increases in beta-MHC, alpha-skeletal actin, ANP, and collagen I and III mRNAs in the nonischemic LV and RV were significantly suppressed by treatment with cilazapril. Depressed SR Ca(2+)-ATPase mRNA (nonischemic LV, 0.7-fold, P < 0.05 vs. control; RV, 0.5-fold, P < 0.05 vs. control) at 3 months after MI was significantly restored to normal levels by cilazapril. Cilazapril improved the adverse remodeling process by attenuating the progression of systolic and diastolic dysfunction, and prevented abnormal cardiac gene expression following MI.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Effects of cyclooxygenase-2 selective and nitric oxide-releasing nonsteroidal antiinflammatory drugs on mucosal ulcerogenic and healing responses of the stomach.

Effects of selective cyclooxygenase-2 (COX-2) inhibitors (NS-398) and nitric oxide (NO) -releasing aspirin (NO-ASA) on gastric ulcerogenic and healing responses were examined in comparison with nonselective COX inhibitors such as indomethacin and aspirin (ASA). Hypothermic stress (28-30 degrees C, 4 hr) induced gastric lesions in anesthetized rats with an increase of acid secretion. The lesions induced by hypothermic stress were markedly worsened by subcutaneous administration of both indomethacin and ASA but were not affected by either NS-398 or NO-ASA, although the increased acid secretion during hypothermia was not affected by any of the drugs. On the other hand, the healing of gastric ulcers induced in mice by thermal cauterization (70 degrees C, 15 sec) was significantly delayed by daily subcutaneous administration of indomethacin and ASA as well as NS-398, but not by NO-ASA. COX-2 mRNA was not detected in the intact mucosa but was positively expressed in the ulcerated mucosa, most potently on day 3 after ulceration. Prostaglandin contents in the intact mouse stomach were reduced by indomethacin, ASA, and NO-ASA, while the increased prostaglandin generation in the ulcerated mucosa was inhibited by all drugs including NS-398. After subcutaneous administration of NO-ASA to pylorus-ligated rats and mice, high amounts of NOx were detected in both the gastric contents and serum. In addition, both NS-398 and NO-ASA showed an equipotent antiinflammatory effect against carrageenan-induced paw edema in rats as compared with indomethacin and ASA. These results suggest that both indomethacin and ASA not only increased the mucosal ulcerogenic response to stress but impaired the healing response of gastric ulcers as well. The former action was due to inhibition of COX-1, while the latter effect was accounted for by inhibition of COX-2 and was mimicked by the COX-2-selective inhibitor NS-398. NO-ASA, although it inhibited both COX-1 and COX-2 activity, had no deleterious effects on gastric ulcerogenic and healing responses.

Animals↗
PubMed1998

Role of nitric oxide in regulation of gastric acid secretion in rats: effects of NO donors and NO synthase inhibitor.

1. The role of nitric oxide (NO) in the regulation of acid secretion was examined in the anaesthetized rat. 2. A rat stomach was mounted in an ex vivo chamber, instilled with 2 ml of saline every 15 min, and the recovered sample was titrated at pH 7.0 against 0.1 N NaOH by use of an automatic titrator for acid secretion. Gastric mucosal blood flow (GMBF) was measured simultaneously by laser Doppler flowmeter. 3. Intragastric application of NO donors such as FK409 (3 and 6 mg ml[-1]) and sodium nitroprusside (SNP; 6 and 12 mg ml[-1]) as well as i.p. administration of cimetidine (60 mg kg[-1]), a histamine H2-receptor antagonist, significantly inhibited the increase in acid secretion in response to pentagastrin (60 microg kg(-1) h(-1), i.v.), in doses that increased gastric mucosal blood flow (GMBF). 4. Intragastric application of FK409 (6 mg ml[-1]) increased both basal and stimulated acid secretion induced by YM-14673 (0.3 mg kg(-1), i.v.), an analogue of thyrotropin-releasing hormone (TRH), but had no effect on the acid secretory response induced by histamine (4 mg kg(-1) h(-1), i.v.). 5. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1), i.v.) did not affect basal acid secretion, but significantly potentiated the increase in acid secretion induced by YM-14673 and slightly augmented the acid secretory response to pentagastrin. 6. Both pentagastrin and YM-14673 increased the release of nitrite plus nitrate (NOx), stable NO metabolites, into the gastric lumen, and these changes were completely inhibited by prior administration of L-NAME (10 mg kg(-1), i.v.). 7. Pentagastrin caused an increase in luminal release of histamine and this response was significantly suppressed by intragastric application of FK409 (6 mg ml[-1]). 8. These results suggest that either exogenous or endogenous NO has an inhibitory action on gastric acid secretion through suppression of histamine release from enterochromaffin-like (ECL) cells.

Animals↗
PubMed1998

Increased susceptibility of gastric mucosa to ulcerogenic stimulation in diabetic rats--role of capsaicin-sensitive sensory neurons.

1. We examined the gastric mucosal blood flow (GMBF) and ulcerogenic responses following barrier disruption induced by sodium taurocholate (TC) in diabetic rats and investigated the role of capsaicin-sensitive sensory neurons in these responses. 2. Animals were injected streptozotocin (STZ: 70 mg kg(-1), i.p.) and used after 5, 10 and 15 weeks of diabetes with blood glucose levels of > 350 mg dl(-1). The stomach was mounted on an ex-vivo chamber under urethane anaesthesia and exposed to 20 mM TC plus 50 mM HCl for 30 min in the presence of omeprazole. Gastric transmucosal potential difference (PD), GMBF, and luminal acid loss (H+ back-diffusion) were measured before and after exposure to 20 mM TC, and the mucosa was examined for lesions 90 min after TC treatment. 3. Mucosal application of TC caused PD reduction in all groups; the degree of PD reduction was similar between normal and diabetic rats, although basal PD values were lower in diabetic rats. In normal rats, TC treatment caused luminal acid loss, followed by an increase of GMBF, resulting in minimal damage in the mucosa. 4. The increased GMBF responses associated with H+ back-diffusion were mitigated in STZ-treated rats, depending on the duration of diabetes, and severe haemorrhagic lesions occurred in the stomach after 10 weeks of diabetes. 5. Intragastric application of capsaicin increased GMBF in normal rats, but such responses were mitigated in STZ diabetic rats. The amount of CGRP released in the isolated stomach in response to capsaicin was significantly lower in diabetic rats when compared to controls. 6. The deleterious influences on GMBF and mucosal ulcerogenic responses in STZ-diabetic rats were partially but significantly antagonized by daily insulin (4 units rat(-1)) treatment. 7. These results suggest that the gastric mucosa of diabetic rats is more vulnerable to acid injury following barrier disruption, and this change is insulin-sensitive and may be partly accounted for by the impairment of GMBF response associated with acid back-diffusion and mediated by capsaicin-sensitive sensory neurons.

Animals↗
PubMed1998

Establishment of a GM-CSF-dependent megakaryoblastic cell line with the potential to differentiate into an eosinophilic lineage in response to retinoic acids.

We recently established a human granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent cell line (HML) from colony-constituent cells grown by peripheral blood cells of a patient with acute megakaryoblastic leukaemia. The HML cells possessed megakaryocytic features, as determined by cytochemical, electron microscopic and flow cytometric analysis. In the present study we examined the effects of retinoic acid (RA) on the development of HML cells. All-trans-RA, 13-cis-RA and 9-cis-RA at 10(-8) mol/l to 10(-5) mol/l inhibited the GM-CSF-dependent cell growth. Some of the RA-treated cells contained prominent azurophilic granules and were positive for peroxidase. They also reacted with Biebrich scarlet, Luxol fast blue and a monoclonal antibody against eosinophil peroxidase. In addition, exposure to RA increased the frequency and the intensity of major basic protein-positive cells. However, eosinophil-derived neurotoxin and eosinophil cationic protein were not detected or were only detected at a low level in the lysates of the HML cells treated with RA. Although IL-5 alone could not stimulate cell growth, the addition of IL-5 to the cultures containing stem cell factor + all-trans-RA was required for the expression of the eosinophilic phenotype. These results suggest that the HML cell line is a megakaryoblastic cell line with the potential to differentiate into the eosinophilic lineage. HML cells may be a useful model for elucidating the eosinophilic differentiation programme.

Cell Differentiation↗
PubMed1998

Platelet-like particle formation in the human megakaryoblastic leukaemia cell lines, MEG-01 and MEG-01s.

The platelet-sized particle formation in the human megakaryoblastic leukaemia cell line MEG-01 and its subline MEG-01s was examined. MEG-01 and MEG-01s cells spontaneously released platelet-sized particles into the culture medium, in which the cells occasionally extended cytoplasmic processes similar to those of megakaryocyte proplatelets. Scanning electron microscopic images showed cytoplasmic processes elongated from blebs on the MEG-01 and MEG-01s cell surface and were constricted between segments of platelet size. Immunofluorescence staining with anti-tubulin antibody showed that the cytoplasmic processes contained microtubules that were organized into a ring, which is a characteristic of circulating platelets. Some platelet-sized particles, probably released by ruptures at the sites of the process constriction, were metabolically active in an MTT assay (about 50%). Some particles also expressed the platelet-specific glycoproteins GPIIb, IIIa and GMP-140. Rarely, in response to thrombin, particles underwent a shape change from spherical to a shape with irregular membrane protrusions and fine filopodia, and aggregating with one another. The particles also had increased GMP-140 (P-selectin) expression with the addition of thrombin. These results show the usefulness of the MEG-01 and MEG-01s cell lines for the study of thrombopoiesis.

Blood Platelets↗
PubMed1998

Decay-accelerating factor (DAF) in stool specimens as a marker of disease activity in patients with ulcerative colitis (UC).

Colonic epithelial cells of patients with UC express DAF in relation to the severity of mucosal inflammation. The aim of this study was to determine whether this factor in stool could be used as a marker of disease activity in UC patients. Stool DAF was measured by use of an immunoassay in 181 stool specimens obtained from 55 patients with UC of various levels of disease activity. Stool DAF concentrations in patients whose UC was active (0.0-785.6 ng/g stool; median 47.1 ng/g; n = 115) were significantly higher than concentrations in patients whose disease was inactive (0.0-48.6 ng/g; median 0.0 ng/g; n = 66) (P < 0.0001). Values in active UC patients also were higher than those in control patients with diarrhoea (0.0-30.0 ng/g; median 0.0 ng/g; n = 26) (P < 0.0001) and in control subjects without apparent colorectal disease (0-20.4 ng/g; median 0.0 ng/g; n = 44) (P < 0.0001). The elevated levels of stool DAF obtained from UC patients in relapse declined markedly in specimens collected after the disease went into remission following medical therapy. Stool DAF levels correlated with the severity of endoscopic and histological findings and the degree of DAF expression on the colonic epithelia. Our results suggest that the measurement of stool DAF is useful as a non-invasive means of monitoring intestinal disease activity in patients with UC.

Adolescent↗
PubMed1998

Cytokine-stimulated release of decay-accelerating factor (DAF;CD55) from HT-29 human intestinal epithelial cells.

Expression of DAF (CD55) is enhanced on colonic epithelial cells of patients with ulcerative colitis (UC), and stool DAF concentrations are increased in patients with active disease. Cytokines are known to modulate DAF expression in various human cells, and lesions of UC reveal altered profiles of cytokine production. In this study, we evaluate the effects of various cytokines, IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, and interferon-gamma (IFN-gamma), on the synthesis and kinetics of DAF protein in HT-29 human intestinal epithelial cells. Using flow cytometry and an ELISA, we found that HT-29 cells constitutively express DAF on the cell surface and spontaneously release DAF into the culture supernatant under standard culture conditions. When the culture supernatant was centrifuged at 100000g, nearly a half of DAF was precipitated, indicating that one half of the released DAF was present as a membrane-bound form and the other half as a soluble form. Analysis of the culture supernatant of biotin surface-labelled HT-29 cells suggested that the soluble form DAF was derived by secretion from within the cell or by cleavage from the cell surface. Among the cytokines, IL-4 markedly, and IL-1beta moderately, enhanced the expression and the release of DAF. Actinomycin D, cycloheximide, and brefeldin A inhibited the increase in DAF release induced by IL-4 and IL-1beta stimulation. These results suggest that DAF is released from intestinal epithelial cells in response to cytokine stimulation and that IL-4 and IL-1beta are possible cytokines involved in DAF release into the colonic lumen of patients with UC.

Anti-Bacterial Agents↗
PubMed1998

Expression of interferon-gamma, interleukin-4 and interleukin-5 mRNA in the nasal mucosal membrane of rats with allergic rhinitis.

The production of immunoglobulin E (IgE) antibody is largely dependent on the ratio between interleukin-4 (IL-4) (a T helper 2 (Th2)-type cytokine) and interferon-gamma (IFN-gamma) (a T helper 1 (Th1)-type cytokine). Interleukin-5 (IL-5) (also a Th2-type cytokine) is an important eosinophil differentiation factor and also co-stimulates B-cell growth and differentiation. The present study was designed to evaluate and compare the expression of IFN-gamma, IL-4 and IL-5 mRNA in the nasal mucosal membrane of sensitized Brown-Norway (BN) rats. Fourteen BN rats were divided into two groups: non-sensitized (control) and sensitized. The sensitized group was injected with ovalbumin (OA) intraperitoneally on three consecutive days. Twenty-one days later, rats were exposed to 1% OA aerosol. Twenty-four hours after exposure to aerosol, nasal mucosa was extracted from both groups and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed. The densities of the bands of IL-4, IL-5 and IFN-gamma mRNA were expressed as percentages against beta-actin mRNA. Our results showed that the mean values for IL-4 and IL-5 mRNA were increased significantly in sensitized rats compared with control rats. In contrast, the mean value for IFN-gamma mRNA was significantly lower in sensitized rats compared with those of the control group. Our data therefore suggest that sensitization of rat nasal mucous membranes results in the predominant expression of Th2-type cytokines.

Airway Resistance↗
PubMed1998

Effect of allergen-specific immunotherapy on interleukin-4, interleukin-5 and interferon-gamma mRNA expression in the nasal mucosa of rats with allergic rhinitis.

To elucidate the mechanism of immunotherapy, we tested the effect of ovalbumin and ovalbumin-pullulan conjugate immunotherapy on the expression of interleukin (IL)-4, IL-5 and interferon-gamma (IFN-gamma) mRNA in the nasal mucosa of sensitized rats. Forty-five rats were injected with ovalbumin intraperitoneally on three consecutive days and later were exposed to ovalbumin aerosol. The rats were injected intradermally, on six consecutive days, with saline, ovalbumin or ovalbumin-pullulan conjugate. Later, nasal mucosa was obtained and reverse transcription-polymerase chain reaction (RT-PCR) was performed. Nasal responses and specific immunoglobulin E (IgE) were measured. Although the immunotherapy significantly decreased nasal airway resistance, dye leakage and histamine content in nasal irrigation after allergen challenge, no significant difference was found in IL-4 and IL-5 mRNA expression or in specific IgE level among the three groups. We conclude that in this allergic model, the improvement of nasal responses after immunotherapy was the result of a mechanism other than decrease of T-helper 2 (Th2) cytokines.

Airway Resistance↗
PubMed1998

Gammadelta T cell receptor repertoire in middle ear effusions in children.

In order to elucidate the immune response in otitis media with effusion, polymerase chain reaction was employed to examine gammadelta T cell receptor repertoire in the middle ear effusions of patients with otitis media with effusion. RNAs were extracted from 13 middle ear effusions of 10 children with otitis media with effusion. Vgamma2 was the most frequently used Vgamma gene. As for Vdelta gene usage, Vdelta2 amplification gave the strongest signal in 10 out of 13 samples. The results suggest that gammadelta T cells bearing Vgamma2/Vdelta2 T cell receptors accumulate in the middle ear effusions in children, and that these T cells may respond to certain bacteria or bacterial products in the middle ear.

Adolescent↗
PubMed1998

Detection of thromboxane A2 receptor mRNA in the nasal mucosa of patients with allergic rhinitis.

Previous reports suggest that thromboxane (TX) A2 plays an important role in bronchial asthma, especially in the development of airway hypersensitivity. Similarly to asthmatic subjects, the nasal mucosa in patients with allergic rhinitis is hypersensitive to non-specific stimuli. Allergic rhinitis is mediated by chemical mediators released from inflammatory cells. However, the involvement of TXA2 in allergic rhinitis has been studied very little. Recently, TXA2 receptors from humans and mice have been characterized at the molecular level. We performed RT-PCR to examine whether TXA2 receptor mRNA expression is elevated higher in allergic rhinitis than in chronic sinusitis. We found that TXA2 receptor mRNA was expressed both in the nasal inferior turbinates with allergic rhinitis and in the maxillary sinus mucosa with chronic inflammation at a similar level. This result suggests that TXA2 receptor mRNA expression is not enhanced in allergic rhinitis.

Adolescent↗