bluuebunny/crossref_metadata_2025_split huggingface dataset:
HLA class II antigens and T lymphocytes in human nasal epithelial cells. Modulation of the HLA class II gene transcripts by gamma interferon
Authors: WANG D. , LEVASSEUR‐ACKER G. M. , ANKOWSKI R. J , KANNY G. , MONERET‐VAUTRIN D. A. , CHARRON D. , LOCKHART A. , SWIERCZEWSKI E. 
Published: April 2006

SummaryBackground Nasal polyps are characterized by a proliferation of the epithelial layer of the mucosa. cellular infiltrates and other pathological changes; however the mechanisms involved in polyp pathogenesis remain largely unclear.Objectives We have taken two different approaches to study the cellular events involved in nasal polyposis.Methods First, through use of immunohistochemical methods, we have studied the expression of HLA class II antigens in epithelial cells of nasal polyps and the distribution of lymphocytes in the epithelium and in the subepithelial layer in patients with clinical conditions, such as asthma, atopy, aspirin intolerance or cystic fibrosis, and in subjects with an absence of concomitant diseases. Second, in order to investigate whether HLA class II expression is controlled at the pre‐ or post‐transcriptional level, we studied the effect of interferon gamma (INFγ) on epithelial cells in primary culture, which were derived from HLA class II negative and HLA class II positive nasal polyps. Total RNA was extracted from the cells and reverse‐transcribed, and the c‐DNA corresponding to DR, DP, DQ loci was amplified by PCRResults Expression of HLA class II antigens by the epithelia of nasal polyps was more common in the presence rather than in the absence of concomitant asthma, atopy or cystic fibrosis (59% versus 409%). HLA‐DR was the only HLA class II antigen expressed in the seven polyps taken from cystic fibrosis patients. The number of CD8+ cells was significantly higher in polyps associated with known clinical conditions and HLA class II antigen expression than it was in ‘isolated’ polyps and in HLA class II negative polyps. RNA transcripts for at least one or all three HLA‐DR, DP and DQ antigens were detected in 10 cultures of the 11 HLA class II positive polyps. Conversely, 8 of 10 cultures derived from HLA class II negative polyps did not express HLA class II transcripts in the absence of INFγ. Adding INFγ (100U/ml) to the latter cell cultures caused expression of transcripts of one or more HLA class II genes.Conclusions We have shown that HLA class II antigens were more frequently detected in polyps of patients with an identified clinical syndrome than in those of asymptomatic subjects. Our results also suggest that IFN γ regulates expression of HLA class II antigens in airway epithelial cells of the nasal polyps at the transcriptional level, and that cultured cells from nasal polyps represent a suitable modei to investigate immune mechanisms involved in diseases such as atopy, asthma and cystic fibrosis.
Interleukin‐8 secretion in patients with allergic rhinitis after an allergen challenge: interleukin‐8 is not the main chemotactic factor present in nasal lavages
Authors: GOSSET P. , TILLIE‐LEBLOND I. , MALAQUIN F. , DURIEU J. , WALLAERT B. , TONNEL A.‐B. 
Published: April 2006

SummaryBackground Interleukin‐8 (IL‐8) is a chemotactic cytokine for neutrophils and primed eosinophils. In allergic rhinitis, allergen exposure triggers leucocyte recruitment.Objective We evaluated in this study IL‐8 secretion and the neutrophil chemotactic activity in nasal lavages collected after a nasal allergen challenge. Moreover, the participation of IL‐8 in the neutrophil chemotactic activity was quantified.Methods Four healthy subjects and 19 patients with allergic rhinitis were exposed to a nasal allergen challenge. As a control, saline challenge was performed in four patients with allergic rhinitis. Concentration of IL‐8 was measured hy ELISA in nasal lavages collected before and after challenge. Neutrophil chemotactic assay was developed using a 48‐well chemotaxis microassembly.Results After allergen challenge, the healthy subjects, the four patients receiving saline and one patient exposed to allergen did not respond; seven patients presented a single early reaction and 11 patients a dual response. For healthy subjects and the four patients exposed to saline, the level of IL‐8 did not increase after challenge in comparison with that at baseline. After allergen challenge, two peaks of IL‐8 release were observed for patients with allergic rhinitis during the early (30 min to 1 h 30 min) and the late periods (3 h 30 min to 9 h 30 min), however the difference was not significant for the early period. During the late period, a significant increase in IL‐8 concentrations was detected for the patients developing a dual response, whereas the difference was not significant for those presenting only an early reaction. The neutrophil chemotactic activity of nasal lavages from patients with allergic rhinitis collected during the early and the late reactions (17 ± 2.1 and 23.3 ± 2.8 neutrophils per high power field (hpf), respectively) was significantly higher than the activity of lavage fluid collected at haseline (9.2 ± 1.8 neutrophils per hpf). Nevertheless, the addition of a neutralizing anti‐IL‐8 antibody inhibited weakly the chemotactic activity of lavage fluid from rhinitic patients collected during the early or the late periods (18 and 11% of inhibition) (P= NS).Conclusion These data show that allergen challenge increased significantly the secretion of IL‐8 for the patients with allergic rhinitis. However, neutralization of IL‐8 in nasal lavages by a specific antibody revealed that the role of this chemokine in granulocyte infiltrate was limited, suggesting that IL‐8 acts in connection with other chemotactic factors in this recruitment.
Identification of neutrophil chemotactie factors in bronchoalveolar lavage fluid of asthmatic patients
Authors: TERAN L. M. , CAMPOS M. G. , BEGISHVILLI B. T. , SCHRÖDER J.‐M. , DJUKANOVIC R. , SHUTE J. K. , CHURCH M. K. , HOLGATE S. T. , DAVIES D. E. 
Published: April 2006

SummaryBackground Although neutrophils have been implicated in bronchial asthma, the mechanism(s) which bring these cells into the airways is poorly understood.Objective To investigate the presence and identity of neutrophil chemotactic factors in bronchoalveolar lavage (BAL) fluid from atopic asthmatic subjects.Method BAL fluid was obtained from 13 subjects (seven asthmatics and six normals). aged 19 to 60 yr, at bronchoscopy. Separation of neutrophil chemotactic activity (NCA) was achieved by FPLC cation exchange chromatography. Fractions were collected and assayed for chemotaxis multiwell micro‐chemotaxes chambers using polycarbonate filters, for the complement peptide C5a/C5a des Arg by radioimmunoassay (RIA) and for interleukin‐8 (IL‐8) by ELISA.Results NCA was found in FPLC fractions of BAL samples in four out of seven asthmatics and each of these subjects had at least three similar peaks of NCA. The major peak of NCA was found to contain immunoreactive C5a/C5a des Arg and chemotaxis. In response to this NCA could be blocked by desensitization of the neutrophils with recombinant C5a. Purified serum derived C5a/C5a des Arg was found to have altered chromatographic properties when added to BAL fluid; this suggested that BAL fluid contained proteins which interacted with the C5a/C5a des Arg. Immunoreactive IL‐8 (iIL‐8) was also detected but its concentration or chemical form was insufficient to induce neutropbil chemotaxis.Conclusion This study demonstrates that bronchial asthmatic lavage fluid contains C5a/C5a des/Arg and iL‐8, together with other as yet unidentified factors which may contribute to neutropbil recruitment in this disease.
Anti‐asthma effect of an antiviral drug, acyclovir: a clinical case and experimental study
Authors: OKADA H. , OHNISHI T , HIRASHIMA M. , FUJITA J. , YAMAJI Y. , TAKAHARA J. , TODANI T. 
Published: April 2006

SummaryBackground Although acyclovir (9‐(2‐hydroxyethoxymethyl) guaninc) is an antiviral drug that inhibits DNA polymerase of herpes virus, we have had the experience of an asthmatic patient's peak flow rate being improved by oral administration of acyclovir.Objective The aim of this experiment is whether acyclovir has anti‐asthma effects using an asthma model in guinea‐pigs.Methods The airway response was induced by a single inhalation of calcium ionophore A23187 (2 mg/mL). The airway obstruction was estimated by the ratio of expiration to inspiration time (E/I). The peribronchial eosinophil infiltration and eosinophil influx into bronchoalveolar lavage (BAL) fluid 7 h after the inhalation were also examined. To assess the effects of acyclovir (1, 10, and 100 mg/kg), aminophylline (20mg/kg) and pemirolast potassium (TBX, 20mg/kg) on A23187‐induccd asthmatic response, the drugs were intraperitoneally administered before the inhalation.Results The immediate airway obstruction was significantly suppressed by acyclovir (10 mg/kg) and aminophylline, whereas different doses of acyclovir (1 and 100mg/kg) and TBX showed only a small inhibitory effect on the airway obstruction. On the other hand, the peribronchial eosinophilia was most successfully inhibited by TBX. Acyclovir (10 mg/kg) and aminophylline also suppressed the eosinophilia significantly. Furthermore, acyclovir significantly suppressed eosinophil influx into BAL fluid, whereas aminophylline and TBX weakly suppressed the influx.Conclusion These results suggest that acyclovir exhibits not only antiviral but also anti‐asthma activity.
The use of serum eosinophil cationic protein (ECP) in the management of steroid therapy in chronic asthma
Authors: WEVER A. M. J. , WEVER‐HESS J. , HERMANS J. 
Published: April 2006

SummaryBackground Corticosteroid therapy has become the mainstay in the treatment of asthma. However, the risk‐benefit balance in the patient calls for assessment of the state of inflammation in the airways. In this respect serum eosinophil cationic protein (ECP) might be a marker, which can easily be measured in a clinical setting. Studies have indicated a relation between level of serum ECP and activity and severity in asthma.Objective To investigate the feasibility to guide steroid therapy on the basis of the level of serum ECP in patients with chronic asthma.Methods Twenty adult patients on maintenance inhaled steroid therapy visited the chest clinic once every 2 months over a 12‐month period. At each visit a short history, blood sample for ECP and number of eosinophils, baseline spirometry, and histamine inhalation provocation test (PC20) were obtained. On the basis of level of ECP, adjustments in daily dose of steroids were considered. Data were compared with those of a previous 6‐month ECP evaluation study in these same patients.Results In 10 patients mean dose of inhaled steroids was decreased 25%. ECP rose slightly (antilogged mean from 9.06 to 11.8μg/L) and lung function decreased slightly (mean FEV1%predicted from 85.5 to 81.6). In seven patients mean dose of inhaled or oral (n= 2) steroids was increased 25%. In this group ECP decreased but remained elevated at 20μg/L (antilogged mean from 30.5 to 25.6μg/L) and lung function improved (mean FEV1%predicted from 67.2 to 74.5). In both groups patients' scores of asthmatic well‐being increased significantly, and PC20 did not show a trend. Exacerbation rate remained the same in the decreased and the no change group (n= 3, in which no substantial change in steroid dose occurred), but was reduced by about 50% in the increased group.Conclusion From this observational study it is concluded that adjusting steroid therapy guided by serum ECP‐level may be helpful in tailoring asthma treatment.
Studies of the effects of inhaled magnesium on airway reactivity to histamine and adenosine monophosphate in asthmatic subjects
Authors: HILL J. , LEWIS S. , BRITTON J. 
Published: April 2006

SummaryBackground Magnesium is a cation with smooth muscle relaxant and anti‐inflammatory effects and may therefore have a role in the therapy of asthma. Several studies have investigated the effects of intravenous magnesium in acute or stable asthma, but little is known about the effects of inhaled magnesium.Objective To measure the effects of a single inhaled nebulized dose of 180 mg magnesium sulphate on airway reactivity to a direct‐acting bronchoconstrictor (histamine) and an indirect‐acting bronchoconstrictor (adenosine monophosphate [AMP]) in asthmatic subjects.Objective Two separate randomized, double‐blind, placebo‐controlled crossover studies, each involving 10 asthmatic subjects. In the histamine study, airway reactivity to histamine was measured and lung function allowed to recover spontaneously over 50 min before administering nebulized magnesium sulphate or saline placebo. Airway reactivity to histamine was then measured at 5 and 50 min. In the AMP study, a single measurement of airway reactivity was made 5 min after magnesium or placebo.Results In the histamine study, the provocative dose required to reduce FEV1 by 20% (PD20FEV1) was significantly lower after magnesium than after placebo, by a mean (95% CI) of 1.02 (0.22–1.82) doubling doses at 5 min (P= 0.018), and 1.0 (0.3–1.7) doubling doses at 50 min (P= 0.01). In the AMP study, PD20FEV1 was also significantly lower at 5 min after magnesium than after saline, by 0.64 (0.12–1.16) doubling doses (P= 0.023), though this difference was not statistically significant after adjustment for differences in baseline FEV1 on the two study days.Conclusions Inhaled magnesium did not protect against the effects of these direct and indirect bronchoconstrictor stimuli in subjects with asthma, and may have increased airway reactivity to histamine.
Loratadine and desethoxylcarbonyl‐loratadine inhibit the immunological release of mediators from human FcɛRI+cells
Authors: GENOVESE A. , PATELLA V. , DE CRESCENZO G. , DE PAULIS A. , SPADARO G. , MARONE G. 
Published: April 2006

SummaryBackgroundLoratadine, a novel histamine H1‐receptor antagonist, is effective in the treatment of patients with seasonal and perennial rhinitis and some allergic skin disorders. Histamine and other chemical mediators are synthesized and immunologically released by human peripheral blood basophils and tissue mast cells (FcɛRI+cells).ObjectiveTo evaluate the effects of loratadine and its main metabolite, desethoxylcarbonyl‐loratadine (des‐loratadine), on the immunological release of preformed (histamine and tryptase) andde novosynthesized mediators (leukotriene C4: LTC4and prostaglandin D2: PGD2) from human FcɛRI+cells.MethodsHuman FcɛRI+cells purified from peripheral blood and from skin (HSMC) and lung tissue (HLMC) were preincubated with loratadine and des‐loratadine before immunological challenge with Der p 1 antigen or anti‐FcɛRI. The release of preformed mediators (histamine and tryptase) andde novosynthesized eicosanoids was evaluated in the supernatants of human FcRI+cells.ResultsPreincubation (15m in, 37°C) of purified (36–74%) basophils with loratadine (3 × 10–6–10–4M) and des‐loratadine before Der p 1 antigen or anti‐FcɛRI challenge concentration‐dependency (5–40%) inhibited the release of histamine and LTC4. Loratadine (3 × 10–6–l0–4M) and des‐loratadine also inhibited (10–40%) histamine, LTC4, and PGD2release from purified HLMC (16–68%) activated by anti‐FcɛRI. Loratadine (3 × 10–6–10–4M) and des‐loratadine caused concentration‐dependent inhibition (10–40%) of histamine, tryptase. LTC4, and PGD2release from purified HSMC (24– 72%) immunologically challenged with anti‐FcɛRI.ConclusionThese results indicate that loratadine and its main metabolite have anti‐ inflammatory activity by inhibiting the release of preformed andde novosynthesized mediators from human FcɛRI+cells.
Prognostic factors for toluene diisocyanate‐induced occupational asthma after removal from exposure
Authors: PARK H.‐S. , NAHM D.‐H. 
Published: April 2006

SummaryBackground
The outcome of isocyanatc‐induced occupational asthma remains to be further defined. There have been few studies on the role of specific antibodies in prognosis of toluene diisocyanate (TDI) induced occupational asthma. Moreover, to the best of our knowledge, there have been no studies on the improvement pattern of airway hyper‐responsiveness (AH). We analysed the prognostic factors that affected the outcome of 35 toluene diisocyanate‐induced occupational asthma.Objectives
To define clinical and laboratory parameters predicting favourable prognosis for TDI‐induced occupational asthma.Methods and results
After confirmation of bronchial sensitivity by TDI hronchoprovocation test (BPT), 35 patients were recommended to avoid exposure to TDI; they were also given anti‐asthmatic medications including inhaled steroids and monitored for 2 years. Seventeen (49%) recovered completely with disappearance of airway hyperresponsiveness (AH) to methacholine during the follow‐up period (mean duration: 12 months, range of 3–30 months). Eleven (31%) showed a significant improvement in AH for first year, which improvement stabihzed in the next year with mild symptoms. Seven (20%) patients did not show any evidence of improvement in AH and had persistent symptoms. Favourable prognosis was associated with a short duration of asthmatic symptoms before diagnosis (P < 0.05), immediate cessation of exposure after diagnosis (P < 0.05), milder degree of AH at diagnosis (P < 0.05), and the presence of specific IgE antibodies to TDI‐human serum albumin conjugate (0.05 < P < 0.1). No association was found with atopic and smoking status, age, exposure duration, or length of latent period (P > 0.05).Conclusion
These data suggest that early detection of TDI‐induced asthma and immediate cessation of exposure are important factors for a favourable prognosis.
Inhibitory activity of loratadine and descarboxyethoxyloratadine on histamine‐induced activation of endothelial cells
Authors: MOLET S. , GOSSET P. , LASSALLE P. , CZARLEWSKI W. , TONNEL A.‐B. 
Published: April 2006

SummaryBackground
The allergic inflammatory reaction is characterized by leucocyte adherence and infiltration processes which are controlled by the expression of adhesion molecules on the surface of vascular endothelium. One of the main mediators implicated in allergic reactions is represented by histamine. Histamine is a potent activator of endothelial cells (EC): it induces the expression of P‐selectin on the surface of endothelium and the secretion of IL‐6 and IL‐8.Objectives
Loratadine (L), a histamine H1‐antagonist, and one of its active metabolites, descarboxyethoxyloratadine (DCL), were studied at different concentrations for their ability to reduce the histamine‐induced activation of human umbilical vein EC (HUVEC).Methods
HUVEC were stimulated in the presence of histamine at 10‐6M, 10‐5M and 10‐4M. We assessed by ELISA the expression of P‐selectin on EC surface, as well as cytokine production in EC supernatants of 24 h culture.Results
Our results showed that for a 10‐4 M‐histamine stimulation, L and DCL have a similar inhibitory effect on P‐selectin expression (IC50= 13 × 10‐9 M and 23 × 10‐9 M, respectively). L and DCL inhibited significantly IL‐6 and IL‐8 secretion induced by histamine with a more powerful efficiency of the active metabolite. For the dose of 10‐4 M histamine, a 50% inhibition of IL‐6 secretion was obtained for a dose of DCL equal to 2.6 × 10‐12 M whereas the same magnitude of effects were only reached for a higher concentration of L (0.3 × 10‐6 M). Similar results were obtained for IL‐8 (IC50 = 0.2 × 10‐6M for L and 10‐9 M for DCL). Analysis of IL‐8 mRNA expression by RT‐PCR was in accordance with these data.Conclusions
These results demonstrate that both L and DCL are active to reduce the histamine‐induced activation of EC. Interestingly, DCL seems to be effective at lesser concentrations especially to inhibit cytokine secretion.
IgE crossreactivity between mugwort pollen (Artemisia vulgaris) and hazelnut (Abellana nux) in sera from patients with sensitivity to both extracts
Authors: CABALLERO T. , PASCUAL C. , GARCÍA‐ARA M. C. , OJEDA J. A. , MARTÍN‐ESTEBAN M. 
Published: April 2006

SummaryBackgroundAn association between sensitization toCompositaepollens and hypersensitivity to hazelnut has been previously described. There is no previous invitrostudy about crossreactivity between mugwort pollen and hazelnut.ObjectivesTo study mugwort pollen and hazelnut allergens and to assess if there is IgE crossreactivity between mugwort pollen and hazelnut.MethodsA serum pool formed by 28 individual sera with specific IgE to mugwort pollen and hazelnut was used to investigate IgE crossreactivity. RAST‐inhibition, SDS‐PAGE/IEF immunoblotting inhibition assays were performed by preineubation of the sera with mugwort pollen and hazelnut.ResultsRAST to hazelnut was inhibited up to 63% by mugwort pollen, but the mugwort pollen RAST was only inhibited up to 36% by hazelnut. In SDS‐PAGE immunoblotting mugwort pollen showed nine allergens ranging from < 16 to 65kDa and hazelnut had four main allergens: 42kDa, 17kDa and < 16kDa (two bands). In the SDS‐PAGE immunoblotting inhibition hazelnut partially inhibited all the mugwort pollen bands, except that with 19kDa, whereas mugwort pollen produced a nearly total inhibition of all the hazelnut allergens. In isoeleetrofocusing immunoblotting mugwort pollen had two groups of allergens: pI 7.5–8.5 and pi 3.5–5.2 and hazelnut one group of allergens: pI 5.2–5.8. In the isoeleetrofocusing immunoblotting inhibition hazelnut produced a partial inhibition of all the bands of mugwort pollen and mugwort pollen partially inhibited all the allergenic bands of hazelnut.ConclusionsThe RAST and SDS‐PAGE/IEF immunoblotting inhibition results provide evidence of IgE cross reactivity between mugwort pollen and hazelnut allergens. The inhibition of hazelnut by mugwort pollen is higher than the inhibition of mugwort pollen by hazelnut in both RAST inhibition and SDS‐PAGE immunoblotting inhibition. These results suggest that mugwort pollen allergens would behave as primary immunogens in the association between sensitivity to mugwort pollen and hazelnut.
Role of leukotrienes in post‐allergic propranolol‐induced bronchoconstriction in guinea‐pigs
Authors: FUJIMURA M. , SONGÜR N. , ISHIURA Y. , MIZUHASHI K. , MYOU S. , MATSUDA T. 
Published: April 2006

SummaryBackground
Administration of propranolol can provoke bronchoconstriction only in asthmatic patients. Recently we developed an animal model for propranolol‐induced bronchoconstriction (PIB). Our working hypothesis is that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction.Objectives
Our goal in this study was to determine which products of arachidonate 5‐lipoxygenase pathway are involved in the PIB.Methods
Propranolol at a concentration of 10mg/mL was inhaled 20min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea‐pigs. Two different sulfidopeptide leukotriene (s‐LT) antagonists, ICI198 615 in the doses of 0.03 and 0.3 mg/kg and vehicle and KCA757 in the doses of 1 and 5 mg/kg and vehicle, and a LTB4 antagonist ONO4057 in the doses of 1 and 10 mg/kg and vehicle were injected intravenously 15min after antigen challenge. Effects of an anticholinergic agent atropine sulphate (5 mg/kg) and an α‐adrenergic biocker pbentolamine (0.3 and 3 mg/kg) were exatnined in the same way.Results
Bronchoconstriction occurred when 10 mg/mL of propranolol was inhaled 20 min after antigen challenge. Both ICI198 615 and KCA757 administered intravenously 15 min after antigen challenge reduced the PIB in a dose‐dependent manner while ONO4057 did not alter the PIB. Atropine or phentolamine did not change the PIB.Conclusions
These results suggest that mediator mechanism, but not cholinergic or α‐adrenergic nerve, is important in the PIB which developed after the allergic bronchoconstriction in our guinea‐pig model and that s‐LTs but not LTB4 have an important role in the pathophysiology of the PIB.