bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bronchial inflammation and the common cold: a comparison of atopic and non‐atopic individuals
Authors: TRIGG C. J. , NICHOLSON K. G. , WANG J. H. , IRELAND D. C. , JORDAN S. , DUDDLE J. M. , HAMILTON S. , DAVIES R. J. 
Published: April 2006

SummaryBackground
Cold virus infections are associated with asthma attacks and with increased bronchial responsiveness even in normal subjects. Possible mechanisms include epithelial damage, interaction with adhesion molecules or with T‐helper cell subsets.Objective
To determine whether colds increase lower airway inflammation, comparing atopic with non‐atopic normal subjects.Methods
Thirty healthy volunteers (15 atopic) took part. Basehne tests included viral serology. microbiological culture and polymerase chain reaction for rhinovirus infection (HRV‐PCR), histamine bronchial provocation and bronchoscopy. Twenty subjects (eight atopic) underwent repeat tests when they developed a cold.Results
Forced expiratory volume in one second (FEV1) was significantly lower during colds (‐0.19L [95% confidence mterval ‐0.10, ‐0.29], P= 0,0004) and there was a significant increase in bronchial responsiveness (+0.62 doublings of the dose‐response slope [+0.24, +1.00], P=0.003). Eight subjects (two atopic) had a diagnosed viral infection: two HRV. three coronavirus (HCV), one HRV + HCV, one parainfluenza III(PI) and one respiratory syncytial virus (RSV) (also Haemophilus influenzae). In biopsies, during colds, total eosinophils (EG1+) increased significantly (geometric mean 6.73‐fold [1.12,40.46], P=O.04). Activated eosinophils (EG2+) only increased significantly in the subgroup without diagnosed viral infection and particularly in atopic rhinitics. T‐suppressor (CD8+) cells also increased significantly (median +178.3 cells mm2, P= 0.004). Epithelial expression of intercellular adhesion molecule‐1 (ICAM‐1) expression increased in four atopic rhinitics during colds. Bronchial washings showed a significant increase in neutrophils (GM 1.53‐fold [1.04,2.25], P= 0.02).Conclusion
Lower airway inflammation was present in atopic and non‐atopic normal subjects with colds. Atopic subjects differed in that they were less likely to have positive virological tests and were more likely to show activated eosinophilia in the lower airway, despite a similar spectrum of symptoms.
Effect of cetirizine on the inflammatory cells in mosquito bites
Authors: KARPPINEN A. , RANTALA I. , VAALASTI A. , PALOSUO T. , REUNALA T. 
Published: April 2006

SummaryBackground
Mosquito bites frequently cause wealing and delayed papules which appear within a few hours after the bites and may persist for several days. Cetirizine is an effective drug against mosquito bites by decreasing wealing and also the size and pruritus of the delayed bite papules.Objectives
To characterize inflammatory cells in the delayed mosquito‐bite lesions, and to study the effect of cetirizine on the inflammatory cell response.Methods
Twenty‐six mosquito‐bite sensitive subjects received cetirizine 20 mg (14 subjects) or placebo (12 subjects) in a double‐blind fashion. Aedes aegypti‐bites were given on a forearm and serial punch biopsies were taken at 2‐, 6‐ and 24 h after the bite exposure, Eosinophils, neutrophils, mast cells, mononuclear cells and T‐ helper (CD4+) and suppressor (CD8+) lymphocytes were counted from dermal infiltrates.Results
Eosinophils and neutrophiis were found already in 2‐h bite lesions. Moreover, the number of mononuclear and CD4+ cells increased significantly (P < 0,01) from 2‐ to 24‐h bite lesions. Unexpectedly, the overall numbers of eosinophils (P < 0.05), mononuclear cells (P < 0.01) and CD4f cells (P < 0.01) were significantly higher in the cetirizine‐treated subjects compared with the placebo‐treated subjects.Conclusions
The results suggest that the inflammatory cell response in the delayed mosquito‐bite lesions is similar to that occurring in allergic late‐phase responses, i.e. an early influx of eosinophils, neutrophils and subsequent accumalation of CD4+ lymphocytes. The reason for the high numbers of eosinophils and CD4+ cells in the cetirizine‐treated subjects is not known.
Airway function correlates with circulating eosinophil, but not mast cell, markers of inflammation in childhood asthma
Authors: RAO R. , FREDERICK J. M. , ENANDER I. , GREGSON R. K. , WARNER J. A. , WARNER J. O. 
Published: April 2006

SummaryBackground
Lung function tests, including forced expiratory volume in one second (FEV1), forced expiratory flow at 25–75% of vital capacity (FEF25–75%) and provocation concentrations of histamine which reduce FEV] by 20% (PC20), are used as indicators of airway form and function in bronchial asthma. Recently, markers of eosinophil activation in bronchial lavage and serum have been suggested as a measure of eosinophil mediated inflammation in the airways. These include eosinophil cationic protein (ECP), eosinophil protein X (EPX) (also known as eosinophil derived neuro‐toxin) and eosinophil peroxidase (EPO). Similarly, serum tryptase has been used as a marker of mast cell activation in systemic anaphylaxis.Objectives
We measured both sets of indices in a group of children with moderately severe asthma to assess the contribution of eosinophil and mast cell mediated events to airflow limitation and bronchial hyperresponsiveness.Methods
Forty‐eight children aged 5–10 years had spirometric assessments, histamine challenges and blood sampling on the same occasion. After analysis of sera, the indices were compared.Results
The eosinophil markers ECP and EPX correlated very well with each other. They showed a moderate negative correlation with PC20 for histamine. EPX was also found to negatively correlate with FEV, and FEF25–75%. Serum tryptase levels showed no such correlates with airway function.Conclusion
These results suggest that serum markers of eosinophil activation correlate with airway function in childhood asthma, and may be of value in assessing the severity of the disease. It further supports the notion that childhood asthma has a similar immunopathology to that occurring in adults, with predominance of eosinophil mediated inflammation.
Damage to respiratory epithelium by guinea‐pig eosinophils stimulated with IgG‐coated Sepharose beads
Authors: HIRATA A. , MOTOJIMA S. , FUKUDA T. , MAKINO S. 
Published: April 2006

SummaryBackground
There are no reports of respiratory epithelial damage induced by immuiioglobulin‐stimulated eosinophils.Objective
We tried to induce damage to respiratory epithelium by guinea‐pig (GP) eosinophils stimulated with guinea‐pig IgG (GP‐lgG)‐coated Sepharose 4B beads. Methods GP tracheal epithelium was cultured together with GP eosinophils that had been collected from the peritoneal cavity, purified on a Percoll gradient, and stimulated with GP‐lgG‐coated beads (GP eosinophils:beads = 20:1). Damage to the epithelium was observed with an inverted microscope.Results
After 24 h of culture with three 106 eosinophils. irregularity of the surface of the epithelium, desquamation. shedding of cilia, and abnormal beating of cilia were observed. This damage was first observed after 12 h of incubation, and was more severe at 24 h. No damage was found when beads coated with human serum albumin (HSA) were used. GP eosinophils stimulated with GP‐IgG released significantly more EPO than those stimulated with HSA. at 6 and 24 h. Heparin and eatalase partially inhibited the epithelial damage. O2‐production by eosinophils was also enhanced with GP‐IgG‐coated beads. Conclusion Both granule basic proteins and reactive oxygen radicals may be responsible for epithelial damage, probably via an EPO + H2O2+ halide system. These results confirmed that stimulated eosinophils can damage respiratory epithelium.
Neuroregulation of the nose and bronchi
Authors: WIDDICOMBE J. G. 
Published: April 2006

SummaryThe vascular beds, submucosal glands, and airway vasculature are the three primary effector tissues in the airways, and all are under the control of the parasympathetic (vagal) and sympathetic nervous systems. Parasympathetic nerves play a more important role in smooth muscle contraction and gland secretion. The complex neurogenic mechanisms initiated by activation of sensory nerves have been clarified to a large extent by studies on experimental animals. For example, inflammation or an allergic response will cause neurogenic inflammation due to axon reflexes; central nervous reflexes will modulate activity in all of the effector tissues; and these reflex responses will be modulated by local reflexes via parasympathetic ganglia. Similar mechanisms are suspected in humans, but their importance still needs to be fully established.
Pentoxifylline attenuates LPS‐induced bronchial hyperresponsiveness but not the increase in exhaled nitric oxide
Authors: ROLLA G. , BUCCA C. , BRUSSINO L. , DUTTO L. , COLAGRANDE P. , POLIZZI S. 
Published: April 2006

SummaryBackground Inhaled endotoxin (LPS) may cause a transient increase in airway responsiveness, possibly through a cytokine‐mediated airway inflammation, which is associated with an increase in nitric oxide synthesis and release. Objective We wondered whether pentoxifylline (PTX), which may attenuate cytokine release induced by LPS. could inhibit LPS‐induced increase in airway responsiveness.Objective Methacholine (Mch) bronchial responsiveness was assessed 2 and 24 h after saline or LPS inhalation in eight subjects with bronchial hyperresponsiveness (PD20FEV1 610 ± 53 μg), treated with iv saline or PTX, in a double‐blind crossover design. Nitric oxide (NO) in the exhaled air, which was expected to increase after LPS inhalation, and PEFR values were also measured at baseline, hourly for 6h and 24 h later.Results After LPS inhalation PEFR decreased significantly compared with placebo inhalation, reaching a maximum decrease of 11.25 ± 1.05 and 4.5 ± 0.84% of baseline, at 2h, respectively during saline and PTX infusion, P < 0.001. Exhaled NO were elevated after LPS compared with placebo inhalation at 1h (35.6 ± 4.8 vs 18 ± 2.8 ppb, P < 0.001), with no difference during saline or PTX infusion. Exhaled NO remained elevated until the 6th hour. PD20FEVI 2h after LPS inhalation was significantly lower than after placebo inhalation both during saline infusion (234 ± 29 vs 625 ± 62 μg, P < 0.001) and during PTX infusion (441 ± 47 vs 616 ± 48 μg, P < 0.001), the difference between saline and PTX being significant (P < 0.01). At 24 h no difference in PEFR, PD20FEV1 and exhaled NO was observed in comparison with pre‐study values.Conclusion PTX attenuates both the decrease in airway patency and the increase in bronchial responsiveness induced by LPS inhalation, without any significant change in exhaled NO, which is increased by LPS inhalation.
Sibship size and self‐reported inhalant allergy among adult women
Authors: STRACHAN D. P. , HARKINS L. S. , GOLDING J. ,   the ALSPAC Study Team
Published: April 2006

SummaryBackgroundAn association of allergic sensitization with small families and low birth order has been described and attributed to a protective effect of early infection. The influence of like‐sex and unlike‐sex siblings has not been investigated, although the severity of viral infections may be greater if acquired from unlike‐sex siblings.ObjectiveTo investigate the association of self‐reported inhalant allergy with family composition.MethodsReports of allergy to grass, dust or cats by 11042 pregnant women recruited to a longitudinal study of pregnancy and childhood in Avon, UK, were analysed in relation to respondent's age, maternal age and sibship composition (older and younger brothers and sisters) by multiple logistic regression.ResultsThe prevalence of self‐reported inhalant allergy decreased with increasing numbers of brothers (test for trend:P< 0.0001), but was unrelated to the number of sisters. The unadjusted prevalences for subjects with none, one, two and three or more brothers were 26%, 23%, 20% and 17%, respectively. The corresponding prevalences for numbers of sisters were 23%, 24%, 22% and 23%. After adjustment for total sibship size, offspring of older mothers were more likely to report allergy (test for trend:P< 0.001), but there was no association with position in the sibship.ConclusionAlthough it is not possible to determine whether brothers speciflcally, or unlike‐sex siblings in general, are inversely associated with inhalant allergy, these findings are consistent with the hypothesis that patterns of sibling interaction within young families influence the risk of future aeroallergen sensitization.
Major grass pollen allergen Lol p 1 binds to diesel exhaust particles: implications for asthma and air pollution
Authors: KNOX R. B. , SUPHIOGLU C. , TAYLOR P. , DESAI R. , WATSON H. C. , PENG J. L. , BURSILL L. A. 
Published: April 2006

SummaryBackground Grass pollen allergens are known to be present in the atmosphere in a range of particle sizes from whole pollen grains (approx. 20 to 55 μim in diameter) to smaller size fractions < 2.5 μ (fine particles, PM2.5). These latter particles are within the respirable range and include allergen‐containing starch granules released from within the grains into the atmosphere when grass pollen ruptures in rainfall and are associated with epidemics of thunderstorm asthma during the grass pollen season. The question arises whether grass pollen allergens can interact with other sources of fine particles, particularly those present during episodes of air pollution.Objective We propose the hypothesis that free grass pollen allergen molecules, derived from dead or burst grains and dispersed in microdroplets of water in aerosols, can bind to fine particles in polluted air.Methods We used diesel exhaust carbon particles (DECP) derived from the exhaust of a stationary diesel engine, natural highly purified Lol p 1, immunogold labelling with specific monoclonal antibodies and a high voltage transmission electron ‐microscopic imaging techniqueResults DECP are visualized as small carbon spheres, each 30–60 nm in diameter, forming fractal aggregates about 1–2μ in diameter. Here we test our hypothesis and show by in vitro experiments that the major grass pollen allergen, Lol p I. binds to one defined class of fine particles, DECP.Conclusion DECP are in the respirable size range, can bind to the major grass pollen allergen Lol p I under in vitro conditions and represent a possible mechanism by which allergens can become concentrated in polluted air and thus trigger attacks of asthma.
Immune effector cells induced by complete Freund's adjuvant exert an inhibitory effect on antigen‐specific type 2 T helper responses
Authors: CHUANG Y.‐H. , CHIANG B.‐L. , CHOU C.‐C. , HSIEH K.‐H. 
Published: April 2006

SummaryBackground II has hecn well documented that environmental factors such as antigenpresenting cells and related cytokines could affect the development of T helper cells.Objective The purpose of this study is to investigate the effect of different adjuvants on T cell development.Methods Ovalbumin (OVA) combined with aluminum hydroxide (Alum) plus pertussis toxin (PT) or complete Freund's adjuvant (CFA) were used to sensitize mice; the production of IgG and IgE anli‐OVA antibodies was then followed. In addition, OVA‐specific proliferative responses and cytokine production by spleen cells were also investigated.Results The data showed that the adjuvants themselves could modify the pattern of immune response: (1) IgG2a > anti‐OVA antibody was higher in mice sensitized with OVA + CFA compared to that of mice sensitized with OVA + Alum + PT; (2) the ratio of IFN‐γ/IL‐4 produced by OVA‐stimutated spleen cells was higher in mice sensitized with OVA + CFA than that of mice sensitized with OVA + Alum + PT; (3) increased percentage of γδ T cells was noted in the peritoneal exudate cells of OVA + CFA immunized mice; and (4) the immune response of mice sensitized wilh OVA + Alum+ PT was inhibited by the adoptively transferred ascitic cells from OVA + CFA immunized mice.Conclusion In general, the data suggested higher IgG2a and the ratio of IFN‐γ/IL‐4 was noted In mice sensitized with OVA + CFA. Further elucidation of the regulatory mechanism of allergen‐specific T helper cells development and exploration of possible agents for inmiunotherapy might shed light on the management of atopic diseases.
Elevated levels of substance P in tears of patients with allergic conjunctivitis and vernal keratoconjunctivitis
Authors: FUJISHIMA H. , TAKEYAMA M. , TAKEUCHI T. , SAITO I. , TSUBOTA K. 
Published: April 2006

SummaryBackground Recetit studies have suggested that the nervous system may participate in inflammatory processes. Substance P (SP) acts as a chemical mediator as well as a neurotransmitter.Objective In order to clarify the pathogenesis of ocular allergic diseases, we assessed the concentration of SP in tears.Methods Using a highly sensitive and specific double‐antibody enzyme immunoassay (EIA), we determined the SP concentration in tears of 10 patients with seasonal allergic conjunctivitis, 10 with atopic dermatitis without keratoconjunctivitis (AD), 13 with vernal keratoconjunctivitis (VKC) and 65 normal controls. Giemsa's staining for brush cytology samples and histocytological study by immunocytochemical staining of giant papillary conjunctival cells from VKC and normal controls was conducted.Results The mean SP level was low in the normal controls and AD, whereas patients with seasonal allergic conjunctivitis and VKC showed significant elevation of SP (P<0.01). Brush cytology samples showed conjunctival epithelial cells with lymphocytes, neutrophils and eosinophils that were not seen in normal subjects. Histocytological examination demonstrated SP positive cells in the conjunctiva of patients with VKC, but not in normal controls.Conclusion This study suggests that the increased level of SP in tears may contribute to the pathogenesis and severity of ocular allergic diseases.
Altered compartimentalization of transforming growth factor‐β in asthmatic airways
Authors: MAGNAN A. , RETORNAZ F. , TSICOPOULOS A. , BRISSE J. , VAN PEE D. , GOSSET P. , CHAMLIAN A. , TONNEL A. B. , VERVLOET D. 
Published: April 2006

SummaryBackground Asthma is characterized by alterations of the bronchial epithelium associated with inflammatory cell infiltrates and sub‐epithelial fibrosis. Transforming Growth Factor‐β (TGF‐β) is an anti‐inflammatory and fibrosing cytokine normally present in bronchial epithelial cells and also potentially produced by inflammatory cells. Thus, TGF‐β could play a role in the asthmatic process, and its expression could be modified in asthmatic airways.Objective To test this latter hypothesis, we studied the bronchial distribution of TGF‐β in asthmatic patients.Methods TGF‐β1, 2, 3 distribution was studied by immunohistochemistry in bronchial biopsies from 12 asthmatic patients and 10 non‐asthmatic subjects.Results Bronchial epithelial cells from asthmatics were negative or faintly positive while a bright staining was detected in these from non‐asthmatics (P < 0.0l). In both groups, when inflammatory cells were present beneath the basement membrane, they were stained by the anti‐TGF‐β antibody.Conclusion This study shows an altered compartimentalization of TGF‐β in asthma. (a) TGF‐β is scarse in asthmatic bronchial epithelial cells, which could favour the perennization of the bronchial inflammation, and (b) TGF‐β is present in inflammatory cells beneath the basement membrane, where it could be involved in the frequent sub‐epithelial fibrosis.
Constitutive mRNA and immunoreactivity for IL‐2 in human nasal mucosa
Authors: MOSS R. B. , NAGATA H. , GOFF J. , OKUBO K. , HAUSEFELD J. , KALINER MICHAEL A. 
Published: April 2006

SummaryBackground The nasal mucosa is the initial site in the upper airway of host defence against antigenic challenge in the form of airborne allergens, irritants, toxins and infectious agents, and yet little is known about nasal mucosal cytokine expression and function. We hypothesized that IL‐2 might play a role in immunocompetence of the upper airway.Methods IL‐2 immunoreactivity was measured by ELISA in nasal secretions and by Western blot. Immunohistochemistry and electron microscopy were performed on turbinated tissue. mRNA for IL‐2 was evaluated by RTPCR and Southern hybridization.Results IL‐2 immunoreactivity was demonstrated by Western blot and quantitated by an enzyme immunoassay. Immunohistochemical and electron microscopy analysis of turbinate tissue revealed interstitial staining for IL‐2. By RTPCR, IL‐2 message was evident in 5/5 atopies and 5/5 non‐atopics. IL‐2 message was expressed in all subjects by Southern hybridization to an internal probe after PCR.Conclusion This study has demonstrated constitutive expression of IL‐2 protein and mRNA in the upper airway of heallhy individuals. The further characterization of cytokines in the upper airway could provide useful insights into immune regulation at the mucosal level.
IgE response to fur animal allergens and domestic animal allergens in fur farmers and fur garment workers
Authors: SAVOLAINEN J. , UITTI J. , HALMEPURO L. , NORDMAN H. 
Published: April 2006

SummaryObjective The aim of this study was to compare the IgE response to the most commonly farmed fur animals with that to domestic animals.Methods IgE‐immunoblotting and RAST‐inhibition analyses were performed using RAST‐positive sera from fur workers sensitized to fur allergens and sera from patients sensitized to domestic animal allergens.Results The urine extracts of mink, blue fox, silver fox, racoon dog and fitchew contained more protein bands than the fur extracts did. Allergens with the same molecular weight were found in all of the fur and urine extracts. The most prominent allergenic bands had molecular weights of 62–67 kDa, 23–25 kDa and 18–19 kDa. With crossreacting sera the reciprocal RAST inhibition with all five animal extracts indicated common IgE‐binding epitopes, probably common allergens (especially the 62–67 kDa bands). Urine and fur contain common allergens, since urine allergens strongly inhibited the IgE‐binding to fur allergens. The IgE binding to allergenic bands of fur animal extracts was also observed in immunoblotting when dog and cat RAST‐positive sera were used, but not for cow RAST‐ positive sera. RAST inhibition of dog‐positive sera with fur animal extracts and fur‐positive sera with dog extract confirmed the crossreactivity of these IgE antibodies. No such inhibition was seen with cow extract.Conclusion The results of the RAST inhibition and immunoblotting suggest that fur animals have IgE binding epitopes or allergens in common with cat and dog – possibly albumin but not with cow.