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At least 1,351 records · Page 75Linked to original sources
PubMed2002

Wegener's granulomatosis presenting as necrosis of the left mainstem bronchus.

A patient with pansinusitis, nasal septum necrosis, and saddle nose deformity showed necrosis of the left mainstem, upper, and lower bronchi, with complete loss of left lung perfusion and ventilation. Pneumonectomy was performed. Histological findings showed extensive necrotizing and granulomatous bronchial inflammation with vasculitis of the bronchial arteries and the pulmonary vein. Wegener's granulomatosis was diagnosed, despite a negative cytoplasmic pattern of antineutrophil cytoplasmic antibodies and the lack of renal involvement.

Bronchial Diseases↗
PubMed2005

Nerve growth factor is released by IL-1beta and induces hyperresponsiveness of the human isolated bronchus.

Nerve growth factor (NGF) is a neurotrophic factor essential for the development and survival of neurons, and is also an important mediator of inflammation. It is released by airway cells stimulated by interleukin (IL)-1beta. As IL-1beta induces airway hyperresponsiveness (AHR) to the tachykinin NK-1 receptor agonist [Sar9,Met(O2)11]-substance P in human isolated bronchi, the aim of this study was to determine whether IL-1beta was able to induce NGF release from isolated bronchi, and whether NGF might participate into IL-1beta-induced AHR. IL-1beta (10 ng x mL(-1); 21 degrees C; 15 h) increased the release of NGF from human isolated bronchi in vitro, and, in organ bath studies, the response of human bronchi to [Sar9,Met(O2)11]-substance P (0.1 microm). A significant correlation was found between these responses. AHR induced by IL-1beta was abolished by a blocking anti-human NGF antibody. Finally, NGF (1 ng x mL(-1); 37 degrees C; 0.5 h) by itself induced a significant increase in [Sar9,Met(O2)11]-substance P responsiveness. By contrast, it did not change the maximal contraction to acetylcholine. In conclusion, the present study clearly demonstrated that nerve growth factor may participate in the airway hyperresponsiveness induced by interleukin-1beta, which supports the neuro-immune cross-talk that may be active in the development of hyperresponsiveness in the human airways, and suggests nerve growth factor is active in the airways in asthma.

Analysis of Variance↗
PubMed1994

A rare case of inflammatory pseudotumour of the bronchus, occurring in an achondroplastic woman.

An inflammatory pseudotumour of the lung in an achondroplastic woman is described. The occurrence of both conditions in the same patient probably represents a coincidental finding. However, recurrent pulmonary infections, as frequently seen in achondroplasia, may be relevant, because a history of antecedent infection is noted in one third of cases of inflammatory pseudotumours. Despite extensive debridement of the pseudotumour by neodymium yttrium aluminium garnet (NdYAG) laser therapy, early recurrence occurred.

Achondroplasia↗
PubMed1997

Mast cell tryptase potentiates histamine-induced contraction in human sensitized bronchus.

The mast cell plays a pivotal role in the early asthmatic response via release of mediators, which directly influence airway smooth muscle tone. Canine mast cell tryptase has been reported to potentiate the contractile response of canine isolated airways to histamine. The aim of this study was to investigate whether human mast cell tryptase potentiated contractile responses in human isolated bronchi. The effect of tryptase differed according to the sensitization status of the bronchi. In lung tissue from sensitized patients (those whose bronchial tissue contracted in response to the application of any of four common antigens) 90 ng.mL-1 of human purified lung tryptase markedly potentiated the contractile response to histamine. The maximal response as a percentage of maximal contraction to acetylcholine was 80 +/- 8% in control tissues and 119 +/- 6% in tryptase treated tissues (n = 4; p < 0.05). Tryptase, at a dose of 200 ng.mL-1, also potentiated responses but to a lesser degree, 100 +/- 5% (n = 4; p < 0.05). In nonsensitized bronchi, neither 90 nor 200 ng.mL-1 tryptase had any significant effect on histamine responses. The increased response in the presence of tryptase in sensitized tissue was inhibited by the calcium voltage-dependent channel antagonist, verapamil (10(-6) M). We have shown, for the first time, that human mast cell tryptase potentiates contraction in sensitized bronchi via a calcium-related mechanism. These findings provide a link between a mast cell derived product and in vitro human airway hyperresponsiveness.

Acetylcholine↗
PubMed1997

Carcinoma of the bronchus in the Yorkshire region of England 1976-1990: trends since 1984.

We wished to confirm that, in patients with lung cancer, trends in demography and histology, together with modest improvements in survival, first seen in the 1976-1983 cohorts, continued to 1990. All lung cancer patients resident in Yorkshire are notified to the Cancer Registry, whose database was analysed for this report. A total of 38,275 patients were notified. There was no change in annual notification for males but an increase from 513 to 815 annual notifications in females between 1976 and 1990. Mean age increased by 3 yrs, in males to 67.4 yrs and in females to 67.2 yrs. Histological confirmation rate increased from 43% to 60% (mean age from 60.8 to 64.5 yrs). Annual notifications of adenocarcinoma increased consistently from 108 to 253. Two year surgical survival improved from 37.4 to 44.3%, doubling in subjects aged > or = 70 yrs to 43.8%. Over the 15 year period, there was no improvement in survival aged < 60 yrs, but a significant improvement in the 60-69 and > or = 70 yrs age groups. Analysis of survival by quartiles showed significant improvement at all levels (first interval 20 to 24 days, median 79 to 91 days, third interval 224 to 266 days). The modest improvement in outlook was confirmed, confined to older subjects after 1983, and partially masked by increasing age. Survival after surgery is now independent of age.

Adenocarcinoma↗
PubMed1997

MDR1-Pgp 170 expression in human bronchus.

MDR1 P-glycoprotein (Pgp 170), a member of the adenosine triphosphate (ATP) binding cassette transporters, acts as an efflux pump for various hydrophobic agents, particularly for xenobiotics such as benzo(a)pyrene. It has also been shown to regulate cell-volume activated chloride channels. Pgp 170 could, therefore, be of particular importance in cellular mechanisms of defence in the airways and in the control of mucus layer composition. For these reasons, we evaluated the precise localization of Pgp 170 in human adult airways. Fresh non-neoplastic bronchial specimens were collected from 33 patients (26 smokers, four exsmokers and three nonsmokers) who underwent surgery for lung carcinoma. The presence of MDR1 messenger ribonucleic acid (mRNA) was demonstrated by reverse transcriptase chain reaction (RT-PCR) in bronchial epithelial cells collected by gentle scraping from either smokers, exsmokers or nonsmokers. Immunodetection of Pgp 170 using a panel of monoclonal antibodies (MRK16, JSB1, C219, C494) was performed either on cryostat or paraffin-embedded sections of histologically normal bronchial tissue. Pgp 170 was constantly detected with intense labelling at the apical surface of ciliated epithelial cells from the surface epithelium or ciliated collecting ducts, and on apical and lateral surfaces of serous cells from bronchial glands. No staining of mucus-secreting cells was observed. Pgp 170 was also demonstrated at the luminal surface of endothelial cells of bronchial capillaries. In conclusion, the expression of MDR1 P-glycoprotein in bronchial structures, particularly at the epithelial apical surface, suggests important roles for this transmembrane protein in human airways.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Immune sensitization of equine bronchus: glutathione, IL-1beta expression and tissue responsiveness.

BACKGROUND: Increasing clinical epidemiological and experimental evidence indicates that excess of production of reactive oxygen free radicals (ROS) induced by an oxidative stress is involved in the pathogenesis of a number of human airway disorders, as well as equine recurrent airway obstruction. Free-radicals modulate the activation of transcription factors, such as nuclear factor-(NF)-kappaB and activator protein (AP)-1, in several different cells. This activation leads to expression of many pro-inflammatory cytokines, including interleukin (IL)-1beta. We have hypothesized that equine airway sensitization might induce an oxidative stress and increase the ROS production, which in turn might enhance a production of IL-1beta and airway hyperresponsiveness. METHODS: We have examined the effect of passive sensitization on IL-1beta mRNA expression and electrical field stimulation (EFS)-induced contraction in equine isolated bronchi, and the potential interference of reduced-glutathione (GSH), an antioxidant, with these responses. Bronchi passively sensitized with serum from animals suffering from heaves and having high total level of IgE, and control tissues, either pretreated or not with GSH (100 microM), were used to quantify IL-1beta mRNA. Other tissues were used to study the effect of EFS (3-10-25 Hz). RESULTS: Mean IL-1beta mRNA expression was higher in passively sensitized than in control rings. GSH significantly (p < 0.05) reduced the IL-1beta mRNA expression only in passively sensitized bronchi. ELF induced a frequency-dependent contraction in both non-sensitized and passively sensitized tissues, with a significantly greater response always observed in sensitized tissues. GSH did not modify the EFS-induced contraction in non-sensitized bronchi, but significantly (p < 0.05) decreased it in passively sensitized tissues. CONCLUSION: Our data indicate that the passive sensitization of equine bronchi induces inflammation and hyperresponsiveness. These effects might be due to an oxidative stress because a pretreatment with GSH decreased the increased IL-1beta mRNA expression and responsiveness to EFS of passively sensitized bronchi.

Animals↗
PubMed2000

Inspiratory aerodynamic valving in the avian lung: functional morphology of the extrapulmonary primary bronchus.

The form, geometry and epithelial morphology of the extrapulmonary primary bronchi (EPPB) of the domestic fowl (Gallus gallus var. domesticus) and the rock dove (Columba livia) were studied microscopically and by three-dimensional computer reconstruction to determine the structural features that may be involved in the rectification of the inspired air past the openings of the medioventral secondary bronchi (MVSB), i.e. the inspiratory aerodynamic valving (IAV). In both species, the EPPB were intercalated between the clavicular and the cranial thoracic air-sacs. A notable difference between the morphology of the EPPB in G. g. domesticus and C. livia was that, in the former, the EPPB were constricted at the origin of the MVSB, while a dilatation occurred at the same site in the latter. In both species, a highly vascularized, dorsally located hemispherical epithelial swelling was observed cranial to the origin of the MVSB. The MVSB were narrow at their origin and variably angled relative to the longitudinal axis of the EPPB. Conspicuous epithelial tracts and folds were observed on the luminal aspect of the EPPB in both C. livia and G. g. domesticus. From their marked development and their orientation relative to the angled MVSB, these properties may influence the flow of the air in the EPPB. It was concluded that features such as syringeal constriction, an intimate topographic relationship between the EPPB and the cranial air-sacs, prominent epithelial tracts and folds, an epithelial swelling ahead of the origin of the first MVSB (corresponding to the 'segmentun accelerans'), and narrowing and angulation of the MVSB at their origin, may together contribute to IAV to a variable extent. In as much as the mechanism of pulmonary ventilation and mode of airflow in the parabronchial lung are basically similar in all birds, the morphological differences observed between G. g. domesticus and C. livia suggest that either the mechanism of production of IAV or its functional efficiency may be different, at least in these two species of birds.

Animals↗
PubMed1975

[Effect of prostaglandin E1 on the isolated stomach, small intestine, bronchus and uterus of experimental animals and its intestinal effect in vivo].

The stomach, intestine and uterus were contracted by PGE1. Stimulating effects of ACh and serotonin were augmented in some of these organs, especially in guinea pig uterus. ACh- and serotonin-induced bronchial contraction, however, decreased after administration of PGE1. Bronchial relaxation induced by adrenaline or noradrenaline was unaffected or increased. Antiadrenergic effects were not detected in the organs tested. ACh-induced contractions of frog rectus abdominus was augmented by PGE. The potentiating effect of PGE1 was almost the same in degree as that of physotigmine, although cholinesterase inhibitory effect was not detected in PGE1. Intravenous injection of PGE1 (10 mug/kg) into rabbits caused a relaxation of the intestine, which was contrary to the result with the isolated organ. Administration of PGE1 (1 mug/100 g, i.p. or 0.1, 1 mug/100 g, i.v.) did not show any curative effects on intestinal paralysis in cecectomized rats. The mechasism of action of PGE1 on rat uterus was found to be calcium-dependant.

Abdominal Muscles↗
PubMed1997

Abnormal modulation of cholinergic neurotransmission by endogenous nitric oxide in the bronchus of rats with hyperresponsiveness induced by allergen challenge.

The involvement of endogenous nitric oxide (NO) in bronchial cholinergic neurotransmission was compared between normal rats and airway hyperresponsive (AHR) rats. Male Wistar rats were sensitized and repeatedly challenged with dinitrophenylated (DNP)-Ascaris antigen. Twenty-four hours after the last antigenic challenge, enhancements of both the electrical field stimulation (EFS)-induced bronchoconstriction and acetylcholine (ACh) release were observed. NG-Monomethyl-L-arginine (L-NMMA; NO synthase inhibitor, 0.1 mM) augmented the EFS-induced bronchoconstriction and ACh release without affecting exogenously applied ACh-induced bronchoconstriction in normal rats. Interestingly, the augmentative effects of L-NMMA seen in normal rats were not manifested in AHR rats. Sodium nitroprusside inhibited the EFS-induced bronchoconstriction in a concentration-dependent manner; the inhibition was much larger than that of exogenously applied ACh-induced constriction in both normal and AHR rats. Furthermore, dibutyryl cGMP (3 mM) inhibited the EFS-induced bronchoconstriction with no effect on the ACh-induced bronchoconstriction in both normal and AHR rats. These findings suggest that endogenous NO may have a modulatory role in bronchial cholinergic neurotransmission in normal rats and that the augmented ACh release in the AHR rats may result from the defect of endogenous NO-induced modulation of cholinergic nerve transmission.

Acetylcholine↗