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Bronchial Epithelium (bronchial + epithelium)
Selected AbstractsMorphological Studies on the Development of the Bronchial Epithelium of the Fetal Camel LungANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005G. Kamel Light microscopic observations revealed that in camel foetuses of 25 mm crown-to-rump length (CRL) the primordial tubular system of the prospective lung was formed of several tubules lined by undifferentiated columnar epithelium. Intra-epithelial neuroendocrine cells were the first elements to be differentiated in the lining epithelium of the primordial tubular system of the prospective lung as early as 25 mm CRL. On reaching 50,67 mm CRL, the primordial tubular system started to differentiate into two systems of primordial tubules, the prospective bronchial or light tubules and the future respiratory or dark tubules. The lining epithelium of the prospective bronchial tubules revealed a clear evidence of ciliogenesis as early as 80 mm CRL. From 800 mm CRL onwards, the bronchial epithelium demonstrated ciliated and non-ciliated secretory cells. The non-ciliated secretory cells of the bronchial epithelium of fetal camel lung showed moderate reaction to AB/PAS technique, for the first time, in fetuses reaching 600 mm CRL. [source] T-box gene products are required for mesenchymal induction of epithelial branching in the embryonic mouse lungDEVELOPMENTAL DYNAMICS, Issue 1 2003Judith A. Cebra-Thomas Abstract The regulation of signaling pathways is a prerequisite for coordinating the induction between mesenchymal and epithelial tissues during morphogenesis. Mesenchymal FGF10 is known to be an important paracrine factor regulating the branching morphogenesis of the bronchial epithelium. By using antisense oligonucleotides (AS ODNs) and in vitro culture of embryonic lungs, we demonstrate that the transcription factors Tbx4 and Tbx5 are critical for the expression of mesenchymal FGF10. Treatment of embryonic lung cultures with AS ODNs to Tbx4 and Tbx5 reduces the level of these transcripts, suppresses Fgf10 expression in the mesenchyme, and completely eliminates the formation of new lung branches. If FGF10 is locally replaced in these AS ODN-treated lungs, epithelial branching is restored. These studies provide evidence that the production of branching signals by the lung mesenchyme is mediated by T-box genes. © 2002 Wiley-Liss, Inc. [source] Mechanisms of virus-induced asthma exacerbations: state-of-the-art.ALLERGY, Issue 5 2007A GA2LEN, InterAirways document Viral infections of the respiratory tract are the most common precipitants of acute asthma exacerbations. Exacerbations are only poorly responsive to current asthma therapies and new approaches to therapy are needed. Viruses, most frequently human rhinoviruses (RV), infect the airway epithelium, generate local and systemic immune responses, as well as neural responses, inducing inflammation and airway hyperresponsiveness. Using in vitro and in vivo experimental models the role of various proinflammatory or anti-inflammatory mediators, antiviral responses and molecular pathways that lead from infection to symptoms has been partly unravelled. In particular, mechanisms of susceptibility to viral infection have been identified and the bronchial epithelium appeared to be a key player. Nevertheless, additional understanding of the integration between the diverse elements of the antiviral response, especially in the context of allergic airway inflammation, as well as the interactions between viral infections and other stimuli that affect airway inflammation and responsiveness may lead to novel strategies in treating and/or preventing asthma exacerbations. This review presents the current knowledge and highlights areas in need of further research. [source] LKB1 protein expression in neuroendocrine tumors of the lungPATHOLOGY INTERNATIONAL, Issue 2 2008Randa Mahmoud Sobhi Amin During a recent investigation of LKB1 gene abnormality in lung lesions, strong expression of LKB1 protein in normal neuroendocrine (NE) cells of the bronchial epithelium was found. Because LKB1 functions as a tumor suppressor gene, the question of whether alteration of LKB1 expression is related to the development of pulmonary NE tumors of various grades was investigated. LKB1 immunohistochemistry was examined in a total of 68 primary pulmonary NE tumors consisting of 30 specimens of small cell lung carcinoma (SCLC), 23 large cell neuroendocrine carcinomas (LCNEC), two atypical carcinoids, and 13 typical carcinoids. Loss or low expression (<20% immunoreactive cells) of LKB1 protein expression was more frequently observed in high-grade NE tumors (SCLC and LCNEC; 45/53, 84.9%) than in typical and atypical carcinoids (3/15; 20%). The difference in LKB1 immunoreactivity between the high-grade NE tumors and the carcinoid group was statistically significant (P < 0.0001). In conclusion, marked reduction of LKB1 expression in high-grade NE tumors of the lung suggests a possible role of LKB1 inactivation in its tumorigenesis. Although a few previous studies indicated rare genetic alterations of LKB1 in SCLC, further studies including analysis of other NE tumors and focusing on epigenetic abnormalities of LKB1 gene are warranted. [source] Evidence of Temporary Airway Epithelial Repopulation and Rare Clonal Formation by BM-derived Cells Following Naphthalene Injury in MiceTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 9 2007Vladimir B. Serikov Abstract The goal of the study was to investigate participation of bone marrow (BM) cells in the process of airway epithelial restoration after naphthalene-induced injury. We transplanted sex-mismatched green fluorescent protein (GFP) -tagged BM-derived cultured plastic-adherent mesenchymal stem cells into 5Gy-irradiated C57BL/6 recipients. After 1 month of recovery, experimental animals were subjected to 250 mg/kg naphthalene IP. Animals were killed at 2,30 days after naphthalene. By immunofluorescence, immunohistochemistry, and by in situ hybridization for the Y-chromosome, we observed patches of donor-derived cells in the large and small conducting airways, mostly at 2,6 days after injury. GFP+ cells in the epithelium of airways were positive for pancytokeratin and some other epithelial markers. Although rare, GFP+ cells formed clear isolated patches of the bronchial epithelium, consistent with clonal formation; as some cells were also positive for proliferating cell nuclear antigen, a marker of proliferating cells. After day 12, only occasional GFP+ cells were present in the epithelium. These data confirm that bone marrow-derived cultured mesenchymal cells can participate in the recovery of the injured airway epithelium after naphthalene-induced injury with minimal long-term engraftment. Anat Rec, 2007. © 2007 Wiley-Liss, Inc. [source] Cigarette smoke condensate induces nuclear factor kappa-b activity and proangiogenic growth factors in aerodigestive cells,THE LARYNGOSCOPE, Issue 8 2010Joseph Rohrer MD Abstract Objectives/Hypothesis: Aerodigestive cancer risk of both lung and head and neck cancers has been linked to the genotoxic effects of tobacco use. These effects include upregulation of nuclear factor kappa-B (NF,B) and its downstream products associated with both lung and head and neck cancer malignant progression. Study Design: Bench Research. Methods: In the present study we examined the effects of cigarette smoke condensate on functional activation of NF,B in human papillomavirus (HPV)-transformed oral cavity cells (HOK 16B cells) and transformed bronchial epithelium (Beas2B cells) using the head and neck squamous cancer cell line, UMSCC 38, as a comparison. Luciferase reporter gene assays with two types of transiently transfected NF,B reporter genes were employed and downstream NF,B-dependent products, interleukin-6, interleukin-8, and vascular endothelial growth factor, were assayed by enzyme-linked immunosorbent assay. Results: All cell lines were able to dose dependently activate NF,B reporter genes after exposure to cigarette smoke condensate (P < .05). However, the HPV premalignant, transformed cell line had a much more robust NF,B response (3.45-fold) versus the squamous cancer cell line (1.62-fold) and SV40 transformed Beas2B (1.83). Both NF,B reporter genes had similar response curves. Conclusions: This study demonstrates cigarette smoke products might be more potent promoters of an NF,B-dependent progression from HPV+ premalignancy to cancer rather than after tumors are established. Future studies should focus on abrogating NF,B increases during malignant progression and premalignancy. This might be even more relevant in the HPV+ patient with premalignancy. Laryngoscope, 2010 [source] Immunohistochemical Study of HLA-G Expression in Lung Transplant RecipientsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2009O Brugière Human leukocyte antigen-G (HLA-G), a nonclassical HLA class I protein, promotes immune tolerance of solid-organ allografts, yet its role in lung transplantation (LTx) is unknown. We examined the expression of HLA-G in lung allografts through immunohistochemistry by a cross-sectional study of 64 LTx recipients, classified into four groups (stable patients, acute rejection [AR], bronchiolitis obliterans syndrome [BOS] and symptomatic viral shedders). A marked expression of HLA-G in bronchial epithelial cells (BEC) was frequently observed in stable recipients (n = 18/35 [51%]), but not in patients with AR (n = 14) or with BOS (n = 8). HLA-G was also expressed by 4 of 7 symptomatic viral shedders. In addition, HLA-G-positive patients from the stable group (n = 35) experienced lower incidence of resistant AR and/or BOS during long-term follow-up, as compared with their HLA-G-negative counterparts. Finally, in vitro data showed that interferon-,, a cytokine present in lung allograft microenvironment, upregulated HLA-G mRNA and protein expression in primary cultured human BEC. We conclude that HLA-G expression in the bronchial epithelium of lung allograft is elevated in some LTx recipients in association with their functional stability, suggesting a potential role of HLA-G as a tolerance marker. [source] Posttransplant Bronchiolitis Obliterans Syndrome Is Associated with Bronchial Epithelial to Mesenchymal TransitionAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2009S. Hodge Bronchiolitis obliterans syndrome (BOS) compromises lung transplant outcomes and is characterised by airway epithelial damage and fibrosis. The process whereby the normal epithelial configuration is replaced by fibroblastic scar tissue is poorly understood, but recent studies have implicated epithelial mesenchymal transition (EMT). The primary aim of this study was to assess the utility of flow cytometry in detecting and quantifying EMT in bronchial epithelial cells. Large airway brushings were obtained at 33 bronchoscopies in 16 BOS-free and 6 BOS grade 1,3 patients at 2,120 months posttransplant. Flow cytometry was used to assess expression of the mesenchymal markers ,SMA, S100A4 and ED-A FN and HLA-DR. TGF ,1 and HGF were measured in Bronchoalveolar lavage (BAL). Expression of all three mesenchymal markers was increased in BOS, as was HLA-DR. BAL HGF, but not TGF ,1 was increased in BOS. Longitudinal investigation of one patient revealed a 100% increase in EMT markers concurrent with a 6-fold increase in BAL TGF ,1 and the diagnosis of BOS at 17 months posttransplant. Flow cytometric evaluation of bronchial epithelium may provide a novel and rapid means to assess lung allografts at risk of BOS. [source] Morphological Studies on the Development of the Bronchial Epithelium of the Fetal Camel LungANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005G. Kamel Light microscopic observations revealed that in camel foetuses of 25 mm crown-to-rump length (CRL) the primordial tubular system of the prospective lung was formed of several tubules lined by undifferentiated columnar epithelium. Intra-epithelial neuroendocrine cells were the first elements to be differentiated in the lining epithelium of the primordial tubular system of the prospective lung as early as 25 mm CRL. On reaching 50,67 mm CRL, the primordial tubular system started to differentiate into two systems of primordial tubules, the prospective bronchial or light tubules and the future respiratory or dark tubules. The lining epithelium of the prospective bronchial tubules revealed a clear evidence of ciliogenesis as early as 80 mm CRL. From 800 mm CRL onwards, the bronchial epithelium demonstrated ciliated and non-ciliated secretory cells. The non-ciliated secretory cells of the bronchial epithelium of fetal camel lung showed moderate reaction to AB/PAS technique, for the first time, in fetuses reaching 600 mm CRL. [source] Hsp60 and Hsp10 down-regulation predicts bronchial epithelial carcinogenesis in smokers with chronic obstructive pulmonary diseaseCANCER, Issue 10 2006Francesco Cappello MD Abstract BACKGROUND. The relation between smoking, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) is an open field of investigation. A higher frequency of adenocarcinoma has been reported in patients with COPD. Heat shock proteins (Hsps) are implicated in tumoral cell growth and differentiation. The aim of the present study was to investigate the expression of Hsp60 and Hsp10 in bronchial biopsies from smokers with COPD and in 10 lung cancer patients and to evaluate the association between Hsps expression and carcinogenetic steps of LC. METHODS. An immunohistochemical study was performed for Hsp60 and Hsp10 in bronchial biopsies from 35 COPD (postbronchodilator forced expiratory volume in 1 second [FEV1]: 53 ± 19% [mean ± SD]) patients with a history of smoking (53 ± 34 pack/years) and in 10 patients with adenocarcinoma or adenosquamous carcinoma (ASC). Immunopositivity was quantified in the bronchial epithelium and in specimens with ASC. RESULTS. In smokers with COPD, 10 out of 35 patients had a normal bronchial epithelium (NBE), 12 showed basal cell hyperplasia (BCH), 5 squamous metaplasia (SM), and 8 dysplasia (Dy). It was found that 58 ± 23% and 54 ± 23% of NBE and 48 ± 29% and 52 ± 26% of BCH expressed Hsp60 and Hsp10, respectively; in contrast, only 3 ± 3% and 3.6 ± 2% of SM, 1.9 ± 4% and 1.1 ± 2% of Dy expressed Hsp60 and Hsp10, respectively. ASC specimens were negative for Hsps proteins. Interestingly, NBE also present at the edges of ASC specimens was negative for Hsps proteins. CONCLUSIONS. The loss of Hsp60 and Hsp10 immunopositivity is related to the development and progression of bronchial cancer in smokers with COPD. Cancer 2006. © 2006 American Cancer Society. [source] The role of MAP kinases in intracellular signal transduction in bronchial epitheliumCLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2000Puddicombe [source] Isomerism of the right atrial appendages: Clinical, anatomical, and microscopic study of a long-surviving case with asplenia and ciliary abnormalitiesCLINICAL ANATOMY, Issue 3 2003R. Raman Abstract This study describes a case of isomerism of the right atrial appendages (bilateral morphologically right atrial appendages associated with complex congenital cardiac lesions) with ciliary abnormalities. Detailed investigation included gross anatomic dissection, review of the clinical history, and light, confocal, and electron microscopy. Clinically, this 40-year-old, long-surviving male patient had relatively good health until 4 years before death, which was due to cardiac failure. Surgical intervention consisted only of a Blalock-Taussig shunt (anastomosis of the right subclavian artery to the right pulmonary artery) at 6 years of age. Despite the presence of complex cardiac malformations and asplenia, his longevity may be attributed to the connection of the pulmonary veins to the atrium without pulmonary venous obstruction, pulmonary valvar stenosis rather than atresia, no significant atrioventricular valve regurgitation, and no serious infections during his life. Microscopic examination of bronchial epithelium revealed a narrow, disorganized epithelium with abundant goblet cells and short, angulated cilia with a random orientation and possibly an abnormal central microtubule doublet. These abnormalities were not present in controls, and have been noted in primary ciliary dyskinesia (PCD) or Kartagener's syndrome. Because this syndrome has classically been thought to cause random lateralization resulting in a mirror-imaged arrangement of the organs, the occurrence of truly isomeric patterns is not widely recognized. Whereas polysplenia and left bronchial isomerism have been reported to occur in immotile cilia syndrome, this is the first report to present detailed postmortem anatomic evidence of isomerism of the right atrial appendages, right bronchial isomerism, and asplenia in association with microscopy suggesting ciliary abnormalities. Clin. Anat. 16:269,276, 2003. © 2003 Wiley-Liss, Inc. [source] | |||||||||||||