Vitamin A–regulated ciliated cells promote airway epithelium repair in an asthma mouse model

Background: Asthma is a chronic inflammatory airway disease that causes damage to and exfoliation of the airway epithelium. The continuous damage to the airway epithelium in asthma cannot be repaired quickly and generates irreversible damage, repeated attacks, and aggravation. Vitamin A (VA) has multifarious biological functions that include maintaining membrane stability and integrity of the structure and function of epithelial cells. Our research explored the role of VA in repairing the airway epithelium and provided a novel treatment strategy for asthma. Methods: A mouse asthma model was established by house dust mite (HDM) and treated with VA by gavage. Human bronchial epithelial (16HBE) cells were treated with HDM and all-trans retinoic acid (ATRA) in vitro. We analyzed the mRNA and protein expression of characteristic markers, such as acetyl-α-tubulin (Ac-TUB) and FOXJ1 in ciliated cells and MUC5AC in secretory cells, mucus secretion, airway inflammation, the morphology of cilia, and the integrity of the airway epithelium. Results: Findings showed destruction of airway epithelial integrity, damaged cilia, high mucus secretion, increased MUC5AC expression, and decreased Ac-TUB and FOXJ1 expression in asthmatic mice. The VA intervention reversed the effect on Ac-TUB and FOXJ1 and promoted ciliated cells to repair the damage and maintain airway epithelial integrity. In 16HBE cells, we could confirm that ATRA promoted the expression of Ac-TUB and FOXJ1. Conclusion: These results demonstrated that VA-regulated ciliated cells to repair the damaged airway epithelium caused by asthma and maintain airway epithelial integrity. VA intervention is a potential adjunct to conventional treatment for asthma (AU)

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury

Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes (AU)

Anti-inflammatory and anti-remodeling effects of myrtenol in the lungs of asthmatic rats: Histopathological and biochemical findings

Introduction: Asthma is a chronic inflammatory disease of the airways. In this study, we evaluated the anti-inflammatory effects of myrtenol on the inflammatory indices in the pulmonary parenchyma and airways and on the inflammatory and oxidative indices of the bronchoalveolar lavage fluid (BALF) of asthmatic rats. Methods: The allergic asthma was induced by sensitization (two weeks) followed by the inhalation of ovalbumin (four weeks). Animals were divided into two main groups: (1) Histopathology, and (2) measurement of inflammatory and oxidative biomarkers in the BALF. Each main group was subdivided into four subgroups: Control, Asthma, Asthma+Dexamethasone and Asthma + Myrtenol. (-)-Myrtenol (50 mg/kg) or Dexamethasone (2.5 mg/kg) was administered intraperitoneally once a day for one week, at the end of the inhalation period. On day 50, lung histopathologic parameters and inflammatory indices in BALF including INF-gamma, IL-10, IL-1Beta, and TNF-alfa and oxidative stress biomarkers (MDA, SOD, and GPX) were measured. Result: In the Asthma group, leukocyte infiltration, the thickness of smooth muscle and epithelium of airways wall and the number of goblet cells increased. Myrtenol reduced all of the above-mentioned indices except the epithelium thickness. It also inhibited the increase in BALF IL-1Beta, TNF-alfa and MDA and increased the levels of INF-gamma, IL-10 and SOD. Conclusion: Our results suggest that myrtenol reduced damage caused by experimental asthma by reducing the inflammatory indices, normalizing the level of interleukins and balancing oxidative stress in the lungs. It also prevented airway remodeling. Myrtenol may be suggested as a potent herbal medicine for the treatment of allergic asthma

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Quiste de duplicación gástrica de epitelio respiratorio: una lesión infrecuente de difícil diagnóstico diferencial / Gastric duplication cyst with respiratory epithelium: An uncommon injury that has a difficult diferential diagnosis

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From rhinitis to asthma: Is small airway disfunction the clue?

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Airway epithelium plays a leading role in the complex framework underlying respiratory allergy

Airway epithelium is the cellular structure with the greatest surface exposed to a plethora of environmental airborne substances, including microorganisms, respiratory viruses, air pollutants, and allergens. In addition to being a protective physical barrier at the air-liquid interface, the airway epithelium acts as an effective chemical and immunological barrier that plays a crucial role in orchestrating the immune response in the lungs, by supporting the activation, recruitment, and mobilization of immune cells. Airway epithelium dysfunction has been clearly associated with various airway inflammatory diseases, such as allergic asthma. Although it is not fully understood why a person develops respiratory allergy, a growing body of evidence shows that the nature of the host's immune response is strongly determined by the state of the airway epithelium at the time of contact with the inhaled allergen. Our review highlights the physiological state of airway epithelium as a key element in the development of allergy and, particularly, in exacerbation of asthma. We review the role of physiological oxidants as signaling molecules in lung biology and allergic diseases and examine how high exposure to air pollutants (eg, cigarette smoke and diesel particles) can contribute to the increased incidence of respiratory allergy and exacerbation of the disease (AU)

El epitelio pulmonar constituye la barrera celular más susceptible a la acción deletérea de la multitud de agentes que se encuentran en el ambiente, incluidos los alérgenos. Además de prevenir su acceso al organismo, la barrera epitelial de las vías respiratorias juega un papel inmunomodulador crucial, regulando de forma local la acción de las células del sistema inmune subyacentes. Una disfunción epitelial, provocada tanto directa como indirectamente por la acción de los aeroalérgenos, parece ser una de las causas principales de desregulación de la homeostasis pulmonar, causando una respuesta proinflamatoria descontrolada que cada vez más autores atribuyen al origen de las reacciones alérgicas. En esta revisión se quiere destacar el papel de la barrera epitelial pulmonar como regulador de la respuesta inmune en el contexto de la alergia. Las enfermedades crónicas que afectan a las vías respiratorias, tales como el asma alérgica, muestran frecuentemente una función epitelial defectuosa, apoyando así la hipótesis antes mencionada que subyace al origen de la alergia. El impacto de otros contaminantes ambientales -como virus respiratorios, bacterias, humo del tabaco y partículas diésel- sobre la integridad epitelial, así como su influencia en la biología redox pulmonar relacionada con el desarrollo de la respuesta alérgica, también se abordarán en la presente revisión (AU)

Disfunción endotelial medida con flujimetría láser-doppler en pacientes con Síndrome de apneas-hipopneas del sueño. Efecto del tratamiento con presión positiva continua en la vía aérea / Endothelial dysfunction measured with a Laser-Doppler flowmetry in patients with sleep apnea-hypopnea syndrome. The effecto ftreatment with continuous positive airway pressure

INTRODUCCIÓN: El SAHS se relaciona con el desarrollo de enfermedades cardiovasculares, con un aumento de la mortalidad de los pacientes que lo padecen. Dentro del espectro de la afectación cardiovascular, cada día se reconoce como más importante la disfunción endotelial. MATERIAL Y MÉTODOS: Estudio prospectivo de pacientes diagnosticados de SAHS mediante poligrafía respiratoria con indicación de CPAP. La función endotelial se ha valorado mediante la técnica no invasiva de flujimetría láser-doppler, realizada de manera basal y tras 3 meses de tratamiento con CPAP. RESULTADOS: Hemos observado una correlación significativa entre los parámetros oximétricos de la poligrafía respiratoria y algunos parámetros de la flujimetría basal. Además, hemos encontrado un aumento significativo en el valor del área bajo la curva y una disminución del valor de la pendiente de la flujimetría láser doppler (que indica mejoría de la función endotelial) tras la realización del tratamiento con CPAP durante 3 meses

INTRODUCTION: Sleep apnea-hypopnea syndrome (SAHS) is linked to the development of cardiovascular diseases, with increased mortality among these patients. Within the range of cardiovascular affections, the importance of endothelial dysfunction is evermore recognized. MATERIAL AND METHODS: Prospective studies in patients with SAHS using respiratory polygraph with continuous positive airway pressure (CPAP). Endothelial function has been assessed using non-invasive Laser-Doppler Flowmetry, both basal and after 3 months of treatment with CPAP. RESULTS: A significant correlation was observed between the respiratory polygraph oximetry parameters and certain basal flowmeter parameters. Moreover, a significant increase in the value of the area under the curve(AUC) and a decrease in the slope of the Laser-Doppler flowmetry was seen (thus indicating an improvement of endothelial function) after a 3-month treatment with CPAP

Linfoma de tejido linfoide asociado con mucosas con afectación traqueal secundaria: un diagnóstico infrecuente / Tracheal Secondary Involvement by mucosa-associated lymphoid tissue Lymphoma - A Rare Diagnosis

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Effect of exercise duration on pro-oxidants and pH in exhaled breath condensate in humans

Exercise promotes pulmonary oxidative imbalance. In this regard, some evidence has been obtained from the study of exhaled breath condensate (EBC) during urban races, in which the factors involved in the occurrence of this process are still not characterized. In this paper, under laboratory conditions, both the role of time of exercise on the generation of pro-oxidants (H2O2, NO2-) and pH have been assessed in EBC of 16 under-trained subjects who completed three tests of cycloergometric exercise at low intensity (30 % of VO2 max) with a duration of 10, 30, and 90 min. Samples were obtained as follows: immediately before and at 80 min post exertion in each test. In the 90-min test, an increase in H2O2, NO2- concentration in EBC at 80 min post exertion with no changes in the pH was observed. Total O2 consumption and total ventilation weakly correlated with the changes in H2O2 and NO2-. In conclusion, the concentration of pro-oxidants in the EBC depends on the duration of the exercise when it is performed at low intensity under laboratory conditions (AU)

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Evaluación del antígeno galactomanano y la PCR en tiempo real de Aspergillus para el diagnóstico de aspergilosis invasiva / Evaluation of galactomannan antigen and Aspergillus real time PCR for diagnosis of Invasive Aspergillosis

Introducción. Comparar las pruebas de antígeno galactomanano (AG) y moleculares (PCRrt) con el cultivo para el diagnóstico de aspergilosis invasiva (AI). Material y métodos. Se analizaron 472 muestras: 388 respiratorias, 84 sueros, de 271 pacientes. En las respiratorias se realizó cultivo y AG y en los sueros AG. En caso de discordancia entre ellas se realizó PCR. Resultados. El AG resultó positivo en 22 sueros de 84, 21 tenían esta prueba positiva en muestra respiratoria. De 62 sueros con AG negativo, 45 fueron también negativas en muestras respiratorias. El cultivo fue positivo en 37, coincidiendo todas con AG positivo. Comparando cultivo con AG, éste mostró un VPP= 23%, VPN=100%, S= 100% y E=52%. La PCRrt respecto al cultivo mostró un VPP= 69%, VPN= 89%, S= 64% y E= 82%. En los sueros entre AG y PCR encontramos 60% de discrepancias. Conclusiones. Consideramos muy útil la detección de AG en suero combinada con cultivo y AG en muestras respiratorias para el diagnóstico de AI, precisando PCRrt más estudios para su estandarización y establecer puntos de corte (AU)

Introduction. The aim of the study was to compare the galactomannan antigen (GA) and molecular biology (PCRrt) tests with the culture in the diagnosis of invasive aspergillosis (IA). Material and methods. Four hundred and seventy two samples were analyzed: 388 respiratory and 84 serum samples from 271 patients. Culture and GA were evaluated in the respiratory samples and GA in the serum samples. PCR was used when discrepancies were observed among culture and GA tests. Results. The detection of GA in serum was positive in 22 (of 84), 21 had the test positive respiratory sample. Of the 62 sera with negative GA, 45 were also negative respiratory specimens. The culture was positive in 37 of which were positive for GA. Comparing culture with AG, it showed PPV=23%, NPV=100%, S=100% and E=52%. The PCR showed respect to culture: PPV=69%, NPV=89%, S=64% and E=82%. In sera were found in 60% discrepancies between PCRrt and GA. Conclusions. We consider useful the GA detection in serum combined with culture and GA in respiratory samples, for diagnosis of AI. PCR requires further studies for standardization and set breakpoints (AU)

Estudio del efecto de citocinas proinflamatorias en las células epiteliales de pacientes fumadores con o sin EPOC / A study of the Effect of Proinflammatory Cytokines on the Epithelial Cells of Smokers, with or without COPD

Introducción: El humo de tabaco es la principal causa de la inflamación en la EPOC. Los mecanismos quediferencian a los fumadores que desarrollan EPOC son diversos. En este estudio analizamos la diferentepresencia de citocinas en secreciones respiratorias de pacientes fumadores con o sin EPOC y las propiedadessecretoras del epitelio bronquial diferenciado, obtenido de los propios individuos tras su exposiciónal humo de tabaco.Material y métodos: Se estudió a 27 pacientes fumadores, 12 de ellos con EPOC no tratados previamentecon esteroides. En 11 se obtuvo la muestra mediante esputo inducido y el resto procedía del aspiradobronquial tras fibrobroncoscopia. Se determinaron las concentraciones de IL8, IL13 y TNF en el sobrenadante.Se compararon los resultados obtenidos entre individuos con o sin EPOC y se investigó su relacióncon la gravedad de la EPOC expresada según el grado de obstrucción, disnea, presencia de hipersecrecióne intensidad del tabaquismo. Se obtuvieron cultivos de células diferenciadas epiteliales bronquiales,mediante interfase aire-líquido en 4 individuos fumadores. Las muestras fueron expuestas a concentracionescrecientes de humo de tabaco (5-20%) y se determinó la expresión epitelial de ARNm de Muc5AC,IL8 y TNF .Resultados: Los pacientes con EPOC tenían valores significativamente más altos de IL8 que los fumadoressanos (41 [22] vs. 21 [12] pM). Los valores de IL8 se correlacionaron de forma significativa con la gravedadde la obstrucción (r = 0,6; p < 0,05), disnea (r = 0,45; p < 0,05) y la presencia de hipersecreción. No habíarelación entre las citocinas y la intensidad o duración del hábito tabáquico. El humo de tabaco produjoun incremento dependiente de la dosis en la expresión de ARNm para Muc5AC, IL8 y TNF. Conclusiones: Existen diferencias en la producción de citocinas, fundamentalmente IL8, entre individuosfumadores sanos o con EPOC que podrían ser justificadas por la acción directa del humo de tabaco sobrelas células epiteliales (AU)

Introduction: Cigarette smoke is the main cause of inflammation in COPD. The mechanisms that differentiatesmokers who develop COPD are diverse. In this study, we analyzed the presence of cytokines in therespiratory secretions of smokers with or without COPD and the secretory properties of the differentiatedbronchial epithelium obtained from the individuals themselves after exposure to tobacco smoke.Material and methods: Twenty-seven smokers were studied, 12 of whom had COPD that had not beenpreviously treated with steroids. In 11, samples were obtained by means of induced sputum, and the remaining samples were collected from bronchial aspiration after bronchoscopy. Concentrations of IL-8,IL-13 and TNF in the supernatant were determined. The results obtained were compared between individualswith and without COPD, and we studied their relationship with the severity of COPD as expressedby the degree of obstruction, dyspnea, presence of hypersecretion and intensity of smoking. Bronchialepithelial cell cultures were obtained by air-liquid interface in 4 smokers. The samples were exposed toincreasing concentrations of cigarette smoke (5-20%) and the epithelial mRNA expressions of MUC5AC,IL8 and TNF were determined.Results: COPDpatients had significantly higher values of IL-8 than healthy smokers (41 [22] vs. 21 [12] pM).The values of IL-8 correlated significantly with the severity of the obstruction (r = 0.6; p < 0.05), dyspnea(r = 0.45; p < 0.05) and the presence of hypersecretion. There was no relationship between cytokines andthe intensity or duration of the tobacco habit. Cigarette smoke produced a dose-dependent increase inthe expression of RNAm for Muc5AC, IL8 and TNF .Conclusions: There are differences in cytokine production (fundamentally IL8) between smokers and smokerswith COPD which could be explained by the direct action of cigarette smoke on epithelial cells (AU)

Incarceración total de prótesis fonatoria en la mucosa traqueoesofágica. Informe de una nueva complicación con el uso de prótesis fonatorias / Total voice prosthesis incarceration in the trachaeo-oesophageal mucosa. Report of a new complication when using phonatory prostheses

Presentamos los casos de 3 pacientes atendidos en el Servicio de Otorrinolaringología de nuestro centro por haber presentado un carcinoma epidermoide de laringe que requirió laringectomía total. Se les realizó fistuloplastia primaria y colocación de prótesis fonatoria Provox. En estos 3 casos se produjo un crecimiento de tejido granulomatoso alrededor de la fístula, que acabó por enterrar completamente la prótesis fonatoria en la mucosa traqueoesofágica. En dos de los casos fue posible la extracción de la prótesis mediante esofagoscopia rígida. En el otro caso, se precisó la realización de un abordaje externo mediante incisión periestomal para lograr la extracción de la prótesis. En los pacientes en que se pudo extraer la prótesis se recolocó una nueva en el acto. En el otro caso, se esperó a la completa cicatrización del tejido para realizar una fistuloplastia secundaria a los 3 meses de la intervención (AU)

We report the cases of three patients seen at the Otolaryngology Department after presenting a laryngeal carcinoma that required total laryngectomy, followed by trachaeo-oesophageal puncture and Provox voice prosthesis positioning. In all cases the growth of granulomatous tissue totally incarcerated the prosthesis in the trachaeo-oesophageal mucosa. In two of the cases the prosthesis could be extracted by oesophagoscopy and a new prosthesis was positioned in the same surgery. In the other case an external approach was performed using a peristomal wound to extract the prosthesis. In this case a new trachaeo-oesophageal puncture was performed 3 months after the extraction (AU)

Endobronchitis by Scedosporium apiospermum in a child with cystic fibrosis

Presentamos un caso de endobronquitis por Scedosporium apiospermum en una niña con fibrosis quística. El diagnótico se confirmó mediante laboratorio. La citología del aspirado bronquial mostró la presencia de grandes cantidades de micelio dicotomizado septado. El cultivo del aspirado bronquial en tres muestras consecutivas, mostró la presencia de Scedosporium apiospermum en cultivo puro. El estudio de la superficie de la mucosa, mediante microscopia electrónica de barrido, reveló la presencia de micelio escaso, contrastando con la presencia de una gran cantidad de conidias. La microscopia electrónica de transmisión realizada en los cortes de la mucosa bronquial, reveló la presencia de infiltrado inflamatorio constituido por macrófagos, leucocitos polimorfonucleares y una gran cantidad de micelio dicotomizado y macrófagos con micelio y conidis en el interior de fagosomas. La paciente fue tratada con anfotericina B e itraconazol(AU)

A case of endobronchitis by Scedosporium apiospermum in a child with cystic fibrosis is presented. The bronchial aspirate's cytology showed the presence of a large amount of septated-dichotomized hyphae. The bronchial aspirate's culture showed the presence of Scedosporium apiospermum in a pure culture of three consecutive samples. The scanning electron microscopy study of the mucosal surface revealed scarce mycelia with the presence of abundant conidiae. The transmission electron microscopy of the mucosa revealed inflammatory infiltrates constituted by macrophages, polymorphonuclear leukocytes, a lot of dichotomized mycelia and macrophages with hyphae and conidiae within the phagosomes. The patient was treated with amphotericin B and itraconazole(AU)

Coristoma con heterotopia gástrica y respiratoria en un neonato / Choristoma with gastric and respiratory heterotopy in a neonate

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Expresión de las anexinas A1 y A2 en la mucosa del tracto aerodigestivo superior / Expression of annexins A1 and A2 in the mucosa of the upper aerodigestive tract

Introducción: Las anexinas A1 y A2 se han relacionado con el mantenimiento de la integridad tisular. Han sido identificadas en varios tejidos humanos pero su expresión en el tracto aerodigestivo superior es poco conocida. El objetivo de este trabajo es estudiar la expresión de estas proteínas en la mucosa del tracto aerodigestivo superior. Material y métodos: Se estudian muestras de mucosa respiratoria (nasal y laríngea) y digestiva (de cavidad oral y faringe) de pacientes intervenidos de cirugía no oncológica. La expresión de las anexinas A1 y A2 se estudia por inmunohistoquímica. Resultados: Ambas anexinas se expresan tanto en el epitelio ciliado pseudoestratificado como en el plano poliestratificado no queratinizado, pero con un patrón diferente; la anexina A1 se expresa en las células más diferenciadas, mientras que la A2 lo hace en las menos diferenciadas (con la excepción de los cilios de las células ciliadas). Conclusión: Aunque las anexinas A1 y A2 están estructural y filogenéticamente relacionadas, su diferente expresión en la mucosa del tracto aerodigestivo superior sugiere que participan en funciones claramente diferenciadas (AU)

INTRODUCTION: Annexins A1 and A2 have been related with the maintenance of tissue integrity. They have been identified in a wide variety of tissues, but little is known regarding their expression in upper the aerodigestive tract. The aim of this work is to describe the expression of these proteins in the mucosa of the upper aerodigestive tract. MATERIAL AND METHODS: Tissue samples from respiratory (nasal and laryngeal) and digestive (oral and pharyngeal) mucosa from non-oncological patients were studied. Annexin A1 and A2 expression was determined by immunohistochemistry. RESULTS: Both annexins were expressed in the ciliated and in the stratified non-keratinized epithelia, but with a different pattern; ANXA1 was expressed in the more differentiated cells whereas ANXA2 was expressed in the less differentiated ones (with the exception of the cilia of ciliated cells). CONCLUSION: Although annexins A1 and A2 are structurally and philogenetically related its expression pattern in the upper aerodigestive tract suggests that they have different functions (AU)

Rhinitis as a precursor for asthma / Rinitis precursora de asma

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