scholarly journals Dissimilarity of Airway and Lung Tissue Microbiota in Smokers Undergoing Surgery for Lung Cancer

2020 ◽  
Vol 8 (6) ◽  
pp. 794
Author(s):  
Lena Reinhold ◽  
Andreas Möllering ◽  
Sönke Wallis ◽  
Emanuel Palade ◽  
Kathrin Schäfer ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Upper Airway ◽  
Lung Parenchyma ◽  
Lower Airway ◽  
Tissue Samples ◽  
Peripheral Lung ◽  
Lower Airways ◽  
Human Airways ◽  
Rdna Analysis

Human airways are continuously colonized by microaspiration of microbiota. Less is known about the presence, origin and composition of microbiota in the lung parenchyma. In a study of 13 patients undergoing surgery for peripheral lung cancer microbiota composition was comparatively evaluated in upper airway, lower airway and lung tissue samples using 16S rDNA analysis. Bacterial density decreased stepwise from upper to lower airways and tissue. On a taxonomic level upper and lower airway microbiota were similar whereas lung tissue showed marked dissimilarities compared to lower airways that may reflect different environmental conditions shaping local microbiota and host immunity.

PneumoniaCheck: A Device for Sampling Lower Airway Aerosols

2010 ◽  
Vol 4 (4) ◽  
Author(s):  
Tamera L. Scholz ◽  
Prem A. Midha ◽  
Larry J. Anderson ◽  
David N. Ku
Keyword(s):  
Upper Airway ◽  
Lower Airway ◽  
High Quality ◽  
Effective Separation ◽  
Specimen Collection ◽  
Collection Device ◽  
Lower Lung ◽  
Lower Airways ◽  
Selective Collection

The pathogens causing pneumonia are difficult to identify because a high quality specimen from the lower lung is difficult to obtain. A new specimen collection device is designed to collect aerosol specimens selectively from the lower lung generated during deep coughing. The PneumoniaCheck device utilizes a separation reservoir and Venturi valve to segregate contents from the upper and lower airways. The device also includes several specially designed features to exclude oral contaminants from the sample and a filter to collect the aerosolized pathogens. Verification testing of PneumoniaCheck demonstrates effective separation of upper airway gas from the lower airway gas (p<0.0001) and exclusion of both liquid and viscous oral material (p<0.0001) from the collection chamber. The filters can collect 99.9997% of virus and bacteria sized particles from the sampled lower lung aerosols. The selective collection of specimens from the lower airway may aid in the diagnosis of specific pathogens causing pneumonia.

scholarly journals Alteration of Inflammatory Mediators in the Upper and Lower Airways under Chronic Intermittent Hypoxia: Preliminary Animal Study

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Eun Jung Lee ◽  
Woon Heo ◽  
Joo Young Kim ◽  
Hyungchul Kim ◽  
Min Jung Kang ◽  
...  
Keyword(s):  
Immune System ◽  
Sleep Apnea ◽  
Lung Tissue ◽  
Inflammatory Mediators ◽  
Intermittent Hypoxia ◽  
Allergic Inflammation ◽  
Upper Airway ◽  
Lavage Fluid ◽  
Lower Airway ◽  
Obstructive Sleep

Purpose. We hypothesized that CIH may affect the upper airway immune system and aimed to verify whether CIH can induce airway inflammation in a murine obstructive sleep apnea (OSA) model. Methods. C57BL6 male mice were exposed to intermittent hypoxia (CIH group; 5 ~ 21% FiO2, 120 sec cycles, 12 h/d, n=6) or room air (Sham group, n=6) for up to 4 weeks in identical chambers. Nasal and lung tissues and lavage fluid were collected and analyzed by multiplex assay. Lung lavage fluid was also utilized for FACS analysis to determine eosinophil count. Results. We determined the protein level of 24 different cytokines, chemokines, and inflammatory mediators. Among various cytokines, levels of IL-1α, IL-1β, IL-4, IL-6, and IL-13 were significantly elevated in nose or lung tissue from the CIH group. In addition, MCP-1 and periostin were elevated in nose and lung tissue and lavage fluid from the CIH group. Conclusions. CIH for 4 weeks altered the levels of inflammatory mediators in both the nose and lungs of mouse model. We suggest that the airway immune system may be deteriorated by CIH and allergic inflammation in the upper or lower airway could be worsened by sleep apnea.

scholarly journals Upper Airway Cough Syndrome in Pathogenesis of Chronic Cough

2020 ◽  
pp. S35-S42
Author(s):  
M. Lucanska ◽  
A. Hajtman ◽  
V. Calkovsky ◽  
P. Kunc ◽  
R. Pecova
Keyword(s):  
Chronic Cough ◽  
Sensory Nerve ◽  
Upper Airway ◽  
Vagal Afferents ◽  
Upper Airways ◽  
Cough Reflex ◽  
Postnasal Drip ◽  
Common Causes ◽  
Lower Airways ◽  
Human Airways

Cough is one of the most important defensive reflexes. However, extensive non- productive cough is a harmful mechanism leading to the damage of human airways. Cough is initiated by activation of vagal afferents in the airways. The site of their convergence is particularly the nucleus of the solitary tract (nTS). The second-order neurons terminate in the pons, medulla and spinal cord and there is also the cortical and subcortical control of coughing. Upper airway cough syndrome (UACS) – previously postnasal drip syndrome - is one of the most common causes of chronic cough together with asthma and gastroesophageal reflux. The main mechanisms leading to cough in patients with nasal and sinus diseases are postnasal drip, direct irritation of nasal mucosa, inflammation in the lower airways, upper airway inflammation and the cough reflex sensitization. The cough demonstrated by UACS patients is probably due to hypersensitivity of the upper airways sensory nerve or lower airways sensory nerve, or a combination of both. Further studies are needed to clarify this mechanism.

scholarly journals Regulation of Interaction between the Upper and Lower Airways in United Airway Disease

2019 ◽  
Vol 7 (2) ◽  
pp. 27 ◽  
Author(s):  
Akira Kanda ◽  
Yoshiki Kobayashi ◽  
Mikiya Asako ◽  
Koichi Tomoda ◽  
Hideyuki Kawauchi ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inhaled Corticosteroids ◽  
Upper Airway ◽  
Airway Disease ◽  
Comprehensive Approach ◽  
Lower Airway ◽  
T Helper 2 ◽  
Neural Modulation ◽  
Lower Airways ◽  
Novel Therapeutic

The concept of united airway disease comprises allergic rhinitis (AR) with asthma, and eosinophilic chronic rhinosinusitis (ECRS) with asthma. It embodies a comprehensive approach to the treatment of upper and lower airway inflammation. The treatment of upper airway inflammation reduces asthma symptoms and decreases the dose of inhaled corticosteroids (ICS) necessary to treat asthma. However, little is known about the mechanisms of interaction between upper and lower airway inflammation. Here we review these mechanisms, focusing on neural modulation and introduce a novel therapeutic approach to united airway disease using a fine-particle ICS. Our understanding of the relationship between the upper and lower airways and its contribution to T helper 2 (Th2)-skewed disease, such as AR and/or ECRS with asthma, has led us to this novel therapeutic strategy for a comprehensive approach to the treatment of upper airway inflammation with asthma.

Expression ofinterleukin-18andinterleukin-18 receptormRNA in lung tissue samples from non small lung cancer

2015 ◽  
Author(s):  
Charoula Eleni Giannakopoulou ◽  
Irene Papadopoulou ◽  
Grigorios Stratakos ◽  
George Kaltsakas ◽  
Fotis Vlastos ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Tissue Samples

Physiologic Differentiation of Upper and Lower Airway Obstruction

1977 ◽  
Vol 86 (5) ◽  
pp. 630-632 ◽  
Author(s):  
Frank F. Davidson ◽  
George W. Burke
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Lower Airway ◽  
Flow Volume ◽  
Initial Part ◽  
Maximal Flow ◽  
Volume Curve ◽  
Flow Volume Curve ◽  
Lower Airways ◽  
Lower Airway Obstruction

Usual lower airway obstruction and fixed upper airway obstruction can be differentiated physiologically by means of the flow-volume curve. Normally, maximal flow decreases nearly linearly as lung volume decreases during expiration. In lower airway obstruction, this decrease is greatest at the beginning of expiration resulting in a curve that is concave upward. In fixed obstruction (stenosis) flow is constant throughout the initial part of forced maximal expiration and throughout virtually all of inspiration. This results in a plateau or flat curve which is characteristic and different from the curve in obstruction of lower airways. Cases in which this differentiation is clinically important are discussed.

scholarly journals Lungs and hypoxia: a review of the literature

2021 ◽  
Vol 15 (1) ◽  
pp. 76-83
Author(s):  
Mustafa F. Sargon
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Tissue ◽  
Chronic Hypoxia ◽  
Lung Parenchyma ◽  
Lung Cancer Cells ◽  
Lung Fibroblasts ◽  
Lung Maturation ◽  
Micro Rnas ◽  
Molecular Studies

Acute, intermittent or chronic hypoxia have negative effects on lung maturation during the embryological period which has been shown by many experimental models designed on animal studies. The receptors responsible from the development of lungs in fetal period are affected from hypoxia. Hypoxia also affects the morphometry, anatomy and microscopy of lung tissue in the adults. In acute phase of hypoxia; lung parenchyma showed destructive oxidative changes. However, in later phases repair and proliferative processes were observed in the lung tissue. Damage to the lining layer of alveoli, accumulation of alveolar macrophages, oedematous changes in the lung parenchyma, mild oedema, inflammatory cell infiltration, increased number of type II pneumocytes and pulmonary fibrosis are the main findings in cases of hypoxia. Chronic hypoxia accentuates lung growth by increasing the lung parenchyma. Decrease of capillary volume and suppression of elastin repair in lung fibroblasts are other clinically important microscopic findings in hypoxia. Many molecular studies found in the literature revealed micro-RNAs to be involved in modulation of hypoxia-induced pulmonary hypertension. In animal models submitted to acute hypobaric hypoxia; the researchers detected an increase in eNOS mRNA which is responsible of the immediate response, producing nitric oxide that caused vasodilation and bronchodilation in lung tissue. In other molecular studies; suppression of many immune molecules, major changes at the levels of various enzymes and growth factors were detected in the researches. Additionally; hypoxia causes to an increase in the amount of lung cancer cells and therefore; induces the metastases of lung cancer cells to brain tissues.

Measurement of upper and lower airway resistance and conductance in man

1964 ◽  
Vol 19 (6) ◽  
pp. 1059-1069 ◽  
Author(s):  
Richard W. Blide ◽  
H. David Kerr ◽  
William S. Spicer
Keyword(s):  
Direct Measurement ◽  
Airway Resistance ◽  
Lateral Pressure ◽  
Upper Airway ◽  
Normal Subjects ◽  
Lower Airway ◽  
Upper Airway Resistance ◽  
Human Lungs ◽  
Lower Airways ◽  
Airway Conductance

The resistances to flow in the upper (Ruaw) and lower (Rlaw) airway of human lungs were measured simultaneously with total airway resistance (Raw) and the volume of thoracic gas (Vtg) using the plethysmographic method and lateral pressure taps at the tracheal and oral levels. Ruaw is found to decrease slightly in a curvilinear fashion with increasing Vtg while its reciprocal, Guaw, is linearly related to Vtg with a negative Vtg intercept in normal subjects. Lower airway conductance (Glaw) is linearly related to Vtg with a slope of approximately 1.0 liters/sec per cm H2O per liter. From the partitioned resistances it is deduced that total airway conductance (Gaw) is curvilinear but approximately linear over the majority of the Vtg. A method of calculating resistance and conductance in the upper and lower airways from Raw versus Vtg data is presented using the equation Raw = Vtg/(A @#X002B; B Vtg) where B2/A @#X003D; dGlaw/ dVtg. Three hundred and sixty-two records of Raw versus Vtg data from 22 normal, asthmatic, and bronchitic subjects are then evaluated by this method and the results compared to those obtained by direct measurement. intrathoracic or lower airway conductance; intrathoracic or lower airway resistance; extrathoracic or upper airway conductance; extrathoracic or upper airway resistance Submitted on November 8, 1963

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