Trachea

Brand‐Saberi, Beate; Schäfer, Thorsten

doi:10.1016/j.thorsurg.2013.09.004

Cited by 83 publications

(43 citation statements)

References 19 publications

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“…Generally the BEM had an increased rate of mucus accumulation, as a consequence of a higher number of mucus-secreting cells with respect to NHBEs cultured on transwell membranes (data not shown). The mucociliary escalator is essential for the respiratory tract physiology and requires the participation of both ciliated (CCs) and goblet cells (GCs) [ 19 , 20 ]. Scanning electron microscopy (SEM) analysis of the BEM indicated a high-grade of mucinous differentiation ( Fig 3a ) and a well-distributed carpet of cilia covering the apical surface of the epithelium ( Fig 3d ).…”

Section: Resultsmentioning

confidence: 99%

3D Reconstruction of the Human Airway Mucosa In Vitro as an Experimental Model to Study NTHi Infections

et al. 2016

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We have established an in vitro 3D system which recapitulates the human tracheo-bronchial mucosa comprehensive of the pseudostratified epithelium and the underlying stromal tissue. In particular, we reported that the mature model, entirely constituted of primary cells of human origin, develops key markers proper of the native tissue such as the mucociliary differentiation of the epithelial sheet and the formation of the basement membrane. The infection of the pseudo-tissue with a strain of NonTypeable Haemophilus influenzae results in bacteria association and crossing of the mucus layer leading to an apparent targeting of the stromal space where they release large amounts of vesicles and form macro-structures. In summary, we propose our in vitro model as a reliable and potentially customizable system to study mid/long term host-pathogen processes.

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Section: Resultsmentioning

confidence: 99%

3D Reconstruction of the Human Airway Mucosa In Vitro as an Experimental Model to Study NTHi Infections

et al. 2016

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“…These results suggest that the impact of CSS exposure on the allergic nasal mucosa may differ by histological compartment. The respiratory mucosa exists both in the nose and in the trachea and bronchi (Brand-Saberi and Schafer, 2014). Recently, AEP, which is most typically caused by cigarette smoking, has been reported and gradually became known (Allen et al, 1989;Shiota et al, 2000;De Giacomi et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Effects of Cigarette Smoke on the Nasal Respiratory and Olfactory Mucosa in Allergic Rhinitis Mice

Ueha

Kondo

et al. 2020

Front. Neurosci.

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Objective: Cigarette smoke (CS) exposure reportedly enhances allergic airway inflammation. However, some studies have shown an association between current cigarette smoke exposure and a low risk for allergic rhinitis. Thus, the impact of CS exposure on allergic rhinitis remains poorly understood. The purpose of this study was to investigate the effects of CS on the respiratory mucosa (RM) and the olfactory epithelium (OE) of mice with allergic rhinitis, as the effects may differ depending on the nasal histological compartments.Methods: Eight-week-old male BALB/c mice were used for this study. We developed a mouse model of smoking by intranasally administering 10 doses of a CS solution (CSS), and a mouse model of allergic rhinitis by sensitization with intraperitoneal ovalbumin (OVA) injection and intranasal challenge with OVA. We examined the effects of CS on the nasal RM and OE in mice with or without allergic rhinitis using histological, serum, and genetic analyses. First, we examine whether CSS exposure induces allergic responses and then, examined allergic responses in the OVA-sensitized allergic rhinitis mice with or without CSS exposure.Results: Short-term CSS administration intensified allergic responses including increased infiltration of eosinophils and inflammatory cells and upregulation of interleukin-5 expression in the nasal RM of OVA-immunized mice, although only CSS induced neither allergic responses nor impairment of the RM and OE. Notably, repetitive OVA-immunization partially impaired the OE in the upper-lateral area, but CSS administration did not reinforce this impairment in OVA-induced allergic mice.Conclusion: Short-term CSS exposure strengthened allergic responses in the nasal RM and did not change the structure of the OE. These results suggest that patients with allergic rhinitis could experience exacerbation of allergic symptoms after CS exposure.

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“…In the present case without facial and neck burns, the anterior wall thickening of the upper trachea was quickly detected with point-of-care US immediately after laryngoscopic evaluation. The tracheal wall consists of the tunica adventitia, tracheal cartilage, and mucosa containing the tracheal glands [10]. In normal volunteers, hypoechoic cartilaginous rings and a hyperechoic air-mucosa interface are detectable on US [3,9,11].…”

Section: Discussionmentioning

confidence: 99%

Point-of-care ultrasound detection of tracheal wall thickening caused by smoke inhalation

Kameda

Fujita

2014

Crit Ultrasound J

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Smoke inhalation is the leading cause of death due to fires. When a patient presents with smoke inhalation, prompt assessment of the airway and breathing is necessary. Point-of-care ultrasonography (US) is used for the rapid assessment of critically ill or injured patients. We herein present a case report of a 54-year-old male who was transferred to the emergency department with shortness of breath, coughing, carbonaceous sputa, and rhinorrhea after inhaling smoke caused by a fire in his locked bedroom. He had no surface burns on the face and no edema or erosion in the oral cavity. He had hoarseness without stridor. His breath sounds were positive for expiratory wheezes. Laryngoscopy showed light edema and erosive findings on the supraglottic region. Bedside point-of-care US revealed hypoechoic thickening of the tracheal wall. The thickening was confirmed by a computed tomographic scan. The patient was carefully monitored with preparation for emergency airway management and was treated with supplemental oxygen and an aerosolized beta-2 adrenergic agonist in the intensive care unit. The symptoms were subsequently relieved, and reexamination by US after 2 days showed remission of the wall thickening. Point-of-care US may therefore be a useful modality for the rapid diagnosis and effective follow-up of tracheal wall thickening caused by smoke inhalation.

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Trachea

Cited by 83 publications

References 19 publications

3D Reconstruction of the Human Airway Mucosa In Vitro as an Experimental Model to Study NTHi Infections

3D Reconstruction of the Human Airway Mucosa In Vitro as an Experimental Model to Study NTHi Infections

Effects of Cigarette Smoke on the Nasal Respiratory and Olfactory Mucosa in Allergic Rhinitis Mice

Point-of-care ultrasound detection of tracheal wall thickening caused by smoke inhalation

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