Collection and Analysis of Respiratory Mucus from Subjects without Lung Disease

Rubin, Bruce K.; Ramírez, Óscar; Zayas, J. Gustavo; Finegan, Barry A.; King, Malcolm

doi:10.1164/ajrccm/141.4_pt_1.1040

Cited by 83 publications

(81 citation statements)

References 5 publications

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“…At the time the subject was extubated, the ETT was removed from the airway and mucus coating the tube was removed by gently scraping the ETT (37,39).…”

Section: Methodsmentioning

confidence: 99%

Serine Proteases Degrade Airway Mucins in Cystic Fibrosis

et al. 2011

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Airway mucins are the major molecular constituents of mucus. Mucus forms the first barrier to invading organisms in the airways and is an important defense mechanism of the lung. We confirm that mucin concentrations are significantly decreased in airway secretions of subjects with cystic fibrosis (CF) who have chronic Pseudomonas aeruginosa infection. In sputum from CF subjects without a history of P. aeruginosa, we found no significant difference in the mucin concentration compared to mucus from normal controls. We demonstrate that mucins can be degraded by synthetic human neutrophil elastase (HNE) and P. aeruginosa elastase B (pseudolysin) and that degradation was inhibited by serine proteases inhibitors (diisopropyl fluorophosphates [DFP], phenylmethylsulfonyl fluoride [PMSF], and 1-chloro-3-tosylamido-7-amino-2-heptanone HCl [TLCK]). The mucin concentration in airway secretions from CF subjects is similar to that for normal subjects until there is infection by P. aeruginosa, and after that, the mucin concentration decreases dramatically. This is most likely due to degradation by serine proteases. The loss of this mucin barrier may contribute to chronic airway infection in the CF airway.

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“…At the time the subject was extubated, the ETT was removed from the airway and mucus coating the tube was removed by gently scraping the ETT (37,39).…”

Section: Methodsmentioning

confidence: 99%

Serine Proteases Degrade Airway Mucins in Cystic Fibrosis

et al. 2011

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“…Healthy individuals produce much smaller amounts of airway secretions and do not expectorate mucus, but mucus samples from normal airways can be obtained following a standardized protocol of hypertonic saline exposure (270). Mucus samples can also be obtained by endotracheal suctioning of patients without airway diseases who are undergoing surgical procedures (231).…”

Section: E Mucins In Airway Secretions/lung Mucusmentioning

confidence: 99%

Respiratory Tract Mucin Genes and Mucin Glycoproteins in Health and Disease

Rose

Voynow²

2006

Physiological Reviews

945

892

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This review focuses on the role and regulation of mucin glycoproteins (mucins) in airway health and disease. Mucins are highly glycosylated macromolecules (≥50% carbohydrate, wt/wt). MUC protein backbones are characterized by numerous tandem repeats that contain proline and are high in serine and/or threonine residues, the sites of O-glycosylation. Secretory and membrane-tethered mucins contribute to mucociliary defense, an innate immune defense system that protects the airways against pathogens and environmental toxins. Inflammatory/immune response mediators and the overproduction of mucus characterize chronic airway diseases: asthma, chronic obstructive pulmonary diseases (COPD), or cystic fibrosis (CF). Specific inflammatory/immune response mediators can activate mucin gene regulation and airway remodeling, including goblet cell hyperplasia (GCH). These processes sustain airway mucin overproduction and contribute to airway obstruction by mucus and therefore to the high morbidity and mortality associated with these diseases. Importantly, mucin overproduction and GCH, although linked, are not synonymous and may follow from different signaling and gene regulatory pathways. In section i, structure, expression, and localization of the 18 human MUC genes and MUC gene products having tandem repeat domains and the specificity and application of MUC-specific antibodies that identify mucin gene products in airway tissues, cells, and secretions are overviewed. Mucin overproduction in chronic airway diseases and secretory cell metaplasia in animal model systems are reviewed in section ii and addressed in disease-specific subsections on asthma, COPD, and CF. Information on regulation of mucin genes by inflammatory/immune response mediators is summarized in section iii. In section iv, deficiencies in understanding the functional roles of mucins at the molecular level are identified as areas for further investigations that will impact on airway health and disease. The underlying premise is that understanding the pathways and processes that lead to mucus overproduction in specific airway diseases will allow circumvention or amelioration of these processes.

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“…15 In our study the evaluation of macroscopic appearance of the secretions was always performed by 2 investigators. To reduce the subjectivity of those evaluations we used the scale described by Deneuville et al 9 Regarding the samples from the without-lung-disease subjects, the mucus analysis was difficult, because small amounts were collected, so for this group we applied the method described by Rubin et al, 8 in which mucus is collected from the endotracheal tube used during a short surgical procedure in without-lung-disease subjects. The characteristics of the mucus deposited inside and outside the tube was compared.…”

Section: Discussionmentioning

confidence: 99%

“…6 In the without-lung-disease subjects the samples were collected immediately after removal of the endotracheal tube. The secretion sample that was deposited inside the tube was removed with a swab, according to the criteria and procedures described by Rubin et al 8 Respiratory secretions were assessed as follows:…”

Section: Methodsmentioning

confidence: 99%

The Influence of Purulence on Ciliary and Cough Transport in Bronchiectasis

et al. 2013

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BACKGROUND: Individuals with bronchiectasis exhibit colonization and infection of the respiratory system, with a consequent alteration of the macroscopic appearance of secretions, which ranges from mucoid to purulent. Purulence is related to the structural conformation, rheological profile, and transport indexes of mucus. We analyzed and compared the transport properties of respiratory secretions with mucoid appearance versus those with purulent appearance in patients with bronchiectasis and in subjects without lung disease. METHODS: In a simulated cough machine we assessed the mucociliary transport and contact angle of 32 mucoid and 19 purulent samples from subjects with bronchiectasis, and 21 samples from subjects without lung disease. RESULTS: Mucociliary transport was lower in the mucoid samples (0.78 ؎ 0.22) and in the purulent samples (0.73 ؎ 0.22) than in the samples from subjects without lung disease (1 ؎ 0.19). The purulent samples had less displacement in the simulated cough machine (7.57 ؎ 3 cm) than did the mucoid samples (23 ؎ 15 cm) or the samples from subjects without lung disease (34 ؎ 8.4 cm), as did the mucoid samples compared to the samples from subjects without lung disease. The purulent samples had a higher contact angle (25 ؎ 6.1°) than the mucoid samples (17 ؎ 7.8°) or the samples from subjects without lung disease (10 ؎ 2.5°), as did the mucoid samples compared to the samples from subjects without lung disease. CONCLUSIONS: Respiratory secretions in individuals with bronchiectasis have poor transport properties, which manifest as reduced mucociliary transport, reduced mucus transport by cough, and higher contact angle. These features were more accentuated in the purulent samples. This simple classification can be used by therapists to plan treatments, and by researchers to obtain more homogeneity between groups of subjects.

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Collection and Analysis of Respiratory Mucus from Subjects without Lung Disease

Cited by 83 publications

References 5 publications

Serine Proteases Degrade Airway Mucins in Cystic Fibrosis

Serine Proteases Degrade Airway Mucins in Cystic Fibrosis

Respiratory Tract Mucin Genes and Mucin Glycoproteins in Health and Disease

The Influence of Purulence on Ciliary and Cough Transport in Bronchiectasis

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