The Relationship of Sinusitis and Bronchiectasis

Quinn, Lester H.; Meyer, Ovid O.

doi:10.1001/archotol.1929.00620050048003

Cited by 86 publications

(29 citation statements)

References 4 publications

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“…Any change in the lung microbial communities, within an individual or as viewed across disease states, must be the result of a change in one of these three factors. Evidence from our lab and others strongly points to subclinical microaspiration as the primary source of microbial immigration 5,14,20–23 (Dickson et al , submitted). Subclinical microaspiration of pharyngeal secretions among healthy subjects is well-documented.…”

Section: The Immunoecology Of the Respiratory Tract Microbiomementioning

confidence: 60%

The respiratory tract microbiome and lung inflammation: a two-way street

2017

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The lungs are not sterile or free from bacteria; rather, they harbor a distinct microbiome whose composition is driven by different ecological rules than for the gastrointestinal tract. During disease, there is often a shift in community composition towards Gammaproteobacteria, the bacterial class that contains many common lung-associated gram-negative “pathogens.” Numerous byproducts of host inflammation are growth factors for these bacteria. The extracellular nutrient supply for bacteria in the lungs, which is severely limited during health, markedly increases due to the presence of mucus and vascular permeability. While Gammaproteobacteria benefit from airway inflammation, they also encode molecular components that promote inflammation, potentially creating a cyclical inflammatory mechanism. In contrast, Prevotella species that are routinely acquired via microaspiration from the oral cavity may participate in immunologic homeostasis of the airways. v Areas of future research include determining for specific lung diseases (1) whether an altered lung microbiome initiates disease pathogenesis, promotes chronic inflammation, or is merely a marker of injury and inflammation, (2) whether the lung microbiome can be manipulated therapeutically to change disease progression, (3) what molecules (metabolites) generated during an inflammatory response promote cross-kingdom signaling, and (4) how the lung “ecosystem” collapses during pneumonia, to be dominated by a single pathogen.

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Section: The Immunoecology Of the Respiratory Tract Microbiomementioning

confidence: 60%

The respiratory tract microbiome and lung inflammation: a two-way street

2017

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“…However, mineral oil such as liquid paraffin is one of the most frequent sources of exogenous lipid (1). It is postulated that mineral oils could inhibit the cough reflex and ciliary motility, thus facilitating inhalation (8). Another study revealed that mineral oil applied on rabbit and human nasal epithelium markedly impaired the movement of the mucus blanket by altering the physical properties of the secretions (9).…”

Section: Discussionmentioning

confidence: 99%

Exogenous Lipoid Pneumonia Following Ingestion of Liquid Paraffin.

et al. 2002

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An asymptomatic patient with exogenous lipoid pneumonia (ELP) due to silent aspiration of liquid paraffin ingested as a lubricant was diagnosed by bronchoalveolar lavage (BAL). BAL fluid separated into oily upper phase and lower aqueous phase spontaneously. Microscopic analysis of BAL cells revealed the presence of lipid-laden alveolar macrophages. Classic histochemical staining and electron microscope examination indicated that neutral lipid was dominant but phospholipid was also present in the lipidladen macrophages. Together with the history of ingestion of liquid paraffin, we identified that the ingested liquid paraffin was the origin of the neutral lipid in the lipid-laden macrophages observed in the BAL fluid. (Internal Medicine 41: 483-486, 2002)

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“…Diseases of the upper respiratory tract are frequently seen in association with pulmonary disease; in particular, there is a well-established association between bronchiectasis and chronic sinusitis (Thomson, 1914;Quinn and Meyer, 1929;Hogg and Brock, 1950;Szpunar and Okrasinska, 1962). Furthermore, rhino-sinusitis is often associated with a chronic productive cough similar to that of chronic bronchitis (Hinshaw and Garland, 1963).…”

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confidence: 99%

A comparison of changes in the mucous glands and goblet cells of nasal, sinus, and bronchial mucosa

Burton

Dixon

1969

Thorax

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A comparison of mucous gland size in the bronchial and nasal mucosa was performed on material from 24 random necropsies. The Reid index and counts of mucous gland acini were used as measures of hypertrophy. In 14 of these cases the relationship between goblet cell hyperplasia in the sinus mucosa and the presence of chronic bronchitis was investigated by comparing the proportion of goblet cells with the corresponding Reid index. No significant correlation was found between nasal and bronchial mucous gland size, and no association was demonstrated between the proportion of goblet cells in the sinus mucosa and the presence of chronic bronchitis as assessed by the Reid index. These findings suggest that a direct association between chronic bronchitis and chronic sinusitis probably does not exist, and that the inclusion of chronic bronchitis in the 'sino-bronchial syndrome' is not valid. We feel that this term should be restricted to the association of chronic sinusitis with bronchiectasis or adult pulmonary mucoviscidosis. If either infection or air pollution were the predominant cause of mucous gland hypertrophy, changes similar to those found in the bronchi would be expected in the nose and sinuses. Since our results show they are not found there, then some other factor, such as cigarette smoking, must be responsible.

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The Relationship of Sinusitis and Bronchiectasis

Cited by 86 publications

References 4 publications

The respiratory tract microbiome and lung inflammation: a two-way street

The respiratory tract microbiome and lung inflammation: a two-way street

Exogenous Lipoid Pneumonia Following Ingestion of Liquid Paraffin.

A comparison of changes in the mucous glands and goblet cells of nasal, sinus, and bronchial mucosa

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