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Airway inflammation and illness severity in response to experimental rhinovirus infection in asthma.

Zhu J, Message SD, Qiu Y, Mallia P, Kebadze T, Contoli M, Ward CK, Barnathan ES, Mascelli MA, Kon OM, Papi A, Stanciu LA, Jeffery PK, Johnston SL - Chest (2014)

Bottom Line: At acute infection in subjects with asthma, CD4+ cells correlated with chest symptom scores (r = 0.69, P = .029), the fall in the 10% fall in FEV1 (PC10) correlated with neutrophils (r = -0.89, P = .029), the PC10 correlated inversely with CD4+ (r = -0.67, P = .023) and CD8+ cells (r = -0.65, P = .03), the 20% fall in FEV1 was inversely associated with CD20+ cells (r = -0.65, P = .03), and higher epithelial CD8+ cell counts were significantly associated with a greater maximum fall in FEV1 (r = -0.72, P = .03), whereas higher subepithelial mast cell counts were significantly associated with a lower maximum percent fall in peak expiratory flow (r = 0.8, P = .024).In subjects with asthma, rhinovirus infection induces bronchial mucosal neutrophilia and more severe monocyte/macrophage infiltration than in normal subjects.Airway neutrophils, eosinophils, and T and B lymphocytes during infection are related to virus load and physiologic and clinical severity, whereas mast cells are related to greater lung function.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The nature of bronchial mucosal inflammation and its physiologic and clinical significance in rhinovirus-induced asthma exacerbations is unclear. We investigated bronchial mucosal inflammatory response and its association with physiologic and clinical outcomes in an experimental model of rhinovirus-induced asthma exacerbations.

Methods: We used immunohistochemistry methods to detect phenotypes of inflammatory cells infiltrating the bronchial mucosa before and after experimental rhinovirus infection in 10 subjects with asthma and 15 normal subjects.

Results: Compared with baseline, rhinovirus infection significantly increased the number of epithelial (P = .005) and subepithelial (P = .017) neutrophils in subjects with asthma only and subepithelial CD68+ macrophages in both subjects with asthma (P = .009) and normal subjects (P = .018) but more so in those with asthma (P = .021). Numbers of CD45+, CD68+, and CD20+ cells; neutrophils; and eosinophils at day 4 postinfection were positively associated with virus load (r = 0.50-0.72, P = .016-0.03). At acute infection in subjects with asthma, CD4+ cells correlated with chest symptom scores (r = 0.69, P = .029), the fall in the 10% fall in FEV1 (PC10) correlated with neutrophils (r = -0.89, P = .029), the PC10 correlated inversely with CD4+ (r = -0.67, P = .023) and CD8+ cells (r = -0.65, P = .03), the 20% fall in FEV1 was inversely associated with CD20+ cells (r = -0.65, P = .03), and higher epithelial CD8+ cell counts were significantly associated with a greater maximum fall in FEV1 (r = -0.72, P = .03), whereas higher subepithelial mast cell counts were significantly associated with a lower maximum percent fall in peak expiratory flow (r = 0.8, P = .024).

Conclusions: In subjects with asthma, rhinovirus infection induces bronchial mucosal neutrophilia and more severe monocyte/macrophage infiltration than in normal subjects. Airway neutrophils, eosinophils, and T and B lymphocytes during infection are related to virus load and physiologic and clinical severity, whereas mast cells are related to greater lung function.

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Immunohistochemistry-stained cells are seen as red fuchsin positivity. A and B, Subject with asthma at day 4 rhinovirus 16 infection demonstrating more elastase-positive neutrophils (A) and CD68+ monocytes/macrophages (B) in bronchial epithelium and subepithelium. C and D, Subject with asthma at baseline showing fewer neutrophils (C) and CD68+ cells (D). E, Negative control sample shows an absence of signal. Scale bar = 20 μm for all images.
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fig01: Immunohistochemistry-stained cells are seen as red fuchsin positivity. A and B, Subject with asthma at day 4 rhinovirus 16 infection demonstrating more elastase-positive neutrophils (A) and CD68+ monocytes/macrophages (B) in bronchial epithelium and subepithelium. C and D, Subject with asthma at baseline showing fewer neutrophils (C) and CD68+ cells (D). E, Negative control sample shows an absence of signal. Scale bar = 20 μm for all images.

Mentions: Inflammatory cells were present in both the bronchial epithelial and the bronchial subepithelial compartments. Representative photographs are shown in Figures 1A‐E. Elastase-positive neutrophils (Fig 1A) and CD68+ monocytes/macrophages (Fig 1B) appeared to be more frequent in the bronchial mucosa of subjects with asthma during acute infection compared with baseline (Figs 1C, 1D). Application of irrelevant antibodies for the inflammatory cell markers was negative (Fig 1E).


Airway inflammation and illness severity in response to experimental rhinovirus infection in asthma.

Zhu J, Message SD, Qiu Y, Mallia P, Kebadze T, Contoli M, Ward CK, Barnathan ES, Mascelli MA, Kon OM, Papi A, Stanciu LA, Jeffery PK, Johnston SL - Chest (2014)

Immunohistochemistry-stained cells are seen as red fuchsin positivity. A and B, Subject with asthma at day 4 rhinovirus 16 infection demonstrating more elastase-positive neutrophils (A) and CD68+ monocytes/macrophages (B) in bronchial epithelium and subepithelium. C and D, Subject with asthma at baseline showing fewer neutrophils (C) and CD68+ cells (D). E, Negative control sample shows an absence of signal. Scale bar = 20 μm for all images.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4042510&req=5

fig01: Immunohistochemistry-stained cells are seen as red fuchsin positivity. A and B, Subject with asthma at day 4 rhinovirus 16 infection demonstrating more elastase-positive neutrophils (A) and CD68+ monocytes/macrophages (B) in bronchial epithelium and subepithelium. C and D, Subject with asthma at baseline showing fewer neutrophils (C) and CD68+ cells (D). E, Negative control sample shows an absence of signal. Scale bar = 20 μm for all images.
Mentions: Inflammatory cells were present in both the bronchial epithelial and the bronchial subepithelial compartments. Representative photographs are shown in Figures 1A‐E. Elastase-positive neutrophils (Fig 1A) and CD68+ monocytes/macrophages (Fig 1B) appeared to be more frequent in the bronchial mucosa of subjects with asthma during acute infection compared with baseline (Figs 1C, 1D). Application of irrelevant antibodies for the inflammatory cell markers was negative (Fig 1E).

Bottom Line: At acute infection in subjects with asthma, CD4+ cells correlated with chest symptom scores (r = 0.69, P = .029), the fall in the 10% fall in FEV1 (PC10) correlated with neutrophils (r = -0.89, P = .029), the PC10 correlated inversely with CD4+ (r = -0.67, P = .023) and CD8+ cells (r = -0.65, P = .03), the 20% fall in FEV1 was inversely associated with CD20+ cells (r = -0.65, P = .03), and higher epithelial CD8+ cell counts were significantly associated with a greater maximum fall in FEV1 (r = -0.72, P = .03), whereas higher subepithelial mast cell counts were significantly associated with a lower maximum percent fall in peak expiratory flow (r = 0.8, P = .024).In subjects with asthma, rhinovirus infection induces bronchial mucosal neutrophilia and more severe monocyte/macrophage infiltration than in normal subjects.Airway neutrophils, eosinophils, and T and B lymphocytes during infection are related to virus load and physiologic and clinical severity, whereas mast cells are related to greater lung function.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The nature of bronchial mucosal inflammation and its physiologic and clinical significance in rhinovirus-induced asthma exacerbations is unclear. We investigated bronchial mucosal inflammatory response and its association with physiologic and clinical outcomes in an experimental model of rhinovirus-induced asthma exacerbations.

Methods: We used immunohistochemistry methods to detect phenotypes of inflammatory cells infiltrating the bronchial mucosa before and after experimental rhinovirus infection in 10 subjects with asthma and 15 normal subjects.

Results: Compared with baseline, rhinovirus infection significantly increased the number of epithelial (P = .005) and subepithelial (P = .017) neutrophils in subjects with asthma only and subepithelial CD68+ macrophages in both subjects with asthma (P = .009) and normal subjects (P = .018) but more so in those with asthma (P = .021). Numbers of CD45+, CD68+, and CD20+ cells; neutrophils; and eosinophils at day 4 postinfection were positively associated with virus load (r = 0.50-0.72, P = .016-0.03). At acute infection in subjects with asthma, CD4+ cells correlated with chest symptom scores (r = 0.69, P = .029), the fall in the 10% fall in FEV1 (PC10) correlated with neutrophils (r = -0.89, P = .029), the PC10 correlated inversely with CD4+ (r = -0.67, P = .023) and CD8+ cells (r = -0.65, P = .03), the 20% fall in FEV1 was inversely associated with CD20+ cells (r = -0.65, P = .03), and higher epithelial CD8+ cell counts were significantly associated with a greater maximum fall in FEV1 (r = -0.72, P = .03), whereas higher subepithelial mast cell counts were significantly associated with a lower maximum percent fall in peak expiratory flow (r = 0.8, P = .024).

Conclusions: In subjects with asthma, rhinovirus infection induces bronchial mucosal neutrophilia and more severe monocyte/macrophage infiltration than in normal subjects. Airway neutrophils, eosinophils, and T and B lymphocytes during infection are related to virus load and physiologic and clinical severity, whereas mast cells are related to greater lung function.

Show MeSH
Related in: MedlinePlus