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Respirology. 2018 Dec;23(12):1138-1145. doi: 10.1111/resp.13360. Epub 2018 Jun 26.

Inflammation-dependent and independent airway remodelling in asthma.

Author information

1
West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Perth, WA, Australia.
2
School of Human Sciences, University of Western Australia, Perth, WA, Australia.
3
Centre for Neonatal Research and Education, School of Paediatrics and Child Health, University of Western Australia, Perth, WA, Australia.
4
Department of Pathology, University Medical School, Sao Paulo, Brazil.
5
Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
6
Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, VIC, Australia.
7
Department of Respiratory Medicine, Children's Hospital at Westmead, Sydney, NSW, Australia.
8
Department of Pathology and Laboratory Medicine, University of Calgary, Calgary, AB, Canada.
9
School of Medicine and Pharmacology, University of Western Australia, Perth, WA, Australia.

Abstract

BACKGROUND AND OBJECTIVE:

The pathology of asthma is characterized by airway inflammation (granulocytic (GA) or paucigranulocytic (PGA)) and remodelling of airway structures. However, the relationship between inflammatory phenotypes and remodelling is unclear. We hypothesized that some features of airway remodelling are dependent on granulocytic airway inflammation while others are not.

METHODS:

Post-mortem airway sections from control subjects (n = 48) and cases of asthma with (n = 51) or without (n = 29) granulocytic inflammation in the inner airway wall were studied. The thickness of the airway smooth muscle (ASM) layer, basement membrane and inner and outer airway walls, the size and number of ASM cells, the volume fraction of extracellular matrix within the ASM layer, ASM shortening and luminal mucus were estimated. Airway dimensions were compared between the three subject groups.

RESULTS:

In cases of PGA, only the thickness of the ASM layer and basement membrane was increased compared with control subjects. In cases of GA, not only the ASM and basement membrane were increased in thickness, but there was also increased inner and outer airway wall thickness and increased narrowing of the airway lumen due to ASM shortening and mucus obstruction, compared with control subjects. Granulocytic inflammation was observed more often in cases of fatal asthma.

CONCLUSION:

These findings suggest that inner and outer wall thickening coexists with inflammation, whereas thickening of the ASM layer and basement membrane may be present even in the absence of inflammation. Remodelling of the ASM layer and basement membrane may therefore be less susceptible to anti-inflammatory therapy.

KEYWORDS:

airway morphology; asthma; inflammation; stereology

PMID:
29943875
DOI:
10.1111/resp.13360
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