Published ahead of print on January 7, 2004, doi:10.1164/rccm.200308-1167OC Am. J. Respir. Crit. Care Med., Volume 169, Number 6, March 2004, 712-718 A more recent version of this article appeared on March 15, 2004
Submitted on August 26, 2003 Aggregations of Lymphoid Cells in the Airways of Non-Smokers, Smokers and AsthmaticsJohn G Elliot1,1 West Australian Sleep Disorders Research Institute, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia, 2 West Australian Sleep Disorders Research Institute, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia; Faculty of Regional Professional Studies, Edith Cowan University, Bunbury, Western Australia, Australia, 3 West Australian Sleep Disorders Research Institute, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia; School of Pharmacology and Medicine, University of Western Australia, Nedlands, Western Australia, Australia * To whom correspondence should be addressed. E-mail: ajames{at}it.net.au.
Persistent airway inflammation is present in asthma and in smokers with airflow obstruction. Isolated aggregations of lymphoid cells (IALC) may be sites of localised inflammatory cell activation. Their distribution and characteristics in cartilaginous airways were assessed in post-mortem tissue from non-smokers (n=10), smokers (n=9) and cases of nonfatal (n=10) and fatal asthma (n=10). IALC were present in 70-100% of cases, were more often in proximal than distal airways and 80% were confined to the outer airway wall. IALC with area >0.1mm2 were more frequent in both asthma groups (p <0.001). Airways with IALC had increased airway dimensions and greater numbers of eosinophils and lymphomononuclear cells. Within IALC, T and B lymphocytes were segregated and comprised >90% of all cells. Proliferating, apoptotic and antigen presenting cells (Rel-B+ and HLA-DR+) were <5%, 30-40% and <1% of all cells, respectively, and were similar in each case group. Vascular structures were increased (p<0.01) in cases of fatal asthma. These findings show that, even in non-smoking, nonasthmatic cases, IALC are common, show cellular organization and are associated with airway wall inflammation and remodeling. It remains to be determined if IALC contribute to or result from persistent airway inflammation in asthma. Key words: airway inflammation, remodelling
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