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Reduced apoptosis of memory T-cells in the inner airway wall of mild and severe asthma

J. P. Lamb^1,2, A. James^1,3, N. Carroll¹, L. Siena⁴, J. Elliot¹ and A. M. Vignola^4,5

¹ Dept of Pulmonary Physiology, Sir Charles Gairdner Hospital, ² Dept of Physiology, ³ School of Medicine and Pharmacology, University of Western Australia, Nedlands, Australia, ⁴ Instituto di Biomedicinia e Moleculare, ⁵ Cattedra di Malattie Fisiopatologica, Palermo, Italy

CORRESPONDENCE: A. James, Dept of Pulmonary Physiology, Sir Charles Gairdner Hospital, Hospital Avenue, 6009 Nedlands, WA, Australia. Fax: 61 89346 2034. E-mail: ajames@it.net.au

Keywords: Airways inflammation, apoptosis, asthma, lymphocytes, memory T-cell

Received: December 17, 2004
Accepted April 29, 2005

Effector memory T-cells (CD45RO+) may provide pro-inflammatory signals that contribute to the persistent airway inflammation that is characteristic of asthma, and reduced apoptosis of these cells may prolong their effects.

The present authors compared apoptosis of CD45RO+ T-cells in the inner airway wall in nonfatal asthma (n = 7), fatal asthma (n = 7) and control (n = 8) cases. Apoptotic cells were identified using both the terminal deoxynucleotidyl transferase dNTP nick end-labelling (TUNEL) technique and cell morphology.

The percentage of CD45RO+ T-cells that were apoptotic was significantly greater in control cases compared with nonfatal and fatal cases of asthma, respectively, in small (42±19, 16±9, 7±6%), medium (40±12, 15±11, 12±8%) and large airways (42±15, 23±18, 18±12%). The reduction in the percentage of apoptotic CD45RO+ cells in the cases of asthma was observed in both blood vessels and the interstitium in large airways.

In conclusion, these data suggest that reduced apoptosis may prolong the active life of effector memory T-cells in the airways. It is possible that survival signals may be received before cells migrate into the interstitium of the inner airway wall.

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