EDITORIAL

Smoking cessation and airway inflammation in COPD

Why does airway inflammation persist after the smoking stops?

J C Hogg

Correspondence to:
Correspondence to:
Professor J C Hogg
McDonald Research Laboratories, St Paul’s Hospital, Vancouver, Canada, V6Z 1Y6; jhogg@mrl.ubc.ca

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Important new observations on the behaviour of T lymphocytes and plasma cells following prolonged smoking cessation in patients with COPD

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Keywords: plasma cells; T lymphocytes; chronic obstructive pulmonary disease; smoking cessation

The first 150 words of the full text of this article appear below.

The toxic gases and particles generated in tobacco smoke come into contact with lung tissues each time a puff of smoke is inhaled, and this tissue injury recurs in a cyclic fashion as each cigarette is smoked. A 20 pack year smoking history indicates that the subject’s lungs have received 20 of these short cyclic exposures per day for a cumulative total of 7300 exposures per year and 146 000 exposures over the lifetime of their smoking habit. This complex pattern of acute upon chronic inhalation injury reduces the innate defences of the lung by interfering with mucociliary clearance,¹ diminishing the inflammatory cytokine response to other stimuli,² and disrupting the epithelial barrier.^3,4 The tissue damaged by the smoke becomes infiltrated with innate and adaptive inflammatory immune cells and, even though tobacco smoke exposure may suppress the immune response,⁵ the lymphoid cells collect to . . . [Full text of this article]

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