Acute effects of cigarette smoking on inflammation in healthy intermittent smokers

Abstract

Background: Chronic smoking is the main risk factor for chronic obstructive pulmonary disease. Knowledge on the response to the initial smoke exposures might enhance the understanding of changes due to chronic smoking, since repetitive acute smoke effects may cumulate and lead to irreversible lung damage.

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

“…The results in the current study, on both gelatinases and neutrophil counts, correspond well with findings reported in a previous study on induced sputum from intermittent smokers, in spite of the fact that the current study reflects the peripheral and not the proximal airways [6]. The previous study on proximal airways indicated no substantial changes in sputum MMP-9, TIMP-1 or neutrophil counts 24 h after exposure to tobacco smoke [6].…”

“…The previous study on proximal airways indicated no substantial changes in sputum MMP-9, TIMP-1 or neutrophil counts 24 h after exposure to tobacco smoke [6]. However, in contrast to the current study, the study by VAN DER VAART et al [6] did not address MMP-2 and TIMP-2.…”

“…As a consequence, it is still uncertain to what extent acute exposure to tobacco smoke per se leads to an imbalance in the gelatinase homeostasis in the peripheral airways of clinically healthy humans. A study on induced sputum from occasional smokers has shed some light on this by providing evidence that, in the proximal airways, acute exposure to tobacco smoke does cause a transient increase in the number of neutrophils, an inflammatory cell that constitutes a potentially important source of the gelatinase MMP-9 [6]. However, that study did not indicate any differences in MMP-9 or TIMP-1 in the proximal airways after smoke exposure.…”

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

“…CS-induced airway inflammation can already occur after short-term exposure in individuals susceptible for the development of COPD (39,51). To date, little is known about the genetics of CS-induced neutrophilic airway inflammation, in contrast to the genetics of COPD or asthma for which many susceptibility genes have been identified (8,38).…”

The Relationship Between Smoking Intensity and Subclinical Cardiovascular Injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

“…9 Acute exposure to cigarette smoking may be associated with inflammation, thrombosis, endothelial dysfunction, arterial stiffness, and coronary microvascular dysfunction. [10][11][12][13][14][15][16][17] Cohort studies have traditionally been used to examine the chronic effects of smoking, but have rarely been used to evaluate immediate inhalational smoking exposure. 18 Long-term exposure is commonly assessed using smoking duration (years), or cumulative exposure (pack-years).…”