Inhibition of Neutrophil Adherence and Movement by Acute Cigarette Smoke Exposure

Abstract

Peripheral blood neutrophils were harvested and exposed acutely in vitro to physiologically attainable levels of cigarette smoke. The adherence of radiolabeled neutrophils subsequently to alveolar epithelial cell monolayers was measured. In contrast to control cells, smoke-exposed neutrophils were significantly less adherent and failed to increase their adherence following stimulation with phorbol ester or f-met-leu-phe (fMLP). Flow cytometric analysis of the cell surface adhesion protein CD18 demonstrated no significant change in expression following in vitro smoke exposure and, furthermore, no increase in surface CD18 of smoke-exposed cells following consecutive fMLP stimulation was demonstrated. Acute in vivo cigarette smoking of up to 4 cigarettes also did not alter peripheral blood neutrophil CD18 expression. Cell spreading and chemokinesis, but not chemotaxis, was also impaired following in vitro smoke exposure. These data suggest that acute cigarette smoke may impair the crucial neutrophil functions of adherence and movement. However, the chronic effects of cigarette smoke exposure may clearly differ.

Acute effects of cigarette smoke on inflammation and oxidative stress: a review

“…73 75 The expression of CD18 on human PMNs was increased in one study 76 but remained unchanged in another. 71 Surprisingly, ACS decreased the expression of Lselectin on PMNs. 76 The phagocytic capacity of AMs, peritoneal macrophages (PMs), and PMNs was shown to decrease during CS exposure and 30 minutes, 2 and 24 hours after exposure to CS.…”

“…[67][68][69] In contrast, the chemotactic response of blood PMNs exposed directly to CS or CSE appeared to be decreased 70 or unchanged. 71 This suggests that CSE has an indirect effect on PMN chemotaxis.…”

Neutrophils in Periodontal Inflammation

“…As we have recently reviewed (146), tobacco smoke exposure induces systemic neutrophilia (147) and exerts profound effects on human neutrophils including compromised neutrophil maturation (147–148) and inefficient effector function (148–150). Key to the development of destructive, inflammatory periodontal disease may be the tobacco-induced induction of neutrophil-derived elastase (151–152) and metalloproteinase release (148, 153–154); combined with compromised phagocytotic and bacteriocidal capacities, including diminished ability to kill P. gingivalis (148, 155–156) and impaired chemotactic responsiveness (150).…”

“…Key to the development of destructive, inflammatory periodontal disease may be the tobacco-induced induction of neutrophil-derived elastase (151–152) and metalloproteinase release (148, 153–154); combined with compromised phagocytotic and bacteriocidal capacities, including diminished ability to kill P. gingivalis (148, 155–156) and impaired chemotactic responsiveness (150). …”

“…Neutrophils also express receptors for several endogenous immunomodulatory factors that have been shown to be dysregulated in tobacco smokers. These factors include IL-8, ICAM-1 and TNF (150, 159–162). The α7 nicotinic acetylcholine receptor (nAChR)–triggered cholinergic anti-inflammatory pathway is a key endogenous mechanism by which an overly robust pro-inflammatory response to infection is prevented (163–165).…”