Source: Annual Congress 2008 - Mechanisms of respiratory infections: interaction between the pathogen and the host
Disease area: Airway diseases, Respiratory infections

Abstract

The clinical course of Chronic Obstructive Pulmonary Disease (COPD) is associated with acute exacerbations of symptoms, markedly contributed to by bacterial infection, including nontypeable Haemophilus influenzae (ntHi). Evidence suggests that cigarette smoke impacts respiratory host defense; however, the consequences of altered host defense to bacterial infections are poorly understood. The purpose of this study was to investigate, in mice, the impact of cigarette smoke exposure on inflammatory responses elicited by ntHi challenge. Mice were room-air or cigarette-smoke exposed for 8 weeks and subsequently inoculated intranasally with ntHi. We observed significantly increased cell numbers in the BAL of smoke-exposed ntHi challenged mice, as compared to room-air exposed ntHi challenged mice. This was associated with a marked shift in the profile of inflammatory mediators expressed in smoke exposed mice following ntHi challenge. While TNFα expression was significantly attenuated in the BAL of smoke-exposed ntHi challenged mice, levels of a number of inflammatory mediators such as MCP-1, MCP-3, and MIP-1α were significantly increased. A similar shift in inflammatory mediator expression was also observed in cell supernatants of ntHi-stimulated alveolar macrophages from smoke-exposed mice. Taken together our data demonstrate that cigarette smoke-exposure exacerbates inflammatory processes elicited by bacterial infection and profoundly alters the inflammatory mediator profile.
This study was funded in part by the Canadian Institutes of Health Research and AstraZeneca.

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M. R. Stampfli, M. Skrtic, C. C. J. Zavitz, G. J. Gaschler (Hamilton, ON, Canada). Cellular and cytokine profile following in vivo challenge with nontypeable haemophilus influenzae in cigarette smoke exposed mice. Eur Respir J 2008; 32: Suppl. 52, 2284

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