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. 2008;3(1):149-53.
doi: 10.2147/copd.s2108.

Systemic inflammation after inspiratory loading in chronic obstructive pulmonary disease

Affiliations

Systemic inflammation after inspiratory loading in chronic obstructive pulmonary disease

Antonia Fuster et al. Int J Chron Obstruct Pulmon Dis. 2008.

Abstract

Objective: Patients with chronic obstructive pulmonary disease (COPD) present systemic inflammation. Strenuous resistive breathing induces systemic inflammation in healthy subjects. We hypothesized that the increased respiratory load that characterizes COPD can contribute to systemic inflammation in these patients.

Patients and methods: To test this hypothesis, we compared leukocyte numbers and levels of circulating cytokines (tumor necrosis factor alpha [TNFalpha], interleukin-1beta [IL-1beta], IL-6, IL-8, and IL-10), before and 1 hour after maximal incremental inspiratory loading in 13 patients with stable COPD (forced expiratory volume in one second [FEV1] 29 +/- 2.5% ref) and in 8 healthy sedentary subjects (FEV1 98 +/- 5% ref).

Results: We found that: (1) at baseline, patients with COPD showed higher leukocyte counts and IL-8 levels than controls (p < 0.01); and, (2) one hour after maximal inspiratory loading these values were unchanged, except for IL-10, which increased in controls (p < 0.05) but not in patients with COPD.

Conclusions: This study confirms the presence of systemic inflammation in COPD, shows that maximal inspiratory loading does not increase the levels of pro-inflammatory cytokines (IL-1beta, IL-8) in COPD patients or controls, but suggests that the former may be unable to mount an appropriate systemic anti-inflammatory response to exercise.

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Conflict of interest statement

Disclosure Supported, in part, by ABEMAR. There is no conflict of interest.

Figures

Figure 1
Figure 1
Systemic inflammatory markers determined in patients with COPD (open squares) and healthy controls (closed squares), before and after maximal incremental inspiratory loading. *p < 0.05, **p < 0.01 versus controls.

References

    1. Agusti AG, Noguera A, Sauleda J, et al. Systemic effects of chronic obstructive pulmonary disease. Eur Respir J. 2003;21:347–60. - PubMed
    1. American Thoracic Society. Official Statement. Standardization of Spirometry. Am J Respir Crit Care Med. 1995;152:1107–36. 1994 Update. 1995. - PubMed
    1. Anzueto A, Supinski GS, Levine SM, et al. Mechanisms of disease: Are oxygen-derived free radicals involved in diaphragmatic dysfunction. Am J Respir Crit Care Med. 1994;149:1048–52. - PubMed
    1. Barbera JA, Roca J, Ferrer A, et al. Mechanisms of worsening gas exchange during acute exacerbations of chronic obstructive pulmonary disease. Eur Respir J. 1997;10:1285–91. - PubMed
    1. Bury TB, Louis R, Radermecker MF, et al. Blood mononuclear cells mobilization and cytokines secretion during prolonged exercises. Int J Sports Med. 1996;17:156–60. - PubMed

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