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Title[redir]:
Responsiveness of blood and sputum inflammatory cells in Japanese COPD | COPD
Description:
Responsiveness of blood and sputum inflammatory cells in Japanese COPD patients, non-COPD smoking controls, and non-COPD nonsmoking controls Tomotaka Kawayama,1 Takashi Kinoshita,1 Kazuko Matsunaga,2 Akihiro Kobayashi,3 Tomoyuki Hayamizu,4 Malcolm Johnson,5 Tomoaki Hoshino11Division of Respirology, Neurology, and Rheumatology, Department of Medicine, Kurume University School of Medicine, Kurume, 2Department of Respiratory Medicine, Fukuoka Sanno Hospital, Fukuoka, 3Biomedical Data Science Department, 4Medical Affairs Respiratory Department, GlaxoSmithKline, Shibuya-ku, Tokyo, Japan; 5Respiratory Global Franchise, GlaxoSmithKline, Uxbridge, UKPurpose: To compare pulmonary and systemic inflammatory mediator release, pre- and poststimulation, ex vivo, in cells from Japanese patients with chronic obstructive pulmonary disease (COPD), non-COPD smoking controls, and non-COPD nonsmoking controls (NSC).Patients and methods: This was a nontreatment study with ten subjects per group. Inflammatory biomarker release, including interleukin (IL)-6 and -8, matrix metalloproteinase-9, and tumor necrosis factor (TNF)-α, was measured in peripheral blood mononuclear cells (PBMC) and sputum cells with and without lipopolysaccharide or TNF-α stimulation.Results: In PBMC, basal TNF-α release (mean ± standard deviation) was significantly different between COPD (81.6±111.4 pg/mL) and nonsmoking controls (9.5±5.2 pg/mL) (P<0.05). No other significant differences were observed. Poststimulation biomarker release tended to increase, with the greatest changes in the COPD group. The greatest mean increases were seen in the lipopolysaccharide-induced release of matrix metalloproteinase-9, TNF-α, and IL-6 from PBMC. Pre- and poststimulation data from sputum samples were more variable and less conclusive than from PBMC. In the COPD group, induced sputum neutrophil levels were higher and macrophage levels were lower than in either control group. Significant correlations were seen between the number of sputum cells (macrophages and neutrophils) and biomarker levels (IL-8, IL-6, and TNF-α).Conclusion: This was the first study to compare cellular inflammatory mediator release before and after stimulation among Japanese COPD, smoking controls, and nonsmoking controls populations. Poststimulation levels tended to be higher in patients with COPD. The results suggest that PBMC are already preactivated in the circulation in COPD patients. This provides further evidence that COPD is a multicomponent disease, involving both airway and systemic inflammation.Keywords: chronic obstructive pulmonary disease, lipopolysaccharide, peripheral blood mononuclear cells, sputum, tumor necrosis factor-α
Title[redir]:
Responsiveness of blood and sputum inflammatory cells in Japanese COPD | COPD
Description:
Responsiveness of blood and sputum inflammatory cells in Japanese COPD patients, non-COPD smoking controls, and non-COPD nonsmoking controls Tomotaka Kawayama,1 Takashi Kinoshita,1 Kazuko Matsunaga,2 Akihiro Kobayashi,3 Tomoyuki Hayamizu,4 Malcolm Johnson,5 Tomoaki Hoshino11Division of Respirology, Neurology, and Rheumatology, Department of Medicine, Kurume University School of Medicine, Kurume, 2Department of Respiratory Medicine, Fukuoka Sanno Hospital, Fukuoka, 3Biomedical Data Science Department, 4Medical Affairs Respiratory Department, GlaxoSmithKline, Shibuya-ku, Tokyo, Japan; 5Respiratory Global Franchise, GlaxoSmithKline, Uxbridge, UKPurpose: To compare pulmonary and systemic inflammatory mediator release, pre- and poststimulation, ex vivo, in cells from Japanese patients with chronic obstructive pulmonary disease (COPD), non-COPD smoking controls, and non-COPD nonsmoking controls (NSC).Patients and methods: This was a nontreatment study with ten subjects per group. Inflammatory biomarker release, including interleukin (IL)-6 and -8, matrix metalloproteinase-9, and tumor necrosis factor (TNF)-α, was measured in peripheral blood mononuclear cells (PBMC) and sputum cells with and without lipopolysaccharide or TNF-α stimulation.Results: In PBMC, basal TNF-α release (mean ± standard deviation) was significantly different between COPD (81.6±111.4 pg/mL) and nonsmoking controls (9.5±5.2 pg/mL) (P<0.05). No other significant differences were observed. Poststimulation biomarker release tended to increase, with the greatest changes in the COPD group. The greatest mean increases were seen in the lipopolysaccharide-induced release of matrix metalloproteinase-9, TNF-α, and IL-6 from PBMC. Pre- and poststimulation data from sputum samples were more variable and less conclusive than from PBMC. In the COPD group, induced sputum neutrophil levels were higher and macrophage levels were lower than in either control group. Significant correlations were seen between the number of sputum cells (macrophages and neutrophils) and biomarker levels (IL-8, IL-6, and TNF-α).Conclusion: This was the first study to compare cellular inflammatory mediator release before and after stimulation among Japanese COPD, smoking controls, and nonsmoking controls populations. Poststimulation levels tended to be higher in patients with COPD. The results suggest that PBMC are already preactivated in the circulation in COPD patients. This provides further evidence that COPD is a multicomponent disease, involving both airway and systemic inflammation.Keywords: chronic obstructive pulmonary disease, lipopolysaccharide, peripheral blood mononuclear cells, sputum, tumor necrosis factor-α
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Keywords {🔍}
copd, sputum, tnfα, inflammatory, cells, release, lps, nsc, study, pbmc, pulmonary, disease, stimulation, group, patients, controls, inflammation, chronic, cell, data, subjects, obstructive, smoking, systemic, neutrophils, groups, blood, table, biomarkers, japanese, levels, noncopd, glaxosmithkline, biomarker, macrophages, nonsmoking, significant, medical, peripheral, compared, subject, respir, university, interleukin, tumor, necrosis, correlations, airway, increased, mmp,
Topics {✒️}
enzyme-linked immunosorbent assay tumor necrosis factor-alpha single-center study collating author comments received honoraria/consulting fees including fast-track processing dove medical press tobacco anti-idiotypic antibody lps-induced tnf-α release alpha-1-antitrypsin pimz subjects parts phosphate-buffered saline tumor necrosis factor human recombinant tnf-α tomotaka kawayama discloses manuscript login characterize copd-related inflammation favored authors dr kathryn white basal tnf-α release biomarker assay kits salmeterol/fluticasone propionate forced expiratory volume single observer blind editorial support inconsistent findings pre received research grants specific author total cell counts increased responsiveness compared release high amounts major risk factor pulmonary inflammatory responses18 concentration-dependent manner α1-antitrypsin deficiency thermo fisher scientific cigarette smoke condensate offer real benefits potent proinflammatory stimuli gram-negative bacteria ��10 pack-year history /forced vital capacity ��1 pack-year history computed tomography scan european task force21 100× antibiotic-antimycotic solution trypan-blue staining forced vital capacity de-sensitized possibly gave final approval advisory board meetings
Questions {❓}
- COPD is associated with systemic and pulmonary inflammation,3,4 but it remains unclear how the systemic inflammation arises: Is it due to the spillover of inflammation from the lungs?
- Why publish with us?
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