ABSTRACT
<p><b>BACKGROUND</b>It is widely accepted that tumor necrosis factor-α (TNF-α) plays an important role in the pathogenesis of emphysema. This study aimed at investigating the protective effects of anti-TNF-α antibody, infliximab, in the development of emphysema induced by passive smoking in rats.</p><p><b>METHODS</b>Thirty-nine rats were randomly divided into a normal control group (group 1), an emphysema group (group 2), and an infliximab-intervention group (group 3). Rat models of emphysema were established by exposure to cigarette smoking daily for 74 days. After 1 month, the infliximab intervention group was treated with infliximab via subcutaneous injection. The levels of TNF-α, IL-8 and vascular endothelial growth factor (VEGF) in bronchoalveolar lavage fluid (BALF) were measured with enzyme linked immunosorbent assay (ELISA). The number and classification of cells in the BALF were measured. Lung tissue sections stained by hematoxylin and eosin (HE) were observed, and mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were used to examine the percentage of positive cells and distribution of apoptotic cells.</p><p><b>RESULTS</b>The levels of TNF-α and IL-8 in BALF were higher in group 2 than in group 1 and group 3. The MLI was greater in group 2 than that in group 1 and group 3 while MAN was decreased. The concentration of VEGF in BALF of group 2 was significantly decreased as compared with group 1. The total cells and neutrophils number was significantly increased in group 2 as compared with group 1 and group 3, so was the percentage of neutrophils. The number of TUNEL positive cells in the alveolar septa was significantly increased in group 2 as compared with group 1 and group 3.</p><p><b>CONCLUSION</b>Infliximab protects against cigarette smoking-induced emphysema by reducing airway inflammation, attenuating alveolar septa cell apoptosis and improving pathological changes.</p>
Subject(s)
Animals , Male , Rats , Antibodies, Monoclonal , Therapeutic Uses , Bronchoalveolar Lavage Fluid , Chemistry , Cell Biology , Infliximab , Interleukin-8 , Metabolism , Pulmonary Alveoli , Cell Biology , Pulmonary Emphysema , Metabolism , Random Allocation , Rats, Sprague-Dawley , Tobacco Smoke Pollution , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
To investigate the seroprevalence of Helicobacter pylori [H. pylori] in patients with obstructive sleep apnea syndrome [OSAS], and to determine any association between H. pylori infection and severity of OSAS. Two hundred and forty-three subjects were recruited in this cross-sectional study at the Department of Respiratory Medicine in the West China Hospital, Sichuan, P. R. China, from October 2006 to April 2008. Polysomnography [PSG] was used to determine the apnea-hypopnea index [AHI], and enzyme-linked immunosorbent assay was used to test H. pylori IgG. According to the AHI, subjects were divided into 4 groups: the control group [AHI <5/hours], patients with mild OSAS group [AHI: 5-14/hours], moderate OSAS group [AHI: 15-29/hours], and severe OSAS group [AHI: >/= 30/hours]. The prevalence of H. pylori infection in patients with OSAS was 75.5%, and in the controls it was 53.4% [p=0.000]. The prevalence of H. pylori infection in patients with mild OSAS was 57.1%, with moderate OSAS was 76.5%, and with severe OSAS was 90.9%. There were significant differences between patients with moderate and severe OSAS and the controls, as well as among the mild, moderate, and severe OSAS groups. Helicobacter pylori infection may be associated with OSAS. In addition, increased severity of OSAS might be associated with higher seroprevalence of H. pylori