Clinical Features of Patients with Bronchiectasis with Comorbid Chronic Obstructive Pulmonary Disease in China.

BACKGROUND The prevalence of bronchiectasis with comorbid chronic obstructive pulmonary disease (COPD) is rising, which causes extremely high risk of exacerbation and mortality. We aimed to evaluate the differences in clinicopathological manifestations, immune function, and inflammation in bronchiectasis patients with comorbid COPD vs. patients who only have COPD. MATERIAL AND METHODS Clinicopathological characteristics, including common potentially pathogenic microorganisms, lung function, immune function, and inflammation were assessed in bronchiectasis patients with comorbid COPD and in patients who only had COPD. RESULTS Compared to patients who only had COPD, patients with bronchiectasis with comorbid COPD had a higher positive rate of sputum bacteria (45.27% vs. 28.03%, P<0.01). Among them, Pseudomonas aeruginosa (P. aeruginosa) accounted for 25.19% in COPD (4.37%) (P<0.01). Likewise, patients with bronchiectasis with comorbid COPD had worse lung function, worse COPD assessment test scores, and worse Modified Medical Research Council scores. Moreover, compared with COPD only cases, patients with bronchiectasis with comorbid COPD had higher levels of white blood cells (WBC), neutrophils, C-reactive protein (CRP), and procalcitonin (PCT) (all P<0.05). Interestingly, the expression levels of Treg in patients with bronchiectasis with comorbid COPD were lower than in patients with COPD only (P<0.05). Th17 and Th17/Treg levels were higher (P<0.05). Furthermore, remarkable increased level of IL17 and IL-6 and decreased level of IL-10 and TGF-ß were observed in the bronchiectasis combined COPD than in pure COPD (All P<0.05). CONCLUSIONS Our findings suggest that P. aeruginosa is the main pathogen of bacterial infection in bronchiectasis patients with comorbid COPD. These patients have more serious clinical manifestations and immune imbalance, which should be considered when providing clinical treatment.

Functional polymorphisms of CD14 and toll-like receptor 4 in Taiwanese Chinese with Helicobacter pylori-related gastric malignancies.

BACKGROUND/AIMS: Interindividual differences in degrees and extent of gastritis are responsible for the divergent outcomes after H. pylori infection. Cellular responses in gastric inflammation are mediated by lipopolysaccharide of H. pylori, which activate monocytes to express cytokine expression and growth factors via CD14 and toll-like receptor 4 (TLR4). Whether functional polymorphisms of TLR 4 and CD14 account for H. pylori-related gastric malignancies remains unknown. This study aimed to investigate the contribution of CD14 and TLR4 genotypes to the risk of H. pylori-related gastric malignancies in a Chinese population. METHODOLOGY: Genotyping for CD14 (-159C/T) and TLR4 (Asp 299Gly and Thr 399Ile) was performed in 70 patients with gastric mucosa-associated lymphoid tissue lymphoma (MALToma), 204 patients with non-cardia gastric adenocarcinoma (GAC), and 210 unrelated healthy controls. Distribution of genotype and allele frequencies among three groups was compared. RESULTS: The seropositive rate of H. pylori was significantly higher for non-cardia GAC (164/204, 80.4%) and MALToma (66/70, 94.3%) than controls (120/210, 57.5%, p<0.001). A complete absence of Gly or Ile variants was noted for all the studied subjects. The genotype frequencies of CD14 in controls were C/C, 25.7%, C/T, 48.6%, and T/T, 25.7%, and did not deviate from the Hardy-Weinberg equilibrium. The distribution of CD14 genotype did not differ significantly among GAC, MALToma patients, and controls. CONCLUSIONS: These data suggest no apparent association of CD14 polymorphisms with H. pylori-related gastric malignancy and provide evidence for race-specific distribution of TLR4 alleles in Chinese population.