Elevated Circulating CD4+CD25+CD127-/low Regulatory T Cells in Patients with Non-asthmatic Eosinophilic Bronchitis.

PURPOSE: Non-asthmatic eosinophilic bronchitis (NAEB) is a common cause of chronic cough. It is characterized by sputum eosinophilia like asthma but lacks airway hyperresponsiveness. Regulatory T cells (Tregs) are recognized as immune suppressors and are involved in the pathogenesis of asthma. However, the relationship between Tregs and NAEB remains unknown. This study aimed to preliminarily explore the role of Tregs in NAEB by comparing circulating Tregs levels to asthma and healthy controls. METHODS: Fractional exhaled nitric oxide (FeNO), spirometry with bronchial provocation test, sputum induction and blood routine test were performed in all subjects. Peripheral blood mononuclear cells were used to detect the Tregs (CD4+CD25+CD127-/low) by flow cytometry. Relationship between the levels of circulating Tregs and clinical indexes was also observed. RESULTS: A total of 15 patients with NAEB, 20 patients with asthma and 11 healthy controls were included. The absolute numbers of circulating Tregs in the NAEB group (49.8 ± 18.9 × 103 cells/ml) and asthma group (53.3 ± 18.7 × 103 cells/ml) were higher than that in healthy control group (32.7 ± 11.6 × 103 cells/ml) (both P < 0.01). In total, the level of circulating Tregs showed positive correlation with FeNO (r = 0.30, P < 0.05). CONCLUSION: Tregs may play a key role not only in asthmatic patients, but also in patients with NAEB, as reflected by the elevated Tregs in peripheral blood.

Grading Severity of Productive Cough Based on Symptoms and Airflow Obstruction.

The binary approach to the diagnosis of Chronic Bronchitis (CB) is a major barrier to the study of the disease. We investigated whether severity of productive cough can be graded using symptoms and presence of fixed airflow obstruction (FAO), and whether the severity correlates with health status, exposures injurious to the lung, biomarkers of inflammation, and measures of airway wall thickening. Findings from a cross-sectional sample of 1,422 participants from the Lovelace Smokers Cohort (LSC) were validated in 4,488 participants from the COPDGene cohort (COPDGene). Health status was based on the St. George's Respiratory Questionnaire, and Medical Outcomes Study 36-Item Short Form Health Survey. Circulating CC16 levels were quantified by ELISA (LSC), and airway wall thickening was measured using computed tomography (COPDGene). FAO was defined as postbronchodilator FEV1/FVC <0.7. The presence and duration of productive cough and presence of FAO or wheeze were graded into Healthy Smokers, Productive Cough (PC), Chronic PC, PC with Signs of Airflow Obstruction, and Chronic PC with Signs of Airflow Obstruction. In both cohorts, higher grade of severity correlated with lower health status, greater frequency of injurious exposures, greater airway wall thickening, and lower circulating CC16 levels. Further, longitudinal follow-up suggested that disease resolution can occur at every grade of severity but is more common in groups of lower severity and least common once airway remodeling develops. Therefore, severity of productive cough can be graded based on symptoms and FAO and early intervention may benefit patients by changing the natural history of disease.

Value of Exhaled Nitric Oxide (FeNO) And Eosinophilia During the Exacerbations of Chronic Obstructive Pulmonary Disease Requiring Hospital Admission.

The aim of this study was to analyze whether FeNO levels in acute exacerbation of COPD (AECOPD) with hospital admission have better diagnostic value than eosinophilia in blood, and to evaluate its usefulness in predicting a better clinical response. An observational prospective study of patients with AECOPD was carried out. FeNO determinations were made on arrival at the emergency room (ER), at discharge and during stability 3-6 months after discharge. Co-morbidities, bronchodilators, inhaled (IGC) and systemic (SGC) glucocorticoids, eosinophils, systemic inflammation markers (procalcitonin, C-reactive protein), eosinophil cationic protein, and total IgE were collected. Fifty consecutive patients (92% men, mean age 75 ± 6 years) were included in this study. Phenotypes were 26% Asthma-COPD Overlap Syndrome (ACOS), 42% chronic bronchitis (CB) and 32% emphysema. ACOS patients showed significantly higher levels of FeNO (73 ppb) and eosinophils (508 cells/mm3) than the rest (CB: 23 ppb, 184 cells/mm3, emphysema: 27 ppb, 159 cells/mm3; p < 0.05). A significant correlation between FeNO levels measured in ER and eosinophils was observed (r = 0.7; p < 0.001), but not at discharge or in stable phase. No significant association was found with parameters of systemic inflammation and mean stay. In conclusion, the determination of FeNO in AECOPD does not offer advantages over the evaluation of eosinophilia. These parameters rise at arrival in ER, descend at discharge, and remain unchanged in the stable phase. Both present similar diagnostic utility and are able to better identify the ACOS phenotype, which helps select a population that could benefit from a glucocorticoids therapy.

A Randomized, Placebo-controlled Trial of Roflumilast. Effect on Proline-Glycine-Proline and Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease.

RATIONALE: Roflumilast is a therapeutic agent in the treatment of chronic obstructive pulmonary disease (COPD). It has antiinflammatory effects; however, it is not known whether it can affect a biologic pathway implicated in COPD pathogenesis and progression. The self-propagating acetyl-proline-glycine-proline (AcPGP) pathway is a novel means of neutrophilic inflammation that is pathologic in the development of COPD. AcPGP is produced by extracellular matrix collagen breakdown with prolyl endopeptidase and leukotriene A4 hydrolase serving as the enzymes responsible for its production and degradation, respectively. OBJECTIVES: We hypothesized that roflumilast would decrease AcPGP, halting the feed-forward cycle of inflammation. METHODS: We conducted a single-center, placebo-controlled, randomized study investigating 12 weeks of roflumilast treatment added to current therapy in moderate-to-severe COPD with chronic bronchitis. Subjects underwent sputum and blood analyses, pulmonary function testing, exercise tolerance, and quality-of-life assessment at 0, 4, and 12 weeks. MEASUREMENTS AND MAIN RESULTS: Twenty-seven patients were enrolled in the intention-to-treat analysis. Roflumilast treatment decreased sputum AcPGP by more than 50% (P < 0.01) and prolyl endopeptidase by 46% (P = 0.02), without significant improvement in leukotriene A4 hydrolase activity compared with placebo. Roflumilast also reduces other inflammatory markers. There were no significant changes in lung function, quality of life, or exercise tolerance between roflumilast- and placebo-treated groups. CONCLUSIONS: Roflumilast reduces pulmonary inflammation through decreasing prolyl endopeptidase activity and AcPGP. As expected for lower AcPGP levels, markers of neutrophilic inflammation are blunted. Inhibiting this self-propagating pathway lessens the overall inflammatory burden, which may alter the natural history of COPD, including the risk of exacerbation. Clinical trial registered with www.clinicaltrials.gov (NCT 01572948).

[Analysis of polymorphisms of genes associated with immune response and tissue remodeling in occupational chronic bronchitis].

The involvement of polymorphisms of genes encoding immune response-associated molecules (LTA, TNFA, ILB, ILRN, IL8, IL10, VDBP), matrix metalloproteinases (MMP1, MMP2, MMP3, MMP9, MMP12, ADAM33), and tissue and serum inhibitors of proteases (TIMP2, TIMP3, SERPINA1, SERPINA3) in the predisposition to occupational chronic bronchitis was assessed by PCR-RFLP analysis in groups of patients (n = 122) and healthy employees (n = 166). It was found that occupational chronic bronchitis was associated with polymorphisms of VDBP (P(adj) = 0.00005, OR(adj) = 2.06), MMP1 (P(adj) = 0.00002, OR(adj) = 2.57), ADAM33 (P(adj) = 0.0004, OR(adj) = 2.52), and IL8 (P(adj) = 0.0058, OR(adj) = 2.87). The most significant association was observed for the VDBP polymorphism 1296T>G. The VDBP haplotype GC*1S by the loci 1296T>G and 1307C>A was an informative susceptibility marker (P(adj) = 0.0001, OR(adj) = 2.60, 95% CI (1.62-4.19)). There was also a significant interaction between the VDBP polymorphism 1307C>A and the duration of occupational exposure to hazardous factors (P(interaction) = 0.02). Apparently, the investigated polymorphisms of VDBP, MMP1, ADAM33, and IL8 contribute to the genetic susceptibility to chronic bronchitis induced by dust and toxic agents.

Exploration of the Shared Gene Signatures and Molecular Mechanisms between Chronic Bronchitis and Antineutrophil Cytoplasmic Antibody-associated Glomerulonephritis: Evidence from Transcriptome Data.

BACKGROUND: Chronic Bronchitis (CB) is a recurrent and persistent pulmonary inflammation disease. Growing evidence suggests an association between CB and Anti-neutrophil Cytoplasmic Antibody-associated Glomerulonephritis (ANCA-GN). However, the precise mechanisms underlying their association remain unclear. AIMS: The purpose of this study was to further explore the molecular mechanism of the occurrence of chronic bronchitis (CB) associated with anti-neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA- GN). OBJECTIVE: Our study aimed to investigate the potential shared pathogenesis of CB-associated ANCA-GN. METHODS: Datasets of ANCA (GSE108113 and GSE104948) and CB (GSE151052 and GSE162635) were obtained from the Gene Expression Omnibus (GEO) datasets. Firstly, GSE108113 and GSE151052 were analyzed to identify common differentially expressed genes (DEGs) by Limma package. Based on common DEGs, protein-protein interaction (PPI) network and functional enrichment analyses, including GO, KEGG, and GSEA, were performed. Then, hub genes were identified by degree algorithm and validated in GSE104948 and GSE162635. Further PPI network and functional enrichment analyses were performed on hub genes. Additionally, a competitive ceRNA network was constructed through miRanda and spongeScan. Transcription factors (TFs) were predicted and verified using the TRRUST database. Furthermore, the CIBERSORT algorithm was employed to explore immune cell infiltration. The Drug Gene Interaction Database (DGIDB) was utilized to predict small-molecular compounds of CB and ANCA-GN. RESULTS: A total of 963 DEGs were identified in the integrated CB dataset, and 610 DEGs were identified in the integrated ANCA-GN dataset. Totally, we identified 22 common DEGs, of which 10 hub genes (LYZ, IRF1, PIK3CG, IL2RG, NT5E, ARG2, HBEGF, NFATC2, ALPL, and FKBP5) were primarily involved in inflammation and immune responses. Focusing on hub genes, we constructed a ceRNA network composed of 323 miRNAs and 348 lncRNAs. Additionally, five TFs (SP1, RELA, NFKB1, HIF1A, and SP3) were identified to regulate the hub genes. Furthermore, immune cell infiltration results revealed immunoregulation in CB and ANCA-GN. Finally, some small-molecular compounds (Daclizumab, Aldesleukin, and NT5E) were predicted to predominantly regulate inflammation and immunity, especially IL-2. CONCLUSION: Our study explores the inflammatory-immune pathways underlying CB-associated ANCA-GN and emphasizes the importance of NETs and lymphocyte differentiation, providing novel insights into the shared pathogenesis and therapeutic targets.

Low concentrations of serum 25-hydroxyvitamin D associated with increased risk for chronic bronchitis among US adults.

Increasing evidence suggests that vitamin D benefits both innate and adaptive immunity, thereby eliciting an anti-inflammatory effect and reducing the risk of infectious disease. The present study examined the association between serum 25-hydroxyvitamin D (25(OH)D) levels and the risk of chronic bronchitis among US adults. We analysed data from 6872 US adults aged ≥ 20 years who participated in the 2003-6 National Health and Nutrition Examination Survey. Prevalence and OR with 95 % CI of having self-reported chronic bronchitis were estimated by quintiles of 25(OH)D or vitamin D-deficiency status after adjustment for potential confounders. The results showed that the adjusted prevalence of chronic bronchitis ranged from 2.4 (95 % CI 1.4, 3.3) % among adults in the highest quintile of 25(OH)D ( ≥ 30 ng/ml) to 4.1 (95 % CI 2.5, 5.6) % among adults in the lowest quintile ( < 15 ng/ml; P for trend < 0.01). The adjusted OR for chronic bronchitis was 1.85 (95 % CI 1.06, 3.24) in adults with < 15 ng/ml 25(OH)D and 1.77 (95 % CI 1.19, 2.65) in those with 15 to < 20 ng/ml 25(OH)D compared with adults with ≥ 30 ng/ml 25(OH)D. Additionally, the adjusted OR for chronic bronchitis was 1.52 (95 % CI 1.03, 2.26) among adults with vitamin D deficiency ( < 20 ng/ml 25(OH)D) compared with those with ≥ 20 ng/ml 25(OH)D. For every 1 ng/ml increase in 25(OH)D, the likelihood of having chronic bronchitis fell by 2.6 % (P = 0.016). In conclusion, low serum 25(OH)D levels are associated with the increased risk of chronic bronchitis among US adults. The present results provide support for continuing research on the role of vitamin D in lung diseases.

Occupational nonasthmatic eosinophilic bronchitis: current concepts.

BACKGROUND: Nonasthmatic eosinophilic bronchitis (NAEB) is an important cause of chronic cough, since it is present in 10-15% of patients referred for specialist investigation. The syndrome is considered a variant of occupational asthma when it develops as a consequence of occupational exposure, hence it should be considered in the spectrum of work-related airway diseases. OBJECTIVES AND METHODS: The aim of this paper was to update and expand the previous reviews on the clinical and pathophysiological features of NAEB and analyze available data on the occupational causes of the disease. Literature on the topic between the years 1990 and 2010 was reviewed with a Med Line search. RESULTS: The disease is probably underdiagnosed and an occupational origin was demonstrated only in isolated cases, probably due to the rarity of the disease and the lack of systematic evaluation of bronchial inflammation. CONCLUSIONS: In view of the current knowledge on this condition and the development of techniques to evaluate bronchial inflammation, occupational NAEB cannot be neglected any more and has been rightly included in the spectrum of occupational respiratory disorders.

[Immunopathogenetic features of occupational bronchitis].

The article based on research work covers functional, bronchoscopy, microbiologic and immunologic features of chronic dust bronchitis and chronic bronchitis caused by toxic chemicals.

Involvement of mitogen-activated protein kinase activation in cyclooxygenase-2 and transforming growth factor-ß production in alveolar macrophage from chronic bronchitis rats.

OBJECTIVE: Lipopolysaccharides (LPS) activates several signaling pathways in macrophages including mitogen-activated protein kinases (MAPK). Previous studies have investigated effect of LPS on MAPK activation in macrophage of normal rats. In the current study, we investigated the effect of LPS exposure on activation of MAPK in alveolar macrophage (AM) of chronic bronchitis (CB) rats and researched the corresponding cyclooxygenase-2 (COX-2), prostaglandins-2 (PGE(2)) and transforming growth factor- ß (TGF-ß) production and their MAPK signal pathways. METHODS: CB model was established by injection of Bacillus Calmette-Guerin (BCG) and LPS in rats. Special inhibitors of p38, extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinases (JNK) MAPK signal pathways were used to determine the effect of MAPK activation on COX-2, PGE(2), TGF-ß production in AM of CB rats via RT-PCR, western blotting, radioimmunoassay and ELISA. KEY FINDINGS: Synthesis of PGE(2) from AM of CB rats was increased and suppressed by either PD98059 or SB203580. SB203580 and PD98059, (inhibitors of ERK and p38 MAPK), could significantly inhibit COX-2 mRNA and protein expression. Moreover, ERK and p38 MAPK had synergistic effect on COX-2 expression. Inhibitor of ERK MAPK signal transduction could inhibit TGF-ß expression in AM. CONCLUSION: These results demonstrated COX-2, PGE(2) and TGF-ß productions in AM of CB rats were significantly increased, which might be regulated by the different MAPK signaling pathway.

Bronchoalveolar lavage fluid cellular profile in workers exposed to chrysotile asbestos.

The cellular profile of bronchoalveolar lavage fluid (BALF) in asbestos-exposed population remains controversial. We, therefore, aimed to investigate BALF in apparently healthy individuals that were exposed in asbestos-related work for a long period of time. Participants were selected among employees of a car brakes and clutches factory that used chrysotile asbestos. Selection criteria were an employment history of ≥ 15 years and the absence of severe respiratory disease. The total number and type of BALF cells, the existence of dust cells, iron-laden macrophages and asbestos bodies were assessed. Thirty-nine workers (25 men), with a mean age of 46.2 ± 4.2 years and a mean employment time of 23.5 ± 4 years, participated. Asbestos bodies were observed in 14 out of 39 (36%) specimens, dust cells in 37 and iron-laden macrophages in all. Those with asbestos bodies had at least 3 times higher probability to have lymphocytosis (lymphocytes > 11%: 64% vs 28%, p = 0.027) and had an increased percentage of iron-laden macrophages compared to those without asbestos bodies (median values: 42% vs 13%, p = 0.08). Smokers (36%) had less lymphocytes compared to non and ex-smokers (median values: 6% vs. 13%, p = 0.002), and iron-laden macrophages count had a positive relation (r = 0.31, p = 0.05) to lymphocyte count. Asbestos-exposed asymptomatic individuals with the presence of asbestos bodies in the BALF are more likely to have lymphocytic alveolitis while concurrent dust exposure and smoking habits hold a significant role.

[Effects of mangiferin on cytokines in rats with chronic bronchitis and expression of macrophage COX-2 in mice].

OBJECTIVE: To explore the mechanism of anti-inflammatory effect of mangiferin. METHOD: The model of chronic bronchitis in rat was established by LPS + smoke. The activity of SOD, content of MDA and NO in BALF and serum, content of TNF-alpha and IL-8 were determined. The expression of RAW264.7 macrophage COX-2 mRNA induced by LPS in mice was detected by RT-PCR. RESULT: The activity of SOD, the content of NO in BALF and serum in rat with chronic bronchitis were significantly higher with high, medium and low-dose of lg mangiferin (400,200,100 mg x kg(-1)), while the content of MDA, and the content of TNF-alpha and IL-8 in lung tissues were lower. The expression of RAW264.7 macrophage COX-2 mRNA induced by LPS was significantly reduced by mangiferin with 200,100, 50 micromol x L(-1). CONCLUSION: The anti-inflammatory mechanism of mangiferin is to relieve inflammation by raising the activity of SOD and content of NO and reducing the content of MDA and the expression of TNF-alpha, IL-8 and COX-2 mRNA.

[Professional eosinophilic bronchitis: considerations and new diagnostic methods in a clinical case]. / La bronchite eosinofila professionale: considerazioni e nuovi strumenti diagnostici a margine di un caso clinico.

Nonasthmatic eosinophilic bronchitis (NAEB) is a condition characterized by corticosteroid-responsive chronic cough, sputum eosinophilia and absence of symptoms or objective evidence of variable airflow obstruction and airway hyper-responsiveness. Like asthma, NAEB can be associated with exposure to occupational sensitizers and can be considered as being a variant of occupational asthma when it develops as a consequence of work exposure. Few case reports of NAEB caused by workplace exposure have been reported. Bakers are at high risk of developing occupational respiratory disorders and three cases of occupational NAEB have been described. We describe the first case of occupational NAEB due to storage mites in a baker in which the offending agent was identified by means of the basophil activation test (BAT), a new tool which has never been proposed in diagnostic procedures of occupational respiratory allergy. BAT's results allowed the recognition of the offending agent, that is mandatory for diagnosis.

[Colonization resistance and immunological reactivity of children's oropharyngeal mucosa in health and bronchopulmonary pathology].

The study group was comprised of 27 practically healthy children, 51 patients with acute bronchitis, 15 with chronic bronchitis and 11 with pneumonia. It was shown that changes of microbiocoenosis in back of the throat (BOT) were related to increased mucosal contamination with normal microflora and opportunistic microorganisms. The highest degree of contamination was observed in children with acute bronchitis. Normocoenosis was detected only in 13 practically healthy children. The disorders of microbiocoenosis took the form of disbiosis and acute inflammatory processes in patients with acute and chronic bronchitis and pneumonia. However, the large amount of normal flora together with the high Ig level ensured marked colonization resistance as evidenced by the values of natural colonization coefficient of nasopharyngeal epithelium (NCCNE) and balance coefficient (BC). These data suggested development of compensated secondary immunodeficiencies. In patients with acute bronchitis and pneumonia, local synthesis of Ig prevailed. It is shown that BC can be used to screen children for disorders of mucosal immunity. The presence of increased saliva IgE levels in patients with acute and chronic bronchitis supports the generally accepted concept of bronchi as a "shock organ" in allergic condition. It was demonstrated that IgE levels in saliva increase earlier than in serum and may be used as a prognostic criterion in patients with bronchopulmonary pathology.

Biological markers in induced sputum of patients with different phenotypes of chronic airway obstruction.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by a combination of 3 different disorders, namely chronic asthma, chronic bronchitis and pulmonary emphysema, sometimes simultaneously present in the same subject. OBJECTIVES: The aim of our study was to compare sputum inflammatory markers in patients with different phenotypes of chronic airway obstruction. METHODS: Forty-five subjects (forced expiratory volume in 1 s/vital capacity, FEV(1)/VC: 58.8 +/- 12.2%; FEV(1): 49.8 +/- 11.5% of predicted) were classified as chronic asthma (n = 10) or COPD patients (n = 35); the latter were further divided into patients with prevalent chronic bronchitis (n = 24) or prevalent pulmonary emphysema (n = 11) according to clinical history and functional evaluation, and underwent sputum induction and analysis of inflammatory cell and soluble mediators. RESULTS: Patients with chronic asthma showed higher sputum eosinophil percentages and eosinophilic cationic protein levels, and lower neutrophil percentages and neutrophil elastase levels than COPD patients. Neutrophil chemotactic activity in sputum supernatant was higher than the pool of normal subjects both in chronic asthma and COPD patients. No difference in sputum cell composition and levels of soluble mediators was observed between patients with chronic bronchitis and patients with pulmonary emphysema. CONCLUSIONS: The pattern of airway inflammation in induced sputum of patients with chronic asthma is different from that of COPD patients with a similar FEV(1). Among COPD patients, however, the pattern of airway inflammation shows no difference between chronic bronchitis and patients with pulmonary emphysema, suggesting that these two clinically and functionally distinct phenotypes share a common inflammatory pattern as detected by induced sputum.

Validation of assays for inflammatory mediators in exhaled breath condensate.

The use of exhaled breath condensate (EBC) as a tool for noninvasive assessment of lung inflammation is becoming commonplace. Many authors use commercial ELISA kits to measure inflammatory mediators within EBC. However, the very low concentrations of mediators within EBC are often below the commercially validated concentration range of the relevant ELISA and crucially below the linear part of the sigmoid standard curve. The present study seeks to validate a series of assays for use in EBC and to compare the results in EBC with those from matched sol phase sputum samples. The following mediators were measured by ELISA: leukotriene (LT)B(4), interleukin (IL)-8, secretory leukoprotease inhibitor and alpha(1)-antitrypsin (AAT). Myeloperoxidase was measured by chromogenic substrate assay. Mediator concentrations reached the lower limit of quantification in only one assay (AAT) in 19.6% of subjects, while mediator concentrations reached the lower limit of detection in three assays (LTB(4), IL-8 and AAT in 31, 6.5 and 61% of subjects, respectively). No significant correlations were present between any mediators in EBC and sol phase sputum. The results of the present study indicate that care must be exercised when interpreting mediator measurements in exhaled breath condensate and that assays must be validated at concentrations relevant to those found within the biological fluid.

[Immunity in chronic bronchitis patients with significant residual changes after prior pulmonary tuberculosis].

To study the immunological features in chronic bronchitis (CB) patients with great residual changes (GRC) after prior pulmonary tuberculosis, the authors examined two groups: 1) 40 CB patients with GRC after prior pulmonary tuberculosis (a study group) and 2) 30 CB patients without a history of pulmonary tuberculosis. The examination revealed that CB patients with GRC after prior pulmonary tuberculosis were found to have higher T lymphocytes, lower B lymphocytes on an exacerbation of the disease. The phagocytic properties of neutrophils were altered as their high phagocytic activity, decreased oxygen-dependent microbicidal activity of phagocytes with their stimulation. The humoral response remained to be slightly pronounced in CB bronchitis with GRC. The low serum levels of TBC active products may suggest the low activity of lipid peroxidation processes in the study group patients. After prior pulmonary tuberculosis, antioxidative activity preserves to be high in CB patients with GRC.

[Characteristics of the immune system in workers of heavy industry with chronic bronchitis].

Chronic bronchitis is a disease at the base of it we see inflammation process, when under the influence of factors of environment the immune system changes. The author has studied the influence of adverse factors on the state of the immune system of workers of engineering plants with chronic bronchitis. 15 workers of engineering plants with chronic bronchitis have been observed. 8 workers with chronic bronchitis had unhealthy conditions of work (main group) and other 7 workers with chronic bronchitis had not had unhealthy conditions of work (control group). The author revealed workers of engineering plants with chronic bronchitis to have changes of the immune system characterized by the increase in immunoglobulin M by 0.64 +/- 0.3 g/l in comparison with the control group (P < 0.05) and the increase in immunoglobulin G by 5.02 +/- 1.65 g/l (P < 0.05). Immunoglobulin A has decreased by 1.60 +/- 0.45 g/l (p < 0.05) in comparison with the control group. Then, CD3+ was 66.0 +/- 2.9% in the main group and in the control group it was by 4.35 +/- 3.1% greater. It was seen decrease in the activity of T-suppressors of patients with chronic bronchitis who were exposed to unhealthy conditions of work. CD4+ and CD20+ were also different in the main and control groups. It is worthy to note that patients with chronic bronchitis working in unhealthy conditions (main group) had reduced activity of neutrophilic granulocytes while this activity is increased in the workers of the control group. So these data certify that changes in the immune system of workers of engineering plants with chronic bronchitis significantly correlate with the presence of unhealthy conditions in work.

[Immune mechanisms of broncho-pulmonary diseases in aluminium production workers].

Complex clinical examination of aluminium production workers having broncho-pulmonary diseases revealed immunologic criteria of toxic dust bronchitis, diffuse pneumosclerosis and secondary infection-dependent bronchial asthma, caused by combination of occupational hazards. Contribution of allergic environmental factors was shown as they deplete immune reserves in the workers. The authors proved efficiency of contemporary immune modulator polyoxydonium, when included into the complex therapy.

Factors associated with plasma IL-33 levels in patients with chronic obstructive pulmonary disease.

BACKGROUND: Interleukin (IL)-33 promotes T helper (Th)2 immunity and systemic inflammation. The role of IL-33 in asthma has been widely investigated. IL-33 has also been suggested to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). This study investigated the clinical significance and usefulness of plasma IL-33 level in patients with COPD. METHODS: A total of 307 patients with stable COPD from 15 centers, who were in the Korean Obstructive Lung Disease cohort, were enrolled in this study. Plasma IL-33 levels were measured by enzyme-linked immunosorbent assay. We analyzed the association between IL-33 level and other clinical characteristics related to COPD. We also examined the features of patients with COPD who exhibited high IL-33 levels. RESULTS: IL-33 levels varied, but were very low in most patients. Eosinophil count was significantly correlated with a plasma IL-33 level. In addition, old age and current smoking were related to a low IL-33 level. Significantly more patients with a higher IL-33 level had chronic bronchitis compared with those with a low IL-33 level. CONCLUSION: Plasma IL-33 level in patients with stable COPD was related to eosinophil count and chronic bronchitis phenotype. Further studies are needed to identify the precise mechanisms of IL-33/ST2 pathway in patients with COPD.