- Associations of Pulmonary Fibrosis with Peripheral Blood Th1/Th2 Cell Imbalance and EBF3 Gene Methylation in Uygur Pigeon Breeder's Lung Patients. [Journal Article]
- CPCell Physiol Biochem 2018 Jun 15; 47(3):1141-1151
- Background/Aims Pigeon breeder's lung (PBL) results from Th1/Th2 cell imbalance. B cells inhibit the immune activity of Th1, and EBF3 is a key B cell factor. This study explored the relationship betw...
Background/Aims Pigeon breeder's lung (PBL) results from Th1/Th2 cell imbalance. B cells inhibit the immune activity of Th1, and EBF3 is a key B cell factor. This study explored the relationship between EBF3 and Th1/Th2 imbalance in chronic PBL cases complicated with pulmonary fibrosis (PF). Methods Twenty Uygur PBL+PF patients, 20 pigeon breeders without PBL or PF, and 20 healthy individuals without pigeon breeding history constituted the patient I, negative control, and normal control groups, respectively. Peripheral blood specimens and case backgrounds were collected between June 2016 and March 2017. EBF3 gene methylation was analyzed by matrix assisted laser desorption ionization-time of flight mass spectrometry. To compare different mechanisms of PF progression in PBL, samples from 20 Uygur PBL patients without PF (at acute and sub-acute stages) were collected between October 2017 and February 2018, constituting the patient II group. EBF3 mRNA expression was evaluated by real-time polymerase chain reaction. IFN-γ, IL-4 and IL-10 expression and Th1/Th2 imbalance in PBL were evaluated by enzyme-linked immunosorbent assay and flow cytometry. Results CpG-2 and general methylation rates in the patient I group were lower than those in the control groups (P˂0.017). The level of EBF3 mRNA expression in the patient I group was significantly higher than that in any other group. Compared with the control groups, the patient I group showed a significantly higher level of IL-4, whereas the patient II group showed a significantly lower level. IL-10 was also expressed more highly in the patient I group than in any other group (P< 0.01). Flow cytometry showed INF-γ dominance (Th1 cytokine) in PBL at the acute/sub-acute stage and IL-4 dominance (Th2 cytokine) at the chronic stage after PF occurred. The general methylation rate was negatively correlated with the mRNA level, with the latter being positively correlated with the IL-10 level and number of pigeons bred in the past 3 months. IL-4 expression was negatively correlated with INF-γ but positively correlated with PF area and duration of pigeon breeding history. Conclusions After PF occurs in chronic PBL, the inflammation type changes from Th1 dominance to Th2 dominance. During PBL development, IL-10 increases before IL-4 does, which may be associated with EBF3 hypomethylation and the involvement of B lymphocytes.
- Lung disease associated with occupational styrene exposure. [Journal Article]
- AJAm J Ind Med 2018 Jun 13
- Despite reports of pulmonary toxicity due to styrene, guidelines on acceptable styrene exposure levels have been based on risk of cancer and central nervous system and liver toxicity and not on respi...
Despite reports of pulmonary toxicity due to styrene, guidelines on acceptable styrene exposure levels have been based on risk of cancer and central nervous system and liver toxicity and not on respiratory effects. Many reports have linked exposure to styrene vapor in occupational settings to various forms of non-malignant pulmonary disorders including bronchiolitis, hypersensitivity pneumonitis, and occupational asthma. We report two cases in which the same tasks performed in a single workplace resulted in exposure to styrene vapor with subsequent development of acute respiratory symptoms associated with impaired gas exchange and imaging and histopathologic findings consistent with bronchiolitis and organizing pneumonia. Both patients gradually recovered once their workplace exposure to styrene was terminated. Clinicians, employers, and insurers should be aware of the potential for pulmonary toxicity from exposure to styrene.
- Clinical behaviour of patients exposed to organic dust and diagnosed with idiopathic pulmonary fibrosis. [Journal Article]
- RRespirology 2018 Jun 13
- CONCLUSIONS: Group B patients experienced a better outcome compared with (non-exposed) IPF patients, although worse compared with CHP patients. Antifibrotic treatment in group B resulted in a similar beneficial effect compared with group A. Further research is needed to ascertain the diagnostic designation in this exposed usual interstitial pneumonia (UIP) patient group without other CHP features.
- [The respiratory effects of smoking]. [Review]
- RPRev Pneumol Clin 2018 May 21
- A marked increase in the morbidity and mortality of a large number of broncho-pulmonary diseases has been documented in relation to smoking. The influence of tobacco smoking on various respiratory co...
A marked increase in the morbidity and mortality of a large number of broncho-pulmonary diseases has been documented in relation to smoking. The influence of tobacco smoking on various respiratory conditions. is discussed: incidence, severity or natural history modification of some respiratory illnesses: obstructive lung diseases (COPD, asthma), lung cancer, bacterial, viral respiratory infections, with the impact of smoking on tuberculosis. Finally, the relationship of tobacco with diffuse interstitial lung disease: protective role of smoking (controversial in sarcoidosis, real in hypersensitivity pneumonitis). The benefits of smoking cessation are described.
- The Expression of AQP1 IS Modified in Lung of Patients With Idiopathic Pulmonary Fibrosis: Addressing a Possible New Target. [Journal Article]
- FMFront Mol Biosci 2018; 5:43
- Activation of the epithelial-mesenchymal transition process (EMT) by which alveolar cells in human lung tissue undergo differentiation giving rise to a mesenchymal phenotype (fibroblast/miofibroblast...
Activation of the epithelial-mesenchymal transition process (EMT) by which alveolar cells in human lung tissue undergo differentiation giving rise to a mesenchymal phenotype (fibroblast/miofibroblasts) has been well recognized as a key element in the origin of idiopathic pulmonary fibrosis (IPF). Here we analyzed expression of AQP1 in lung biopsies of patients diagnosed with IPF, and compared it to biopsies derived from patients with diverse lung pneumonies, such as hypersensitivity pneumonitis, sarcoidosis or normal lungs. Immunostaining for AQP1 showed a clear increment of AQP1 localized in the alveolar epithelium in biopsies from IPF patients alone. Moreover, to examine the possible participation of AQP1 in the pathophysiology of IPF, we evaluated its role in the pro-fibrotic transformation induced by transforming growth factor (TGF-β) in vitro. Human alveolar epithelial cells (A549), and fibroblasts derived from an IPF patient (LL29), or fibroblasts from healthy normal lung tissue (MRC-5), were treated with TGF-β, and levels of expression of AQP1, as well as those of E-cadherin, vimentin, α-SMA and collagen were analyzed by RT-qPCR, western blot and immunohistochemistry. An increase of AQP1 mRNA and protein after TGF-β treatment (4-72h) was observed either in A549 or IPF fibroblast-LL29 but not in MRC-5 fibroblasts. A gradual reduction of E-cadherin, and increased expression of vimentin, with no changes in α-SMA levels were observed in A549. Whereas in LL29 and MRC-5, TGF-β1 elicited a large production of collagen and α-SMA that was significantly greater in IPF fibroblast-LL29. Changes observed are consistent with activation of EMT by TGF-β, but whether modifications in AQP1 expression are responsible or independent events occurring at the same time is still unknown. Our results suggest that AQP1 plays a role in the pro-fibrotic TGF-β action and contributes to the etiology and pathophysiology of IPF. Understanding AQP1's role will help us comprehend the fate of this disease.
- Hypersensitivity Pneumonitis and Acute Respiratory Distress Syndrome From E-Cigarette Use. [Journal Article]
- PedPediatrics 2018; 141(6)
- Electronic cigarette (e-cigarette) use, or "vaping," is gaining widespread popularity as an alternative to conventional cigarettes among adolescents. Little is known of the health risks of e-cigarett...
Electronic cigarette (e-cigarette) use, or "vaping," is gaining widespread popularity as an alternative to conventional cigarettes among adolescents. Little is known of the health risks of e-cigarette use, especially in children and adolescents. We present a Case Report of a previously healthy 18-year-old woman who presented with dyspnea, cough, and pleuritic chest pain after e-cigarette use. She developed respiratory failure with hypoxia and was intubated, and ultimately met diagnostic criteria for acute respiratory distress syndrome. Chest tubes were placed to drain worsening pleural effusions. Computed tomography of the chest revealed dependent opacities in both lung bases, superimposed smooth interlobular septal thickening, and pleural effusions. Bronchoalveolar lavage revealed cellular debris and reactive mononuclear cells, and cell counts were remarkable for elevated mononuclear cells and eosinophilia. After the results of a workup for an infectious etiology came back negative, the patient was diagnosed with hypersensitivity pneumonitis and intravenous methylprednisolone therapy was initiated. After this the patient rapidly improved, was weaned off vasopressor support, and was extubated. This is the first reported case of hypersensitivity pneumonitis and acute respiratory distress syndrome as a risk of e-cigarette use in an adolescent, and it should prompt pediatricians to discuss the potential harms of vaping with their patients. Hypersensitivity pneumonitis, lipid pneumonia, and eosinophilic pneumonia should be included in the differential diagnosis of patients who exhibit respiratory symptoms after the use of an e-cigarette.
- StatPearls [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- Hypersensitivity pneumonitis (HP) classified as an interstitial lung disease is characterized by a complex immunological reaction of the lung parenchyma in response to repetitive inhalation of a sens...
Hypersensitivity pneumonitis (HP) classified as an interstitial lung disease is characterized by a complex immunological reaction of the lung parenchyma in response to repetitive inhalation of a sensitized allergen. The name HP defines the disease more appropriately than the previous term extrinsic allergic alveolitis, as the inflammation involves not only the alveoli but the bronchioles as well. The severity of the disease and clinical presentation varies depending on the inhaled antigen and quantity. The first detailed clinical descriptions of the disease came out in 1932 describing symptoms in workers exposed to a fungus on Maple bark at a Michigan company and agricultural workers exposed to moldy hay in England. Since these initial observations, numerous exposures have been described from all over the world that causes HP. Traditionally it has been classified into acute, sub-acute and chronic forms based on the time course and the presentation. But more recently classifying it to Acute or Inflammatory HP (symptoms less than six months) and Chronic or fibrotic HP has been proposed based on clinical, radiologic and pathologic characteristics.
- Clinical Genetics in Interstitial Lung Disease. [Review]
- FMFront Med (Lausanne) 2018; 5:116
- Interstitial lung disease (ILD) comprises a heterogeneous group of diffuse parenchymal lung processes with overlapping clinical, radiographic, and histopathologic features. Among the most common and ...
Interstitial lung disease (ILD) comprises a heterogeneous group of diffuse parenchymal lung processes with overlapping clinical, radiographic, and histopathologic features. Among the most common and deadly ILDs are idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis (CHP). As the name implies, the cause of IPF remains elusive, but a variety of genetic and infectious risk factors have been identified. CHP results from chronic inhalation of an organic antigen, usually of avian or mold origin, and may occur in patients with a genetic predisposition. While IPF is treated with anti-fibrotic compounds, CHP is generally treated by suppression of the immune system and elimination of the causative antigen. Despite advances in our understanding of IPF and CHP, there exists substantial variability in the diagnosis and treatment of these disease processes. Furthermore, IPF and CHP natural history and treatment response remain far from uniform, leaving it unclear which patients derive the most benefit from disease-specific therapy. While clinical prediction models have improved our understanding of outcome risk in patients with various forms of ILD, recent advances in genomic technology provides a valuable opportunity to begin understanding the basis for outcome variability. Such advances will ultimately allow for the incorporation of genomic markers into risk stratification and clinical decision-making. In this piece, we highlight recent advances in our understanding of the genomic factors that influence susceptibility and outcome risk among patients with IPF and CHP. Genomic modalities used to identify these genomic markers include genome-wide association studies, analyses of gene expression, drug-gene interaction testing, telomere length determination, telomerase mutation analysis, and studies of the lung microbiome. We then identify gaps in knowledge that should be addressed to help facilitate the incorporation of these genomic technologies into ILD clinical practice.
- The aging lung: tissue telomere shortening in health and disease. [Journal Article]
- RRRespir Res 2018 May 11; 19(1):95
- CONCLUSIONS: These results show a progressive decline in telomere length with age in normal, BOS and RAS lungs. cHP, BOS and RAS lungs demonstrated shorter RTL compared to normal lungs. Lung tissue RTL does not associate with regional disease severity within the lung. Therefore, tissue RTL does not seem to fully reflect peripheral blood telomere length.
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- Current and emerging techniques for the diagnosis of hypersensitivity pneumonitis. [Journal Article]
- ERExpert Rev Respir Med 2018; 12(6):493-507
- Hypersensitivity pneumonitis (HP) is the result of an immunologically induced inflammation of the lung parenchyma in response to inhalation exposure to a large variety of antigens in genetically susc...
Hypersensitivity pneumonitis (HP) is the result of an immunologically induced inflammation of the lung parenchyma in response to inhalation exposure to a large variety of antigens in genetically susceptible individuals. HP shares clinical and radiological features with other acute and chronic interstitial lung diseases and is sometimes difficult to diagnose if exposure to an antigenic agent is not detected. Several classifications and diagnostic criteria have been proposed but are not currently recommended by guidelines from any scientific society. However, advances have been made over the past ten years in improving the diagnosis of HP. Areas covered: This article will provide a summary of the different classification and diagnostic criteria proposed in acute and chronic forms of HP. In addition, we review current diagnostic procedures including antigen detection, high resolution computed tomography, histopathology and provide an overview of emerging techniques. Expert commentary: Important changes are occurring in the field of HP and knowledge of the disease will likely progress enormously in the coming 5 to 10 years as many techniques continue to be developed, including genomic signature and diagnostic biomarkers.