Relationship between radiologic patterns, pulmonary function values and bronchoalveolar lavage fluid cells in newly diagnosed sarcoidosis

Meng

et al. 2020

Exp Biol Med (Maywood)

Smoking has become a major cause of chronic obstructive pulmonary disease through weakening of the respiratory mucus-ciliary transport system, impairing cough reflex sensitivity, and inducing inflammation. Recent researches have indicated that hydrogen sulfide is essential in the development of various lung diseases. However, the effect and mechanism of hydrogen sulfide on cigarette smoke-induced chronic obstructive pulmonary disease have not been reported. In this study, rats were treated with cigarette smoke to create a chronic obstructive pulmonary disease model followed by treatment with a low concentration of hydrogen sulfide. Pulmonary function, histopathological appearance, lung edema, permeability, airway remodeling indicators, oxidative products/antioxidases levels, inflammatory factors in lung, cell classification in bronchoalveolar lavage fluid were measured to examine the effect of hydrogen sulfide on chronic obstructive pulmonary disease model. The results showed that hydrogen sulfide effectively improved pulmonary function and reduced histopathological changes, lung edema, and permeability. Airway remodeling, oxidative stress, and inflammation were also reduced by hydrogen sulfide treatment. To understand the mechanisms, we measured the expression of TGF-β1, TGF-βIand TGF-βII receptors and Smad7 and phosphorylation of Smad2/Smad3. The results indicated that the TGF-β1 and Smad were activated in cigarette smoke-induced chronic obstructive pulmonary disease model, but inhibited by hydrogen sulfide. In conclusion, this study showed that hydrogen sulfide treatment alleviated cigarette smoke-induced chronic obstructive pulmonary disease through inhibition of the TGF-β1/Smad pathway. Impact statement COPD has become a severe public health issue in the world and smoking has become a major cause of COPD. As a result, it is a demandingly needed to explore new potential therapy for cigarette smoke-associated COPD. The present study suggested that H2S treatment improved pulmonary function and reduced histopathological changes, lung edema, permeability, inflammation, airway remodeling and oxidative injury in a COPD model induced by cigarette smoke. Although additional studies are required to elucidate the pharmacodynamics, pharmacokinetics, and pharmacology of H2S in the cigarette smoke-associated COPD, our findings provide an experimental basis for the potential clinical application of H2S in COPD treatment.

“…28 Approximately 200 cells were counted in each sample and classified as neutrophils, lymphocytes, and macrophages according to morphological characteristics. 29…”

Section: Methodsmentioning

confidence: 99%

Hydrogen sulfide alleviates cigarette smoke-induced COPD through inhibition of the TGF-β1/smad pathway

Meng

et al. 2020

Exp Biol Med (Maywood)

“…We had performed literature search looking for a cellular markers that could help to predict the course of sarcoidosis and selected four molecules, e.g., CD31, CD38, CD44, and CD103. Many inflammatory cells and tissue cells with various, sometimes even opposite effects may be positive for CD31, CD38, CD44, and CD103 (23)(24)(25)(26)(27)(28)(29), but while sarcoidosis is driven by T-cell mechanisms, particularly the accumulation of activated CD4 T-cells in the lungs, allowing for T-cell attachment and transmigration through the endothelium (30)(31), research was performed on T cell subpopulations CD4 + and CD8 + . CD31, also known as platelet endothelial cellular adhesion molecule-1 (PECAM-1), is an integral membrane protein expressed by endothelial cells, platelets, dendritic cells, and blood cells, including T lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

CD31+, CD38+, CD44+, and CD103+ lymphocytes in peripheral blood, bronchoalveolar lavage fluid and lung biopsy tissue in sarcoid patients and controls

Aleksonienė¹,

Besusparis²,

Gruslys³

et al. 2021

J Thorac Dis

Self Cite

Background: The mechanisms driving the transition from inflammation to fibrosis in sarcoidosis patients are poorly understood; prognostic features are lacking. Immune cell profiling may provide insights into pathogenesis and prognostic factors of the disease. This study aimed to establish associations in simultaneous of lymphocyte subset profiles in the blood, bronchoalveolar lavage fluid (BALF), and lung biopsy tissue in the patients with newly diagnosed sarcoidosis.Methods: A total of 71 sarcoid patients (SPs) and 20 healthy controls (HCs) were enrolled into the study. CD31, CD38, CD44, CD103 positive T lymphocytes in blood and BALF were analysed. Additionally, the densities of CD4, CD8, CD38, CD44, CD103 positive cells in lung tissue biopsies were estimated by digital image analysis. Results: Main findings: (I) increase of percentage of CD3 + CD4 + CD38 + in BALF and blood, and increase of percentage of CD3 + CD4 + CD44 + in BALF in Löfgren syndrome patients comparing with patients without Löfgren syndrome, (II) increase of percentage of CD3 + CD4 + 103 + in BALF and in blood in patients without Löfgren syndrome (comparing with Löfgren syndrome patients) and increase of percentage of CD3 + CD4 + 103 + in BALF and in blood in more advanced sarcoidosis stage. (III) Increasing percentage of BALF CD3 + CD4 + CD31 + in sarcoidosis patients when comparing with controls independently of presence of Löfgren syndrome, smoking status or stage of sarcoidosis. Several significant correlations were found. Conclusions: Lymphocyte subpopulations in blood, BALF, and lung tissue were substantially different in SPs at the time of diagnosis compared to HCs. CD3 + CD4 + CD31 + in BALF might be a potential supporting marker for the diagnosis of sarcoidosis. CD3 + CD4 + CD38 + in BALF and blood and CD3 + CD4 + CD44 + in BALF may be markers of the acute immune response in sarcoidosis patients. CD4 + CD103 + T-cells in BALF and in blood are markers of the persistent immune response in sarcoidosis patients and are potential prognostic features of the chronic course of this disease.

Advances in Respiratory Medicine

“…Levy et al recommend repeated HRCT scans if the clinical image changes or complications are suspected [36 37]. Unlike X-ray scans, some lesions visible in HRCT demonstrate a relationship with pulmonary function disorders [38][39][40]. Drent et al demonstrated correlations between features visible in HRCT such as thickening of the bronchovascular bundle, intraparenchymal nodules, septal and non-septal lines, or focal pleural thickening on one hand, and results of respiratory functional tests on the other [38].…”

Section: High Resolution Computed Tomographymentioning

confidence: 99%

Imaging Methods for Pulmonary Sarcoidosis

Węcławek

Jastrzębski

2020

Sarcoidosis is a chronic systemic granulomatous disease of unknown etiology. In more than 90% of patients with diagnosed sarcoidosis, mediastinal and hilar lymph nodes are affected. The objective of this paper is to discuss the most important chest imaging methods in pulmonary sarcoidosis. A chest X-ray remains the method of choice at both the diagnostic stage and during follow-up of the disease progress. High-resolution computed tomography allows for a more thorough description of lesions in terms of their location. Research demonstrates the superiority of FDG PET over both aforementioned techniques in the assessment of active inflammatory lesions. Magnetic resonance imaging is currently being used in diagnosing cardiac sarcoidosis. Although EBUS constitutes the basic diagnostic tool, the invasiveness of the method results in it not being used when monitoring the activity of the disease.