Regulation trend of resveratrol on TNF-α,IL-1β,IL-6 expressions in bronchoalveolar lavage fluid of RSV-infected BALB/c mice

2012 ◽  
Author(s):  
LI Jiaxi
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Tnf Α

scholarly journals TGF-β1, IL-6 and TNF-α in Bronchoalveolar Lavage Fluid: Useful Markers for Lung Cancer?

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Zhongbo Chen ◽  
Zhiwei Xu ◽  
Shifang Sun ◽  
Yiming Yu ◽  
Dan Lv ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Tnf Α ◽  
Tgf Β1

Characterization of LPS-induced lung inflammation incftr−/−mice and the effect of docosahexaenoic acid

2002 ◽  
Vol 92 (5) ◽  
pp. 2169-2176 ◽  
Author(s):  
Steven D. Freedman ◽  
Deborah Weinstein ◽  
Paola G. Blanco ◽  
Pedro Martinez-Clark ◽  
Serge Urman ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Membrane Lipid ◽  
Inflammatory Parameters ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Α

The mechanism by which Pseudomonas causes excessive inflammation in the cystic fibrosis lung is unclear. We have reported that arachidonic acid is increased and docosahexaenoic acid (DHA) decreased in lung, pancreas, and ileum from cftr−/−mice. Oral DHA corrected this defect and reversed the pathology. To determine which mediators regulate inflammation in lungs from cftr−/−mice and whether inhibition occurs with DHA, cftr−/−and wild-type (WT) mice were exposed to aerosolized Pseudomonas lipopolysaccharide (LPS). After 2 days of LPS, tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-2, and KC levels in bronchoalveolar lavage fluid were increased in cftr−/−compared with WT mice and not suppressed by pretreatment with oral DHA. Neutrophil levels were not different between cftr−/−and WT mice. After 3 days of aerosolized LPS, neutrophil concentration, TNF-α, and the eicosanoids 6-keto-PGF1α, PGF2α, PGE2, and thromboxane B2were all increased in bronchoalveolar lavage fluid from cftr−/−mice compared with WT controls. Oral DHA had no significant effect on TNF-α levels in cftr−/−mice. In contrast, neutrophils and eicosanoids were decreased in cftr−/−but not in WT mice treated with DHA, indicating that the effects of DHA on these inflammatory parameters may be related to correction of the membrane lipid defect.

Effects of mechanical ventilation at low lung volume on respiratory mechanics and nitric oxide exhalation in normal rabbits

2005 ◽  
Vol 99 (2) ◽  
pp. 433-444 ◽  
Author(s):  
Edgardo D'Angelo ◽  
Matteo Pecchiari ◽  
Patrizia Della Valle ◽  
Antonia Koutsoukou ◽  
Joseph Milic-Emili
Keyword(s):  
Mechanical Ventilation ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Lung Mechanics ◽  
Albumin Concentration ◽  
Open Chest ◽  
Interstitial Pulmonary Edema ◽  
Tnf Α ◽  
Low Volume

Lung mechanics, exhaled NO (NOe), and TNF-α in serum and bronchoalveolar lavage fluid were assessed in eight closed and eight open chest, normal anesthetized rabbits undergoing prolonged (3–4 h) mechanical ventilation (MV) at low volume with physiological tidal volumes (10 ml/kg). Relative to initial MV on positive end-expiratory pressure (PEEP), MV at low volume increased lung quasi-static elastance (+267 and +281%), airway (+471 and +382%) and viscolelastic resistance (+480 and +294%), and decreased NOe (−42 and −25%) in closed and open chest rabbits, respectively. After restoration of PEEP, viscoelastic resistance returned to control, whereas airway resistance remained elevated (+120 and +31%) and NOe low (−25 and −20%) in both groups of rabbits. Elastance remained elevated (+23%) only in closed-chest animals, being associated with interstitial pulmonary edema, as reflected by increased lung wet-to-dry weight ratio with normal albumin concentration in bronchoalveolar lavage fluid. In contrast, in 16 additional closed- and open-chest rabbits, there were no changes of lung mechanics or NOe after prolonged MV on PEEP only. At the end of prolonged MV, TNF-α was practically undetectable in serum, whereas its concentration in bronchoalveolar lavage fluid was low and similar in animals subjected or not subjected to ventilation at low volume (62 vs. 43 pg/ml). These results indicate that mechanical injury of peripheral airways due to their cyclic opening and closing during ventilation at low volume results in changes in lung mechanics and reduction in NOe and that these alterations are not mediated by a proinflammatory process, since this is expressed by TNF-α levels.

scholarly journals Prognostic Assessment of the Inflammatory Process Activity in Sarcoidosis of Respiratory Organs: Potential Use of C-reactive Protein and TNF-α

2017 ◽  
Vol 23 (2) ◽  
Author(s):  
Mykola Ostrovskyy ◽  
Kostiantyn Shvets
Keyword(s):  
Bronchoalveolar Lavage ◽  
Blood Serum ◽  
Peripheral Blood ◽  
Inflammatory Process ◽  
Bronchoalveolar Lavage Fluid ◽  
Research Work ◽  
Lavage Fluid ◽  
Control Group ◽  
Tnf Α ◽  
Α Level

This research work is devoted to the development of new additional criteria for the activity of inflammatory process in sarcoidosis of respiratory organs. The objective is to assess the effectiveness of performed treatment of sarcoidosis of respiratory organs by using low-cost highly-sensitive inflammatory markers.Materials and methods. The study involved 68 patients with lung sarcoidosis before and after the three-month treatment. In addition to general-clinical methods of examination, patients with sarcoidosis were also determined the levels of TNF-α and СRP.Results and their discussion. Patients with active lung sarcoidosis had 17.6 times (p<0.05) increased level of CRP in bronchoalveolar lavage fluid and 9.0 times (p<0.05) increased levels in peripheral blood serum; the levels of TNF-α increased by 4.98 times (p<0.05) in bronchoalveolar lavage fluid and by 3.2 times (p<0.05) in peripheral blood serum as compared to the findings in the control group of patients. The study showed that in the group of patients, where the efficacy of the prescribed therapy was noted, the level of CRP decreased by 2.76 times (p<0.05) in bronchoalveolar lavage fluid and by 2.58 times (p<0.05) in peripheral blood serum, and the concentration of TNF-α decreased by 3.87 times (p<0.05) in bronchoalveolar lavage fluid and by 2.06 times in peripheral blood serum as compared to the initial indices.Conclusions. The decrease of TNF-α level in bronchoalveolar lavage fluid on the background of three-months treatment correlated (r=0.89; p<0.05) to the changes in peripheral blood serum; at the same time the decrease of TNF-α level in peripheral blood serum correlated (r=0.82; p<0.05) to the decrease of CRP in peripheral blood serum of patients with sarcoidosis of respiratory organs. 

scholarly journals Autotaxin levels in serum and bronchoalveolar lavage fluid are associated with inflammatory and fibrotic biomarkers and the clinical outcome in patients with acute respiratory distress syndrome

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Lijuan Gao ◽  
Xiaoou Li ◽  
Hao Wang ◽  
Yue Liao ◽  
Yongfang Zhou ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bronchoalveolar Lavage ◽  
Sofa Score ◽  
Bronchoalveolar Lavage Fluid ◽  
Distress Syndrome ◽  
Lavage Fluid ◽  
Apache Ii Score ◽  
Tnf Α

Abstract Background Autotaxin (ATX) is a secreted glycoprotein that is widely present in extracellular biological fluids and has been implicated in many inflammatory and fibrotic diseases. However, the clinical impact of the release of ATX in patients with acute respiratory distress syndrome (ARDS) remains unclear. Methods Serum and bronchoalveolar lavage fluid (BALF) levels of ATX, interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α, matrix metalloproteinase (MMP)-7, fibronectin, oncostatin M (OSM), and SPARC (secreted protein acidic and rich in cysteine) were collected from 52 patients with ARDS within 24 h of diagnosis. All cytokines were measured by Magnetic Luminex Assay. BALF albumin (BA) and serum albumin (SA) were measured by enzyme-linked immunosorbent assay. Results Serum ATX, MMP-7, and BALF IL-8 levels were significantly higher in patients who did not survive than in those who survived up to 28 days after diagnosis of ARDS (P < 0.05). BALF and serum ATX levels were correlated with IL-6, IL-8, and MMP-7 levels in BALF and serum, respectively. In addition, BALF ATX was positively correlated with BALF TNF-α, fibronectin, OSM, and SPARC as well as the BA/SA ratio, while serum ATX was correlated with severity of illness based on the SOFA score and PaO2/FIO2 ratio. Furthermore, serum ATX was better able to predict 28-day ARDS-related mortality (area under the curve 0.744, P < 0.01) than the SOFA score, APACHE II score, or PaO2/FIO2 ratio. Serum ATX independently predicted mortality in a univariate Cox regression model (P < 0.0001). Conclusion The serum ATX level is a potential prognostic biomarker in patients with ARDS. BALF ATX is associated with pulmonary biomarkers of inflammation and fibrosis, suggesting a role of ATX in the pathogenesis of ARDS.

scholarly journals Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ye Yang ◽  
Lei Huang ◽  
Chongchong Tian ◽  
Bingjun Qian
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Normal Control Group ◽  
Control Group ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α ◽  
Magnesium Isoglycyrrhizinate

Abstract Background Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung diseases with the characteristics of airway remodeling and airflow obstruction. Magnesium isoglycyrrhizinate (MgIG) is an anti-inflammatory glycyrrhizic acid preparation for treating hepatitis. However, whether MgIG can treat other diseases and its action mechanism is still obscure. In this study, we evaluated the anti-inflammatory effect of MgIG in rats with COPD and investigated the underlying mechanisms. Methods Rat model of COPD was constructed by endotracheal-atomized lipopolysaccharide exposure and cigarette smoke induction. Rats were randomly divided into 5 groups: control group, COPD model group, salmeterol fluticasone comparator group, low dose of MgIG group, and high dose of MgIG group. Except for normal control group, the other four groups received sensitization treatment by cigarette smoking and endotracheal-atomization of endotoxin lipopolysaccharide to construct COPD rats model. After model established successfully, the COPD rats in each group received corresponding dose of endotracheal-atomized normal saline, salmeterol fluticasone, and MgIG every day prior to exposure of cigarette smoke from days 30 to 45. Normal control group were treated with normal saline. Finally, All rats were euthanatized. Pulmonary function was measured. Cells in bronchoalveolar lavage fluid were classified, inflammatory factors IL-6 and TNF-α were determined, histopathological analysis was performed by HE staining, and expression of NLRP3 and cleaved caspase-1 in the lung tissue was also determined by Western blotting. Results It showed that MgIG treatment (0.40 or 0.80 mg/kg/day) could recover the weight and the clinical symptoms of rats with COPD, accompanied with lung inflammation infiltration reduction, airway wall attenuation, bronchial mucus secretion reduction. Additionally, MgIG administration reduced inflammatory cells (white blood cells, neutrophils, lymphocytes and monocytes) accumulation in bronchoalveolar lavage fluid and decreased IL-6 and TNF-α production in the serum of COPD rats. Furthermore, MgIG treatment also reduced the expression level of NLRP3 and cleaved caspase-1. Conclusion It indicate that MgIG might be an alternative for COPD treatment, and its mechanism of action might be related to the suppression of NLRP3 inflammasome.

scholarly journals IL-6 knockout alleviates inflammatory response and improve acute lung injury via regulating macrophage polarization in sepsis

2021 ◽  
Author(s):  
Jinxin Zhang ◽  
Kuo Shen ◽  
Jiangang Xie ◽  
Shanshou Liu ◽  
Xiaozhi Bai ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Western Blot ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokines ◽  
Death Rate ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Tnf Α

Abstract Background Sepsis is a fatal disease with a high rate of morbidity and mortality, during which acute lung injury is the earliest and most serious complication. Macrophage plays a crucial role in the initiation and progress of sepsis. This study meant to explore the effect of IL-6 knockout in CLP induced sepsis. Methods In this study, cecal ligation and puncture (CLP) was performed on wildtype and interleukin 6 (IL-6) knockout C57 mice. General condition and death rate of sepsis mice were observed. organ samples (lungs, livers, kidneys and hearts) and serum were collected for histology observation and inflammatory cytokine detection. Lung tissue injury detection were conducted via lung injury score, wet/dry ration and protein concentrations measurement of Bronchoalveolar lavage fluid (BALF). In in vivo studies, RAW264.7 macrophages were transfected with IL-6 specific siRNA and treated with LPS. After exposed to IL-6 specific siRNA and LPS, expression of inflammatory cytokines interleukin 1 (IL-1), tumor necrosis factor-α (TNF-α), IL-6 and interleukin 10 (IL-10) were detected by RT-qPCR, concentration of IL-1 and TNF-α in culture supernatant were detected by ELISA and M1 and M2 markers were detected by western blot and flow cytometry. Results We constructed CLP induced sepsis models and found that inhibition of IL-6 could improve general condition and death rate of sepsis mice. Mice in IL-6 knockout group display improved tissue damage, especially in the lung tissue. IL-6 knockout relieved inflammatory cytokines storm in both serum and bronchoalveolar lavage fluid while polarized macrophage to an anti-inflammatory M2 phenotype. In cell model, inhibition of IL-6 could alleviate LPS induced expression of inflammatory cytokines IL-1, TNF-α, and IL-6 in macrophages. Western blot and Flow cytometry results indicated that expression of M1 markers (iNOS and CD86) in LPS stimulated macrophages were significantly declined while M2 (Arg-1 and CD206) were enhanced when expression of IL-6 was blocked. Conclusion Inhibition of IL-6 alleviated LPS induced inflammation and exerted protective effect in sepsis via regulating macrophage function and polarization.

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