Levels Of Inflammatory Cytokines And Chemokines In Bronchoalveolar Lavage Fluid In Patients With Idiopathic Interstitial Pneumonitis And Collagen Vascular Disease Associated Interstitial Pneumonitis

Abstract BackgroundSepsis 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.MethodsIn 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- (TNF-), IL-6 and interleukin 10 (IL-10) were detected by RT-qPCR, concentration of IL-1 and TNF- in culture supernatant were detected by ELISA and M1 and M2 markers were detected by western blot and flow cytometry.ResultsWe 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-, 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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Lymphadenopathy-Associated Virus Isolated from Bronchoalveolar Lavage Fluid in AIDS-Related Complex with Lymphoid Interstitial Pneumonitis

New England Journal of Medicine ◽

10.1056/nejm198507183130313 ◽

1985 ◽

Vol 313 (3) ◽

pp. 183-183 ◽

Cited By ~ 36

Keyword(s):

Bronchoalveolar Lavage ◽

Interstitial Pneumonitis ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Aids Related Complex ◽

Related Complex

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Effects of Mesenchymal Stem Cells and Their Derived Microvesicles on Pulmonary Toxicity Induced by Petrol Exhaust Nanoparticle; Histological and Immuno-Histochemical Study

Annual Research & Review in Biology ◽

10.9734/arrb/2019/v31i630070 ◽

2019 ◽

pp. 1-14

Author(s):

Sherifa Abd El Salam ◽

Eman Mohamed Faruk ◽

Hanan Fouad ◽

Naglaa Yehia Nafie

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Bronchoalveolar Lavage ◽

Inflammatory Cytokines ◽

Lung Tissue ◽

Pulmonary Toxicity ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Total Proteins ◽

Regenerative Capacity

Background: Diesel vehicles exhaust contains toxic nanoparticles that drastically affect lung tissue due to their direct cytotoxic effects, induction of oxidative stress, inflammatory signaling pathways and DNA damage. Mesenchymal stem cells (MSCs) exhibit anti-inflammatory effects and efficient regenerative capacity in chronic lung diseases. Objectives: Evaluation of the effects of MSCs and MSCs-derived micro vesicles (MSCs-MVs) on pulmonary toxicity induced by diesel exhaust nanoparticles (DENPs). Materials and Methods: Sixty male rats were equally divided into: Group I (Control rats), Group II (DENPs group) received repeated doses of DENPs (180μg/rat) intratracheally every other day for 6 days, Group III (MSCs group) received MSCs intravenously (3×106 cells) after the last dose of DENPs and Group IV (MSCs-MVs group) received MSCs-MVs (0.5 mg/mL) intravenously after the last dose of DENPs. Lung tissue were subjected to histological and immunohistochemical assessment. Inflammatory cytokines and bronchoalveolar lavage fluid (BALF) contents of inflammatory cells, albumin, LDH and total proteins were evaluated. Results: Histological picture of lung tissue in DENPs group showed numerous collapsed alveoli, thick interalveolar septa and marked cellular infiltration. Elastic fibers were markedly decreased by DENPs. Increased optical density of NF-κB/p65 immunoreactivity. Bronchoalveolar lavage fluid showed significant elevation of inflammatory cytokines (TNF-a, IL-6), polymorphonuclear leukocytes (PMN), neutrophils, macrophages, LDH, total proteins and albumin. Treatment with either MSCs or MSCs-MVs led to a significant amelioration of all of the aforementioned studied parameters. Conclusion: MSCs-MVs and MSCs showed significant therapeutic effects against DENPs damaging effects on the lung tissues via their regenerative capacity and anti-inflammatory effects.

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Heparin‐binding protein, lysozyme, and inflammatory cytokines in bronchoalveolar lavage fluid as diagnostic tools for pulmonary infection in lung transplanted patients

American Journal of Transplantation ◽

10.1111/ajt.14458 ◽

2017 ◽

Vol 18 (2) ◽

pp. 444-452 ◽

Cited By ~ 10

Author(s):

Anna Stjärne Aspelund ◽

Helena Hammarström ◽

Malin Inghammar ◽

Hillevi Larsson ◽

Lennart Hansson ◽

...

Keyword(s):

Bronchoalveolar Lavage ◽

Inflammatory Cytokines ◽

Bronchoalveolar Lavage Fluid ◽

Pulmonary Infection ◽

Binding Protein ◽

Lavage Fluid ◽

Diagnostic Tools ◽

Heparin Binding ◽

Heparin Binding Protein

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

10.21203/rs.3.rs-618570/v1 ◽

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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