The role of microRNA regulation in the early inflammatory response: miR-146a and NF-κB signaling in lung inflammation

Pneumologie ◽  
2013 ◽  
Vol 67 (S 01) ◽  
Author(s):  
X Lai ◽  
C Schulz ◽  
F Seifert ◽  
B Dolniak ◽  
O Wolkenhauer ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lung Inflammation ◽  
Microrna Regulation ◽  
Early Inflammatory Response

scholarly journals Lung Inflammation from Single and Repetitive Exposure to Glyphosate

2021 ◽  
Author(s):  
Upkardeep Singh Pandher ◽  
Shelley Kirychuk ◽  
David Schneberger ◽  
Brooke Thompson ◽  
Gurpreet Aulakh ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lung Inflammation ◽  
Leukocyte Infiltration ◽  
Th2 Cytokines ◽  
Once Daily ◽  
Repetitive Exposure ◽  
Lung Histology ◽  
Relevant Dose ◽  
First Time

Abstract Background: Glyphosate is an active ingredient in herbicides used in agriculture worldwide. Exposure to glyphosate has been associated with respiratory dysfunctions in agricultural workers. However, the ability of glyphosate to induce inflammation in the lung is not well studied. Therefore, we evaluated lung inflammatory response to glyphosate at agricultural relevant dose for single and repetitive exposures. Methods: Male C57BL/6 mice were intranasally exposed to glyphosate (1 μg/40 μl) for 1-day or once daily for 5-days, and 10-days. After the exposure periods, mice were euthanized to collect the bronchoalveolar lavage (BAL) fluid and lung tissue. Results: Repetitive exposure to glyphosate for 5-days and 10-days showed an increase of neutrophils in BAL fluid and eosinophil peroxidase levels in lungs, a marker for eosinophils. Leukocyte infiltration in lungs was further confirmed through lung histology. Th2 cytokines including IL-5 and IL-13 were increased in BAL fluid after 10-days of glyphosate exposure whereas IL-4 was not increased. Lung sections from all glyphosate groups showed higher expression for ICAM-1, VCAM-1, and vWF adhesion molecules. TLR-4 and TLR-2 expression was increased in lungs after repetitive exposure to glyphosate. Conclusions: We conclude that repetitive exposure to glyphosate induces migration of neutrophils and eosinophils and release of Th2 cytokines. This study, for the first time, provides evidence for the role of ICAM-1, VCAM-1 and vWF in lungs of glyphosate-treated animals.

Antigen-Induced Eosinophilic Lung Inflammation Develops in Mice Deficient in Chemokine Eotaxin

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3912-3923 ◽  
Author(s):  
Yi Yang ◽  
James Loy ◽  
Rolf-Peter Ryseck ◽  
Daniel Carrasco ◽  
Rodrigo Bravo
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Immunohistochemical Staining ◽  
High Selectivity ◽  
Allergic Diseases ◽  
Mutant Mice ◽  
Cc Chemokine ◽  
Lung Eosinophilia

Abstract The mechanisms that regulate the selective infiltration of eosinophils in certain allergic diseases are still poorly understood. The CC chemokine eotaxin is a potent chemoattractant, highly specific for eosinophils. Recent studies have implicated that eotaxin plays an important role in the recruitment of eosinophils in different inflammation processes. A number of other chemokines, cytokines, and chemoattractants also have chemotactic activities for eosinophils and some of them present high selectivity for eosinophils. To further study the role of eotaxin in inflammation, we generated mutant mice with the eotaxin gene disrupted and replaced by the Escherichia coliβ-galactosidase gene. These mice developed normally and had no histologic or hematopoietic abnormalities. Furthermore, our studies showed that the lack of eotaxin did not affect the recruitment of eosinophils in the inflammation models induced by Sephadex beads and thioglycollate, as well as in an experimental lung eosinophilia model induced by ovalbumin aerosol challenge, even at the onset of the inflammatory response. The replacement of the eotaxin gene by the β-galactosidase gene provided a useful marker to monitor the activity of the eotaxin promoter under normal conditions and after antigen challenges. Immunohistochemical staining suggested that endothelial cells were the major sources of eotaxin expression.

Antigen-Induced Eosinophilic Lung Inflammation Develops in Mice Deficient in Chemokine Eotaxin

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3912-3923 ◽  
Author(s):  
Yi Yang ◽  
James Loy ◽  
Rolf-Peter Ryseck ◽  
Daniel Carrasco ◽  
Rodrigo Bravo
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Immunohistochemical Staining ◽  
High Selectivity ◽  
Allergic Diseases ◽  
Mutant Mice ◽  
Cc Chemokine ◽  
Lung Eosinophilia

The mechanisms that regulate the selective infiltration of eosinophils in certain allergic diseases are still poorly understood. The CC chemokine eotaxin is a potent chemoattractant, highly specific for eosinophils. Recent studies have implicated that eotaxin plays an important role in the recruitment of eosinophils in different inflammation processes. A number of other chemokines, cytokines, and chemoattractants also have chemotactic activities for eosinophils and some of them present high selectivity for eosinophils. To further study the role of eotaxin in inflammation, we generated mutant mice with the eotaxin gene disrupted and replaced by the Escherichia coliβ-galactosidase gene. These mice developed normally and had no histologic or hematopoietic abnormalities. Furthermore, our studies showed that the lack of eotaxin did not affect the recruitment of eosinophils in the inflammation models induced by Sephadex beads and thioglycollate, as well as in an experimental lung eosinophilia model induced by ovalbumin aerosol challenge, even at the onset of the inflammatory response. The replacement of the eotaxin gene by the β-galactosidase gene provided a useful marker to monitor the activity of the eotaxin promoter under normal conditions and after antigen challenges. Immunohistochemical staining suggested that endothelial cells were the major sources of eotaxin expression.

scholarly journals Cytosolic DNA sensor cGAS plays an essential pathogenetic role in pressure overload-induced heart failure

2020 ◽  
Vol 318 (6) ◽  
pp. H1525-H1537 ◽  
Author(s):  
Dan Hu ◽  
Yu-Xia Cui ◽  
Man-Yan Wu ◽  
Long Li ◽  
Li-Na Su ◽  
...  
Keyword(s):  
Heart Failure ◽  
Inflammatory Response ◽  
Cardiac Remodeling ◽  
Therapeutic Target ◽  
Pressure Overload ◽  
Dna Sensor ◽  
Pathogenetic Role ◽  
Early Inflammatory Response ◽  
Sting Pathway

In this study, we first revealed a novel role of cGAS in the regulation of pathological cardiac remodeling and dysfunction upon pressure overload. We found that the cGAS/STING pathway was activated during pressure overload. Moreover, we also demonstrated that inhibition of the cGAS/STING pathway alleviated pathological cardiac remodeling and downregulated the early inflammatory response during pressure overload-induced HF. Together, these findings will provide a new therapeutic target for HF.

scholarly journals A thrombomodulin mutation that impairs activated protein C generation results in uncontrolled lung inflammation during murine tuberculosis

Blood ◽  
2005 ◽  
Vol 106 (8) ◽  
pp. 2761-2768 ◽  
Author(s):  
Sebastiaan Weijer ◽  
Catharina W. Wieland ◽  
Sandrine Florquin ◽  
Tom van der Poll
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Protein C ◽  
Essential Role ◽  
Activated Protein C ◽  
Wild Type ◽  
Anti Inflammatory

AbstractThrombomodulin (TM) plays an essential role in the generation of activated protein C (APC), a mediator with both anticoagulant and anti-inflammatory properties, and is preferentially expressed in lungs. To investigate the role of TM in the coagulant and inflammatory response in the lung during tuberculosis, mice with a mutation in the TM gene (Thbd), which results in a minimal capacity for APC generation (TMpro/pro mice), were intranasally infected with live virulent Mycobacterium tuberculosis. Whereas pulmonary tuberculosis was not associated with activation of coagulation in either wild-type or TMpro/pro mice, 5 weeks after infection TMpro/pro mice displayed an uncontrolled inflammatory response in their lungs, as reflected by higher lung weights, a diminished ability to form well-shaped granulomas, elevated levels of proinflammatory cytokines, and concurrently reduced concentrations of anti-inflammatory cytokines. During a 36-week follow-up after infection with a lower dose of M tuberculosis, 35% of TMpro/pro mice died from week 28 onward versus none of the wild-type mice, and the surviving TMpro/pro mice displayed increased lung inflammation accompanied by higher mycobacterial loads in liver and spleen. These data suggest that a TM mutation that impairs APC generation results in uncontrolled lung inflammation during tuberculosis.

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