scholarly journals Inhibiting Mer receptor tyrosine kinase suppresses STAT1, SOCS1/3, and NF-κB activation and enhances inflammatory responses in lipopolysaccharide-induced acute lung injury

2012 ◽  
Vol 91 (6) ◽  
pp. 921-932 ◽  
Author(s):  
Ye-Ji Lee ◽  
Ji-Young Han ◽  
Jiyeon Byun ◽  
Hyun-Jeong Park ◽  
Eun-Mi Park ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Inflammatory Responses

Src protein tyrosine kinase family and acute inflammatory responses

2006 ◽  
Vol 291 (2) ◽  
pp. L129-L141 ◽  
Author(s):  
Daisuke Okutani ◽  
Monika Lodyga ◽  
Bing Han ◽  
Mingyao Liu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Reperfusion Injury ◽  
Protein Tyrosine Kinase ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Protein Tyrosine

Acute inflammatory responses are one of the major underlying mechanisms for tissue damage of multiple diseases, such as ischemia-reperfusion injury, sepsis, and acute lung injury. By use of cellular and molecular approaches and transgenic animals, Src protein tyrosine kinase (PTK) family members have been identified to be essential for the recruitment and activation of monocytes, macrophages, neutrophils, and other immune cells. Src PTKs also play a critical role in the regulation of vascular permeability and inflammatory responses in tissue cells. Importantly, animal studies have demonstrated that small chemical inhibitors for Src PTKs attenuate tissue injury and improve survival from a variety of pathological conditions related to acute inflammatory responses. Further investigation may lead to the clinical application of these inhibitors as drugs for ischemia-reperfusion injury (such as stroke and myocardial infarction), sepsis, acute lung injury, and multiple organ dysfunction syndrome.

The Role of the Receptor Tyrosine Kinase Ron in Nickel-Induced Acute Lung Injury

2002 ◽  
Vol 26 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Susan A. McDowell ◽  
Ali Mallakin ◽  
Cindy J. Bachurski ◽  
Kenya Toney-Earley ◽  
Daniel R. Prows ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase

scholarly journals THE RON RECEPTOR TYROSINE KINASE REGULATES ACUTE LUNG INJURY AND SUPPRESSES NUCLEAR FACTOR ??B ACTIVATION

Shock ◽  
2007 ◽  
Vol 27 (3) ◽  
pp. 274-280 ◽  
Author(s):  
Alex B. Lentsch ◽  
Peterson Pathrose ◽  
Sarah Kader ◽  
Satoshi Kuboki ◽  
Margaret H. Collins ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Nuclear Factor ◽  
Factor B ◽  
Ron Receptor

scholarly journals LncRNA HOTAIR Increases Inflammatory Responses by Activating NF-κB Pathway in LPS-Induced Acute Lung Injury

2020 ◽  
Author(s):  
XiaoMei Huang ◽  
ZeXun Mo ◽  
YuJun Li ◽  
Hua He ◽  
KangWei Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Noncoding Rna ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
A549 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Lncrna Hotair

Abstract Background Nuclear factor kappa-B (NF-κB) activation increased the expression of cytokines and further lead to lung injury was considered the main mechanism of acute lung injury (ALI). Here, we focus on exploring the potential regulatory mechanism between long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) and NF-κB on LPS-induced ALI. Methods A549 cells were then divided into 4 groups: HOTAIR group, NC group, si-HOTAIR group and si-NC group. These 4 groups were then treated with 1μg/mL lipopolysaccharides (LPS) or without LPS at 37°C for 24 h. The expression level of cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) and LncRNA HOTAIR were evaluated by quantitative Real Time Polymerase Chain Reaction (qRT-PCR) and Enzyme-linked immunosorbent assay (ELISA). Western Blot analysis was adopted for evaluating the level of p-IκBα/IκBα and p-p65/p65. Nuclear translocation of p65 was observed by immunofluorescence staining. Results qRT-PCR and ELISA assay showed that the expression of cytokines (IL-1β, IL-6 and TNF-α) and inflammatory gene HOTAIR was remarkably increased with LPS treatment (p < 0.01). Over-expression of HOTAIR significantly increased the expression of cytokines (including IL-1β, IL-6 and TNF-α) and NF-κB pathway associated proteins (including p-IκBα/IκBα and p-p65/p65), while knockdown of HOTAIR had the opposite effect (p < 0.01). The immunofluorescence assay showed that the level of p65 in the nucleus was significantly higher in the HOTAIR group and significantly lowers in the si-HOTAIR group (p < 0.01). Conclusion HOTAIR may play a pro-inflammatory response through NF-κB pathway in LPS-induced ALI, which may provide a perspective for further understanding the pathogenic mechanism of ALI.

scholarly journals Levonadifloxacin, a Novel Benzoquinolizine Fluoroquinolone, Modulates Lipopolysaccharide-Induced Inflammatory Responses in Human Whole-Blood Assay and Murine Acute Lung Injury Model

2020 ◽  
Vol 64 (5) ◽  
Author(s):  
Anasuya Patel ◽  
Ganesh V. Sangle ◽  
Jinal Trivedi ◽  
Sushant A. Shengule ◽  
Deepak Thorve ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Whole Blood ◽  
Inflammatory Responses ◽  
Immunomodulatory Activity ◽  
Human Whole Blood ◽  
Injury Model ◽  
Cytokine Levels ◽  
Lung Injury Model ◽  
Clinical Benefits

ABSTRACT Fluoroquinolones are reported to possess immunomodulatory activity; hence, a novel benzoquinolizine fluoroquinolone, levonadifloxacin, was evaluated in lipopolysaccharide-stimulated human whole-blood (HWB) and mouse acute lung injury (ALI) models. Levonadifloxacin significantly mitigated the inflammatory responses in an HWB assay through inhibition of proinflammatory cytokines and in the ALI model by lowering lung total white blood cell count, myeloperoxidase, and cytokine levels. The immunomodulatory effect of levonadifloxacin, along with promising antibacterial activity, is expected to provide clinical benefits in the treatment of infections.

Umbelliferone Alleviates Lipopolysaccharide-Induced Inflammatory Responses in Acute Lung Injury by Down-Regulating TLR4/MyD88/NF-κB Signaling

Inflammation ◽  
2019 ◽  
Vol 42 (2) ◽  
pp. 440-448 ◽  
Author(s):  
Dongqiu Wang ◽  
Xia Wang ◽  
Wen Tong ◽  
Yuhong Cui ◽  
Xiuxian Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Responses

scholarly journals Silencing Bruton's tyrosine kinase in alveolar neutrophils protects mice from LPS/immune complex-induced acute lung injury

2014 ◽  
Vol 307 (6) ◽  
pp. L435-L448 ◽  
Author(s):  
Agnieszka Krupa ◽  
Marek Fol ◽  
Moshiur Rahman ◽  
Karen Y. Stokes ◽  
Jon M. Florence ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Immune Complex ◽  
Distress Syndrome ◽  
Bruton’S Tyrosine Kinase ◽  
Bruton's Tyrosine Kinase ◽  
Neutrophil Survival

Previous observations made by our laboratory indicate that Bruton's tyrosine kinase (Btk) may play an important role in the pathophysiology of local inflammation in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). We have shown that there is cross talk between FcγRIIa and TLR4 in alveolar neutrophils from patients with ALI/ARDS and that Btk mediates the molecular cooperation between these two receptors. To study the function of Btk in vivo we have developed a unique two-hit model of ALI: LPS/immune complex (IC)-induced ALI. Furthermore, we conjugated F(ab)2 fragments of anti-neutrophil antibodies (Ly6G1A8) with specific siRNA for Btk to silence Btk specifically in alveolar neutrophils. It should be stressed that we are the first group to perform noninvasive transfections of neutrophils, both in vitro and in vivo. Importantly, our present findings indicate that silencing Btk in alveolar neutrophils has a dramatic protective effect in mice with LPS/IC-induced ALI, and that Btk regulates neutrophil survival and clearance of apoptotic neutrophils in this model. In conclusion, we put forward a hypothesis that Btk-targeted neutrophil specific therapy is a valid goal of research geared toward restoring homeostasis in lungs of patients with ALI/ARDS.

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