Inhibition Of Mer Receptor Tyrosine Kinase Aggravates LPS-Induced Acute Lung Injury Through Blocking STAT1-Induced SOCS3

Author(s):  
Ye-Ji Lee ◽  
Ji-Young Han ◽  
Jihee L. Kang
2002 ◽  
Vol 26 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Susan A. McDowell ◽  
Ali Mallakin ◽  
Cindy J. Bachurski ◽  
Kenya Toney-Earley ◽  
Daniel R. Prows ◽  
...  

Shock ◽  
2007 ◽  
Vol 27 (3) ◽  
pp. 274-280 ◽  
Author(s):  
Alex B. Lentsch ◽  
Peterson Pathrose ◽  
Sarah Kader ◽  
Satoshi Kuboki ◽  
Margaret H. Collins ◽  
...  

2014 ◽  
Vol 307 (6) ◽  
pp. L435-L448 ◽  
Author(s):  
Agnieszka Krupa ◽  
Marek Fol ◽  
Moshiur Rahman ◽  
Karen Y. Stokes ◽  
Jon M. Florence ◽  
...  

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.


2006 ◽  
Vol 291 (2) ◽  
pp. L129-L141 ◽  
Author(s):  
Daisuke Okutani ◽  
Monika Lodyga ◽  
Bing Han ◽  
Mingyao Liu

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.


2012 ◽  
Vol 38 (5) ◽  
pp. 894-905 ◽  
Author(s):  
Takeshi Oyaizu ◽  
Shan-Yu Fung ◽  
Atsushi Shiozaki ◽  
Zehong Guan ◽  
Qiao Zhang ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document