scholarly journals Potential anti-inflammatory role of 2-chloroadenosine treatment during acute lung inflammation in BALB/c mice suffering from Klebsiella pneumoniae B5055-induced acute lung infection

Critical Care ◽  
2013 ◽  
Vol 17 (Suppl 4) ◽  
pp. P68
Author(s):  
Vijay Kumar ◽  
Kusum Harjai ◽  
Sanjay Chhibber
2013 ◽  
Vol 110 (13) ◽  
pp. 5205-5210 ◽  
Author(s):  
T. Murata ◽  
K. Aritake ◽  
Y. Tsubosaka ◽  
T. Maruyama ◽  
T. Nakagawa ◽  
...  

2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Raymond LC Kao ◽  
Xuemei Xu ◽  
Anargyros Xenocostas ◽  
Neil Parry ◽  
Tina Mele ◽  
...  

2014 ◽  
Vol 193 (9) ◽  
pp. 4623-4633 ◽  
Author(s):  
Zongmei Wen ◽  
Liyan Fan ◽  
Yuehua Li ◽  
Zui Zou ◽  
Melanie J. Scott ◽  
...  

PLoS ONE ◽  
2010 ◽  
Vol 5 (4) ◽  
pp. e10183 ◽  
Author(s):  
Adam A. Anas ◽  
Joppe W. R. Hovius ◽  
Cornelis van 't Veer ◽  
Tom van der Poll ◽  
Alex F. de Vos

2010 ◽  
Vol 59 (4) ◽  
pp. 429-437 ◽  
Author(s):  
Shruti Bansal ◽  
Sanjay Chhibber

Acute lung injuries due to acute lung infections remain a major cause ofmortality. Thus a combination of an antibiotic and a compound with immunomodulatoryand anti-inflammatory activities can help to overcome acute lung infection-inducedinjuries. Curcumin derived from the rhizome of turmeric has been used fordecades and it exhibits anti-inflammatory, anti-carcinogenic, immunomodulatoryproperties by downregulation of various inflammatory mediators. Keeping theseproperties in mind, we investigated the anti-inflammatory properties of curcuminin a mouse model of acute inflammation by introducing Klebsiella pneumoniae B5055 into BALB/c mice via the intranasal route. Intranasal instillationof bacteria in this mouse model of acute pneumonia-induced inflammation resultedin a significant increase in neutrophil infiltration in the lungs along withincreased production of various inflammatory mediators [i.e. malondialdehyde (MDA),myeloperoxidase (MPO), nitric oxide (NO), tumour necrosisfactor (TNF)-α] in the lung tissue. The animalsthat received curcumin alone orally or in combination with augmentin, 15 daysprior to bacterial instillation into the lungs via the intranasal route, showeda significant (P <0.05) decrease in neutrophil influxinto the lungs and a significant (P <0.05) decreasein the production of MDA, NO, MPO activity and TNF-α levels.Augmentin treatment alone did not decrease the MDA, MPO, NO and TNF-α levels significantly (P >0.05) as compared tothe control group. We therefore conclude that curcumin ameliorates lung inflammationinduced by K. pneumoniae B5055 without significantly (P <0.05) decreasing the bacterial load in the lung tissue whereasaugmentin takes care of bacterial proliferation. Hence, curcumin can be usedas an adjunct therapy along with antibiotics as an anti-inflammatory or animmunomodulatory agent in the case of acute lung infection.


2016 ◽  
Vol 311 (3) ◽  
pp. L664-L675 ◽  
Author(s):  
Clémence O. Henry ◽  
Emilie Dalloneau ◽  
Maria-Teresa Pérez-Berezo ◽  
Cristina Plata ◽  
Yongzheng Wu ◽  
...  

Cystic fibrosis (CF) is an inherited disease associated with chronic severe lung inflammation, leading to premature death. To develop innovative anti-inflammatory treatments, we need to characterize new cellular and molecular components contributing to the mechanisms of lung inflammation. Here, we focused on the potential role of “transient receptor potential vanilloid-4” (TRPV4), a nonselective calcium channel. We used both in vitro and in vivo approaches to demonstrate that TRPV4 expressed in airway epithelial cells triggers the secretion of major proinflammatory mediators such as chemokines and biologically active lipids, as well as a neutrophil recruitment in lung tissues. We characterized the contribution of cytosolic phospholipase A2, MAPKs, and NF-κB in TRPV4-dependent signaling. We also showed that 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acids, i.e., four natural lipid-based TRPV4 agonists, are present in expectorations of CF patients. Also, TRPV4-induced calcium mobilization and inflammatory responses were enhanced in cystic fibrosis transmembrane conductance regulator-deficient cellular and animal models, suggesting that TRPV4 is a promising target for the development of new anti-inflammatory treatments for diseases such as CF.


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