Role of LOX-1 in Acute Lung Inflammation and Injury.

2009 ◽  
Author(s):  
J Fu ◽  
L Cheng ◽  
M Liang ◽  
P Zhang
Keyword(s):  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1

2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Raymond LC Kao ◽  
Xuemei Xu ◽  
Anargyros Xenocostas ◽  
Neil Parry ◽  
Tina Mele ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals Role of CD14 in a Mouse Model of Acute Lung Inflammation Induced by Different Lipopolysaccharide Chemotypes

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
Keyword(s):  
Mouse Model ◽  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals Anti-inflammatory role of PGD2 in acute lung inflammation and therapeutic application of its signal enhancement

2013 ◽  
Vol 110 (13) ◽  
pp. 5205-5210 ◽  
Author(s):  
T. Murata ◽  
K. Aritake ◽  
Y. Tsubosaka ◽  
T. Maruyama ◽  
T. Nakagawa ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Signal Enhancement ◽  
Acute Lung Inflammation ◽  
Therapeutic Application ◽  
Anti Inflammatory

A crucial role of nitric oxide in acute lung injury secondary to the acute necrotizing pancreatitis

2010 ◽  
Vol 29 (4) ◽  
pp. 329-337 ◽  
Author(s):  
Shi Cheng ◽  
Wen-Mao Yan ◽  
Bin Yang ◽  
Jing-dong Shi ◽  
Mao-min Song ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
No Production ◽  
Acute Lung Inflammation ◽  
Tnf Α ◽  
Acute Necrotizing

To investigate the role of nitric oxide (NO) in acute lung inflammation and injury secondary to acute necrotizing pancreatitis (ANP), 5% sodium taurocholate was retrogradely injected into the biliopancreatic duct of rats to ANP model. These ANP rats were given L-Arginine (L-Arg, 100 mg/kg), L-NAME (10 mg/kg), or their combination by intraperitoneal injection 30 min prior to ANP induction. At 1, 3, 6, and 12 hours after ANP induction, lung NO production, and inducible NO synthase (iNOS) expression were measured. Lung histopathological changes, bronchoalveolar lavage (BAL) protein concentration, proinflammatory mediators tumor necrotic factor alpha (TNF-α), and lung tissue myeloperoxidase (MPO) activity were examined. Results showed that NO production and iNOS mRNA expression in alveolar macrophages (AMs) were significantly increased along with significant increases in lung histological abnormalities and BAL proteins in the ANP group, all of which were further enhanced by pretreatment with L-Arg and attenuated by pretreatment with L-NAME, respectively. These markers were slightly attenuated by pretreatment with combination of L-Arg + L-NAME, suggesting that NO is required for initiating the acute lung damage in ANP rats, and also that L-Arg-enhanced lung injury is mediated by its NO generation rather than its direct effect. MPO activity and TNF-α expression in lung were upregulated in the ANP rats and further enhanced by pretreatment with L-Arg and attenuated by pretreatment with L-NAME, respectively. These results suggest that overproduction of NO mediated by iNOS in the lung is required for the acute lung inflammation and damage secondary to ANP.

The role of hyaluronic acid in SEB-induced acute lung inflammation

2013 ◽  
Vol 146 (1) ◽  
pp. 56-69 ◽  
Author(s):  
Olga N. Uchakina ◽  
Clara M. Castillejo ◽  
Christy C. Bridges ◽  
Robert J. McKallip
Keyword(s):  
Hyaluronic Acid ◽  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals ACUTE LUNG INFLAMMATION INDUCED BY LIPOPOLYSACCHARIDE: ROLE OF INSULIN

Shock ◽  
2003 ◽  
Vol 19 (Supplement) ◽  
pp. 66
Author(s):  
T. C Alba ◽  
R. Curi ◽  
P. Sannomiya
Keyword(s):  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals Lack of CD34 delays bacterial endotoxin-induced lung inflammation

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Gurpreet K. Aulakh ◽  
Sushmita Maltare ◽  
Baljit Singh
Keyword(s):  
Lung Inflammation ◽  
Neutrophil Migration ◽  
Neutrophil Recruitment ◽  
Multiple Time ◽  
Acute Lung Inflammation ◽  
Knock Out ◽  
Time Points ◽  
Bronchiolar Epithelium ◽  
Alveolar Septa

Abstract Background CD34, a pan-selectin binding protein when glycosylated, has been shown to be involved in leukocyte migration to the site of inflammation. However, only one report is available on the expression and role of CD34 in neutrophil recruitment during acute lung inflammation. Methods We proceeded to study the role of CD34 in lung neutrophil migration using mouse model of endotoxin induced acute lung inflammation and studied over multiple time points, in generic CD34 knock-out (KO) strain. Results While there was no difference in BAL total or differential leukocyte counts, lung MPO content was lower in LPS exposed KO compared to WT group at 3 h time-point (p = 0.0308). The MPO levels in CD34 KO mice begin to rise at 9 h (p = 0.0021), as opposed to an early 3 h rise in WT mice (p = 0.0001), indicating that KO mice display delays in lung neutrophil recruitment kinetics. KO mice do not loose endotoxin induced lung vascular barrier properties as suggested by lower BAL total protein at 3 h (p = 0.0452) and 24 h (p = 0.0113) time-points. Several pro-inflammatory cytokines and chemokines (TNF-α, IL-1β, KC, MIP-1α, IL-6, IL-10 and IL-12 p70 sub-unit; p < 0.05) had higher levels in WT compared to KO group, at 3 h. Lung immunofluorescence in healthy WT mice reveals CD34 expression in the bronchiolar epithelium, in addition to alveolar septa. Conclusion Thus, given CD34′s pan-selectin affinity, and expression in the bronchiolar epithelium as well as alveolar septa, our study points towards a role of CD34 in lung neutrophil recruitment but not alveolar migration, cytokine expression and lung inflammation.

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