scholarly journals Toll-like Receptor-4 Polymorphisms and Serum Matrix Metalloproteinase-9 in Newly Diagnosed Patients With Calcified Neurocysticercosis and Seizures

Medicine ◽  
2016 ◽  
Vol 95 (17) ◽  
pp. e3288 ◽  
Author(s):  
Gaurav Lachuriya ◽  
Ravindra Kumar Garg ◽  
Amita Jain ◽  
Hardeep Singh Malhotra ◽  
Arvind Kumar Singh ◽  
...  
2007 ◽  
Vol 39 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Eun-Jung Lim ◽  
Sun-Hye Lee ◽  
Jin-Gu Lee ◽  
Jae-Ryong Kim ◽  
Sung-Su Yun ◽  
...  

2018 ◽  
Vol 64 (4) ◽  
pp. 361-367 ◽  
Author(s):  
Wen-Cheng Yu ◽  
Jin-Peng Cong ◽  
Li-Yun Mi

SUMMARY OBJECTIVE: This study aims at investigating the expressions of TOLL-like receptor 4 (TLR-4) and matrix metalloproteinase 9 (MMP-9)/ tissue inhibitor of metalloproteinase 1 (TIMP-1) in pulmonary blood vessels with chronic obstructive pulmonary disease (COPD) and their relationships with pulmonary vascular remodelling (PVR). METHODS: 60 para-tumour tissues were divided into the COPD group and the control group (n=30); the inflammations, pulmonary artery wall area/total artery area (WA%), and wall thickness/vascular outer diameter (WT%) were compared. The expressions of TLR-4, MMP-9/TIMP-1, and PCNA in pulmonary vascular smooth muscle cells were detected, and their relationships with PVR were then analysed. RESULTS: The inflammations (1.6±0.8), WA% (44.0±6.4), and WT% (27.3±3.3) in the COPD group were higher than in the control group (0.3±0.5, 26.1±2.8, 15.6±1.8), and the expressions of TLR-4 (31.4±147) and MMP-9/TIMP-1 (2.2±2.6) were increased compared to the control group (4.7±4.5, 1.9±12). Correlation analysis: TLR-4 and MMP-9/TIMP-1 were positively correlated with the inflammations (r=0.18, P<0.01), WA% (r=0.68, P<0.01), and WT% (r=0.73, P<0.01), as well as positively correlated with the expression of PCNA (r=0.44, P<0.01); the upregulation of TLR-4 was positively correlated with the expressions of MMP-9 and TIMP-1. CONCLUSIONS: The upregulation of TLR-4 in the pulmonary arterial smooth muscle cells of COPD patients could promote the inflammations and the MMP-9 expression, thus causing abnormal degradation of extracellular matrix, so it played an important role in the process of PVR.


2011 ◽  
Vol 286 (42) ◽  
pp. 36532-36549 ◽  
Author(s):  
Samar Abdulkhalek ◽  
Schammim Ray Amith ◽  
Susan L. Franchuk ◽  
Preethi Jayanth ◽  
Merry Guo ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Stephane Esnault ◽  
Elizabeth A. Kelly ◽  
Sean H. Johnson ◽  
Larissa P. DeLain ◽  
Madeline J. Haedt ◽  
...  

Asthma is often associated with airway eosinophilia, and therapies targeting eosinophils are now available to treat severe eosinophilic asthma. Eosinophilic asthma is often due to a type-2 immune response and production of IL-5, which leads to eosinophilopiesis and recruitment of mature eosinophils in the airways. A concomitant type-2 and type-17 response has been reported in some individuals. IL-17 may be enhanced by IL-1βproduction and can lead to neutrophilic inflammation. In fact, both eosinophilic and neutrophilic (mixed granulocytic) inflammation are simultaneously present in a large population of patients with asthma. In monocyte/macrophage cell populations, release of mature IL-1βoccurs via toll-like receptor ligand-induced activation of the inflammasome. Within the inflammasome, a cascade of events leads to the activation of caspase-1, which cleaves pro-IL-1βprotein into a mature, releasable, and active form. We have demonstrated that eosinophils can release IL-1βin a Toll-like receptor ligand-independent fashion. The objective of this study was to determine the mechanisms underlying the production and maturation of IL-1βin cytokine-activated eosinophils. Using eosinophils from circulating blood and from bronchoalveolar lavage fluid after an airway allergen challenge, the present study demonstrates that cytokine-activated eosinophils express and release a bioactive form of IL-1βwith an apparent size less than the typical 17 kDa mature form produced by macrophages. Using a zymography approach and pharmacological inhibitors, we identified matrix metalloproteinase-9 (MMP-9) as a protease that cleaves pro-IL-1βinto a ~15 kDa form and allows the release of IL-1βfrom cytokine-activated eosinophils. Therefore, we conclude that activated eosinophils produce MMP-9, which causes the release of IL-1βin an inflammasome/caspase-1-independent manner. The production of IL-1βby eosinophils may be a link between the eosinophilic/type-2 immune response and the neutrophilic/type-17 immune response that is often associated with a more severe and treatment-refractory type of asthma.


Sign in / Sign up

Export Citation Format

Share Document