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1

Toll-like receptor expression and function in airway epithelial cells

100%
Greene C. M., McElvaney N. G.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 5
418-427
EN
Toll-like receptors (TLRs) belong to a family of transmembrane proteins that can recognize and discriminate a diverse array of microbial antigens. Following their activation by specific ligands, TLRs initiate intracellular signaling cascades that culminate in the activation of transcription factors and ultimately lead to changes in pro-inflammatory gene expression. The TLR family constitutes an important component of the innate immune system and, although most commonly considered to be associated with immune cell responses, TLRs are also known to be functionally expressed on a variety of other cell types. Epithelial cells represent a significant component of the cellular content of the airways. These cells provide both a barrier to infection and an active defense mechanism against invading microbes. The expression and function of TLRs on airway epithelial cells has been an area of increasing interest in the recent past. This review will summarize advances in our understanding of the role of TLRs in airway epithelial cells.
2

Nitric oxide (NO) in the pathophysiology of asthma and interstitial lung diseases

100%
Kasperska-Zajac A., Rogala R. B., Rogala B., Kasperka-Zajac A.
Postępy Higieny i Medycyny Doświadczalnej
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2001
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vol. 55
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issue 4
525-540
EN
NO is an important mediator of immune and inflammatory responses. NO is produced from L-arginine by three isoforms of nitric oxide synthase (NOS), neuronal (nNOS; NOS1), endothelial (eNOS; NOS3) and inducible (iNOS). Exhaled NO has been shown to be increased in asthma and has been put forward as a marker of airways inflammation. Moreover, increased production of NO and peroxynitrite may be responsible for the oxidative damage and fibrosis seen in interstitial lung diseases. The present review focuses on clinical and laboratory studies that are aimed at identifying the role of NO in the physiopathology of these disorders.
3

Prostaglandin-endoperoxide synthase genes COX1 and COX2 ? novel modifiers of disease severity in cystic fibrosis patients

100%
Czerska K., Sobczynska-Tomaszewska A., Sands D., Nowakowska A., Bak D., Wertheim K., Poznanski J., Zielenski J., Norek A., Bal J.
Journal of Applied Genetics
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2010
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vol. 51
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issue 3
323-330
EN
Cystic fibrosis (CF) is one of the most common autosomal recessive diseases among Caucasians caused by a mutation in the CFTR gene. However, the clinical outcome of CF pulmonary disease varies remarkably even in patients with the same CFTR genotype. This has led to a search for genetic modifiers located outside the CFTR gene. The aim of this study was to evaluate the effect of functional variants in prostaglandin-endoperoxide synthase genes (COX1 and COX2) on the severity of lung disease in CF patients. To the best of our knowledge, it is the first time when analysis of COX1 and COX2 as potential CF modifiers is provided. The study included 94 CF patients homozygous for F508del mutation of CFTR. To compare their' clinical condition, several parameters were recorded, e.g. a unique clinical score: disease severity status (DSS). To analyse the effect of non-CFTR genetic polymorphisms on the clinical course of CF patients, the whole coding region of COX1 and selected COX2 polymorphisms were analysed. Statistical analysis of genotype-phenotype associations revealed a relationship between the heterozygosity status of identified polymorphisms and better lung function. These results mainly concern COX2 polymorphisms: -765G>C and 8473T>C. The COX1 and COX2 polymorphisms reducing COX protein levels had a positive effect on all analysed clinical parameters. This suggests an important role of these genes as protective modifiers of pulmonary disease in CF patients, due to inhibition of arachidonic acid conversion into prostaglandins, which probably reduces the inflammatory process.
4

Concentration of TBA-reactive substances in type II pneumocytes exposed to oxidative stress

88%
Piotrowski W. J., Marczak J., Kurmanowska Z., Gorski P.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
435-440
EN
Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs), as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. Materials We investigated the susceptibility of freshly isolated and cultured rat type II AECs to and Methods: oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS) were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. Results: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0?1.3 vs. 8.3?2.2 nmol/g protein, p=0.0313) and insignificantly in cultured cells (1.7?0.4 vs. 4.4?1.7 nmol/g protein). ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs: 4.5?1.5 vs. 16.2?3.9 nmol/g protein, p=0.0625, and 4.0?0.8 vs.7.6?4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. Conclusions: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may further increase when catalase is inhibited, which suggests an important protective role for catalase.
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