Wyniki wyszukiwania - Biblioteka Nauki

1

The role of pulmonary mast cell in hemorrhagic shock

100%

Humenczyk-Zybala M. , Kasacka I. , Chyczewski L.

Postępy Higieny i Medycyny Doświadczalnej

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2001

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tom 55

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nr 1

121-132

EN

In the course of hemorrhagic shock. Here are multidirectional organ changes that result in intensified disjunction of important organs as well as multiorgan insufficiency syndrome. The syndrome is a cause of high post-traumatic mortality. The general inflammatory reaction of intensive ? liver ? lungs ? immunological system increases in a cascadical way and has a significant role in the pathogenesis of the syndrome. Most cells activated as a result of ischemia and reprefusion participate in the phenomenon.

2

Murine models of susceptibility to tuberculosis

100%

Beamer G. L. , Turner J.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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tom 53

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nr 6

469-483

EN

Approximately one third of the world's population is infected with Mycobacterum tuberculosis, yet each year a small proportion of those individuals progress to an active disease state. Early identification and treatment of such individuals is essential to reduce transmission; however, genetic and immunological correlates of disease progression have not been well established in man. The murine model has been a central tool for the elucidation of protective immune mechanisms that are essential for controlling M. tuberculosis infection. Additionally, the study of inbred mice has revealed significant divergence in the susceptibility and disease progression of individual mouse strains to an infection with M. tuberculosis. The continued study of genetically disparate mouse strains has the potential to identify immune mechanisms that correlate with increasing susceptibility to tuberculosis. These mechanisms will be highly applicable to studies in man and assist in the early detection of individuals that are more vulnerable to the development of reactivation tuberculosis.

3

Regulation of local immunity by airway epithelial cells

100%

Mayer A. K. , Dalpke A. H.

Archivum Immunologiae et Therapiae Experimentalis

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2007

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tom 55

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nr 6

353-363

EN

Epithelial cells are the first line of defense against invading microbial pathogens. They are important contributors to innate mucosal immunity and generate various and sophisticated anti-microbial defense mechanisms, including the formation of a tight barrier and secretion of anti-microbial substances as well as inflammatory mediators. To provide these active defense mechanisms, epithelial cells functionally express various pattern-recognition receptors. Toll-like receptors have been shown to recognize conserved microbial patterns mediating inducible activation of innate immunity. Mucosal surfaces, however, are prone to contact with pathogenic as well as non-pathogenic microbes and, therefore, immune-recognition principles have to be strictly regulated to avoid uncontrolled permanent activation. This review will focus on mechanisms by which epithelial cells regulate mucosal immune responses, thus creating an organ-specific microenvironment. This includes local adaptations in microbial recognition, regulation of local immune homeostasis, and modulation of antigen-presenting cells and adaptive immune responses. These regulatory mechanisms serve the special needs of controlled microbial recognition in mucosal compartments.

4

The role of autoimmunity in the pathogenesis of lung allograft rejection

88%

Wilkes D. S.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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tom 51

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nr 4

227-230

EN

For many patients, lung transplantation is the only definitive treatment modality for different forms of end stage lung disease. However, the lung is rejected more often than any other type of solid organ allografts, and the five year survival is less than that of other transplanted organs. While alloimmunity directed against donor transplantation antigens is believed to be the key mechanism that mediates rejection responses, newer immunosuppressive regimens designed to abrogate alloimmune activation have not improved survival. Accordingly, these data suggest that other antigens are involved in rejection. Autoimmune responses, reported to occur during allograft rejection, could participate in graft destruction. This review article discusses the role of autoimmune responses to type V collagen ([col(V)], a minor collagen in the lung, in the pathogenesis of lung allograft rejection. By recognizing that lung transplant rejection involves both alloimmune and autoimmune responses, scientific investigation may uncover novel targets for therapeutic intervention that could prolong the life of the lung transplant recipient.

5

Neural cell adhesion molecule in breast, colon and lung carcinomas

88%

Zoltowska A. , Stepinski J. , Lewko B. , Serkies K. , Zamorska B. , Roszkiewicz A. , Izycka-Swieszewska E. , Kruszewski W. J.

Archivum Immunologiae et Therapiae Experimentalis

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2001

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tom 49

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nr 2

91-100

EN

Neural cell adhesion molecules (NCAM) play an important role in embryogenesis and in some tumors, especially of neuroectodermal origin. In this study, eighteen cases of invasive breast carcinoma, seven cases of sigmoid colon carcinomas and seventeen cases of the non-small cell lung carcinoma were immunostained for NCAM. The NCAM expression, usually focal, was observed in some cases only. NCAM was expressed in the membranes, in a fine granular pattern. In three cases of breast cancers, also cytoplasmic localisation of NCAM was observed, which may suggest its cytoplasmic formation. Furthermore, in three cases expression of NCAM in histologically normal ductal lobular units adjacent to invasive breast cancers without presence of this antigen in cancer tissue was observed. The immunostaining was weak or absent in sigmoid colon carcinomas. In this study we confirm observation of some authors that NCAM expression occurs in some cases of non-small cell lung carcinomas.

6

Nitric oxide production by pulmonary leukocytes from induced sputum in patients with asthma and its effect on epithelial cell viability

88%

Bienkowska-Haba M. , Liebhart J. , Cembrzynska-Nowak M.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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tom 54

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nr 3

201-207

EN

Nitric oxide (NO) is one of many factors potentially involved in lung remodeling in asthma. The aim of the study was to assess the effect of pulmonary leukocytes from patients with bronchial asthma on alveolar epithelial cell damage in relation to NO production. Materials and Methods: Induced sputum samples were obtained from 25 patients with bronchial asthma and 10 healthy volunteers. Twelve asthmatics were on inhaled corticosteroid treatment and 13 were corticosteroid free. Type II-like alveolar epithelial (A549) cells were cultured for 48 h in the presence of cell-free media from a 24-h culture of leukocytes obtained from the induced sputa (IS-Su). The level of NO was measured in supernatants from the cell cultures and the viability of the A549 cells was established. Results: The levels of NO in IS-Su from corticosteroid-free asthmatics were significantly higher (p=0.001) than those in IS-Su from healthy controls. Furthermore, NO production by A549 cells exposed to IS-Su from steroid-free asthmatics (group A) was significantly higher than that from asthmatics on corticosteroid therapy (group cA) as well as from healthy controls (p=0.01 and p=0.001, respectively). Lower viability of the epithelial cells exposed to IS-Su was observed in group A compared with controls (median: 72% vs. 97.5%; p<0.001). In addition, a negative correlation (RS=?0.706, p<0.001) was found between the levels of NO produced by pulmonary leukocytes and the viability of epithelial cells. Conclusions: The results suggest that in the course of asthma, pulmonary leukocytes may interact with alveolar epithelial cells by inducing an excessive production of NO which, in turn, may contribute to epithelium impairment.

7

Expression of human blood group antigens A and B in kidney and lung of some vertebrates

75%

Tomova E. S. , Popov A. A. , Sarafian V. S.

Folia Biologica

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2001

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tom 49

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nr 3-4

251-257

EN

Human blood group antigens (BGA) are genetically determined glycoproteins found in many cells and tissues of different mammals. Their major biological functions are still undefined. There are few investigations analysing the evolutionary aspect of BGA tissue ditribution. The present study is aimed at examining the expression of human A and B antigens in the kidney and lung of some free-living vertebrates. The biotin-streptavidin-peroxidase immunostaining system was applied on kidney and lung paraffin sections derived from free-living representatives of five different vertebrate classes. Excluding the possibility of any non-specific staining by the application of inhibition tests, A and B antigens were demonstrated most constantly in epithelial cells of renal and respiratory tubules. They were also detected in chondrocytes of fish gills, in some muscular and endothelial cells. Single erythrocytes showed a positive cytoplasmic staining only in some higher vertebrates. Human BGA seem to be conserved carbohydrate structures with biological functions probably related to cell integrity and differentiation.

8

Surfactant proteins SP-A and SP-D in human health and dis

75%

Kishore U. , Lopez B. A. , Kamran M. F. , Saxena S. , Singh M. , Sarma P. U. , Madan T. , Chakraborty T.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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tom 53

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nr 5

399-417

EN

Surfactant proteins A (SP-A) and D (SP-D) are lung surfactant-associated hydrophilic proteins which have been implicated in surfactant homeostasis and pulmonary innate immunity. They are collagen-containing C-type (calcium-dependent) lectins, called collectins, and are structurally similar to mannose-binding protein of the lectin pathway of the complement system. Being carbohydrate pattern-recognition molecules, they recognize a broad spectrum of pathogens and allergens via the lectin domain, with subsequent activation of immune cells via the collagen region, thus offering protection against infection and allergenic challenge. SP-A and SP-D have been shown to be involved in viral neutralization, clearance of bacteria, fungi, and apoptotic and necrotic cells, the down-regulation of allergic reaction, and the resolution of inflammation. Studies on single-nucleotide polymorphism, protein levels in broncho-alveolar lavage, and gene knock-out mice have clearly indicated an association between SP-A and SP-D and a range of pulmonary diseases. In addition, recent studies using murine models of allergy and infection have raised the possibility that the recombinant forms of SP-A and SP-D may have therapeutic potential in controlling pulmonary infection, inflammation, and allergies in humans.