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1

Regulation of local immunity by airway epithelial cells

100%
Mayer A. K., Dalpke A. H.
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2007
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vol. 55
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issue 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.
2

Phospholipid content and lamellar structures in the epididymal epithelial cells of rats treated chronically with lead acetate [Pb(II)]

100%
Wiszniewska B., Marchlewicz M., Piasecka M., Wenda-Rozewicka L., Swider-Al-Amawi M.
Folia Biologica
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1998
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vol. 46
215-224
EN
The electron-microscopic observations accomplished covered epididymal epithelial cells of rats receiving lead acetate for five times longer than the duration of one spermatogenesis. These cells were found to possess a large number of vacuoles and conglomerates containing plicated membranes or tightly packed myelin-like lamellar formations. Further observations also revealed the formation of lamellar structures in mitochondria, dilatation of cisternae in the Golgi apparatus, and increased phagocytosis of spermatozoa by epithelial cells. The presence of a large amount of membranous material correlated with the increased content of phospholipids in epididymal epithelial cells. It may be suggested that the presence of such a great quantity of lamellar structures in epididymal epithelial cells of rats treated chronically with lead is the result of several processes, including the augmented synthesis of membranes associated with encircling the deposits of lead, autophagy in the cells, as well as intensified phagocytosis of spermatozoa.
3

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
|
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.
4

Cellular responses to attaching and effacing bacteria: activation and implication of the innate immune system

88%
Gobert A. P., Wilson K. T., Martin C.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
|
issue 3
234-244
EN
During the last decade, research on attaching-effacing (A/E) bacteria/host cell interactions has revealed much of the molecular basis of colonization and lesion formation. The colonic mucosa represents the first line of defense against these pathogens, and its integrity is required to avoid translocation of bacteria or bacterial soluble factors into the infected host. Therefore, the cellular immune response to A/E pathogens plays an important role in bacterial pathogenesis since it can clear the bacteria or modulate the inflammatory processes. Data obtained from infected patients demonstrate a correlation between the production of pro-inflammatory cytokines and the severity of the disease. In vitro studies of infected epithelial cells have clearly elucidated A/E bacteria-induced host signal transduction events. However, the identification of the bacterial factors responsible for cellular activation remains a subject of controversy. Experimental studies with knock-out mice infected with Citrobacter rodentium, a rodent A/E pathogen, indicate that innate immunity is an essential component of pathogenesis. This review summarizes in vivo and in vitro evidence for the induction and potential role of the innate immune system during infection with A/E bacteria.
5

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.
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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.
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