von Dr. Marcus Gereke
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| [1.] Mag/Fragment 015 01 - Diskussion Zuletzt bearbeitet: 2014-03-10 12:05:44 Graf Isolan | Fehrenbach 2001, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop, Verschleierung |
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| Untersuchte Arbeit: Seite: 15, Zeilen: 1ff (entire page) |
Quelle: Fehrenbach_2001 Seite(n): 41, Zeilen: r. col: 10-13, 20ff |
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| The interaction of alveolar epithelial and capillary endothelial cells is well examined. It was reported that from pulmonary endothelial cells conditioned medium stimulate fetal lung epithelial cell growth (Smith et al., 1986) and that endothelin-1 increases AECII surfactant secretion in vitro via a protein kinase C and Ca2+-mediated pathway (Sen et al., 1994). As a source of endothelin-1, endothelial cells are therefore principally competent to act in a paracrine manner on AECII, which were reported to express the endothelin receptor A (Markewitz et al., 1995). Furthermore, alveolar type II epithelial cells themselves may synthesize endothelin-1 and stimulate endogenous prostaglandin E2 synthesis in an autocrine fashion (Markewitz et al., 1995).
Recently, a very special mechanism of indirect intercellular communication between AECII and endothelial cells has been suggested. Stimulation of alveolar epithelial cells with tumour necrosis (TNF)-α was reported to increase epithelial Ca2+ influx and to activate epithelial cytoplasmic phospholipase A2, and results in basolateral release of arachidonic acid. Free arachidonic acid is thought to increase endothelial Ca2+ influx and expression of P-selectin (Kuebler et al., 2000), which is known to be crucial for initiation of leukocyte adherence. Thus, AECII could act as transducers of an inflammatory signal from the alveolus to the capillary bed to recruit granulocytes to the site of inflammation. Alveolar macrophages are one of the mobile cell types that interact with AECII. Among the multitude of secretory products synthesized and released by alveolar macrophages (Kasper et al., 1996; Lohmann-Matthes et al., 1994) there are some factors that act as mitogens for AECII, such as hepatocyte growth factor (Mason et al., 1994) and heparin-binding epidermal growth factor (Leslie et al., 1997). Conversely, AECII were shown to express the chemokines RANTES and MCP-1, which chemotactically attract macrophages (O´Brien et al., 1998), as well as GM-CSF (Blau et al., 1994; Christensen et al., 1995), which in turn may stimulate macrophage growth (Worgall et al., 1999). Furthermore, SP-A released from AECII modulate macrophage functions such as oxygen radical release (Weissbach et al. 1994) and nitric oxide production (Stamme et al., 2000). Interactions of AECII with leukocytes have just recently come into focus. AECII synthesize some cytokines affecting leukocytes, such as interleukin (IL)-6 or IL-8. |
Little is known about the interaction of alveolar epithelial and capillary endothelial cells. Pulmonary endothelial cell conditioned medium was reported to stimulate foetal lung epithelial cell growth [156]. [...]
Endothelin-1 was observed to increase AE2 cell surfactant secretion in vitro via a protein kinase C and Ca2+-mediated pathway [158]. As a source of endothelin-1, endothelial cells are therefore principally competent to act in a paracrine manner on AE2 epithelial cells, which were reported to express the endothelin receptor A [159]. One has to take into account that AE2 cells themselves may synthesise endothelin-1 and stimulate endogenous prostaglandin E2 synthesis in an autocrine fashion [159]. Recently, a very special mechanism of indirect intercellular communication between AE2 cells and endothelial cells has been suggested based on in situ fluorescence imaging studies in alveoli of isolated perfused lungs [160]. Stimulation of alveolar epithelial cells with tumour necrosis factor (TNF)-a was reported to increase epithelial [Ca2+]; and to activate epithelial cytoplasmic phospholipase A2, and results in basolateral release of arachidonic acid. Free arachidonic acid is thought to increase endothelial [Ca2+]; and expression of P-selectin [160], which is known to be crucial for initiation of leukocyte adherence. Thus, AE2 cells may act as transducers of an inflammatory signal from the alveolus to the capillary bed to recruit granulocytes to the site of inflammation. Interaction with mobile cells Alveolar macrophages Among the multitude of secretory products synthesised and released by alveolar macrophages (for reviews, see [123,161]) there are some factors that act as mitogens for AE2 cells, such as hepatocyte growth factor [162] and heparin-binding epidermal growth factor-like protein [163]. Conversely, AE2 cells were shown to express the chemokines RANTES and MCP-1, which chemotactically attract macrophages [164], as well as GM-CSF [165,166], which in turn may stimulate macrophage growth [167]. Furthermore, SP-A released from AE2 cells may modulate macrophage functions such as, oxygen radical release [168], and nitric oxide production [169]. One has to take into account, however, that there may be species-specific differences [162,163]. Leukocytes Interactions of AE2 cells with leukocytes have just come into focus. AE2 cells may synthesise some cytokines affecting leukocytes, such as interleukin (IL)-6 or IL-8 (see Supplementary Table 2). 156. Smith SK, Giannopoulos G: Influence of pulmonary endothelial cells on fetal lung development. Pediatr Pulmonol 1985, 1: S53–S59. 158. Sen N, Grunstein MM, Chander A: Stimulation of lung surfactant secretion by endothelin-1 from rat alveolar type II cells. Am J Physiol 1994, 266:L255–262. 159. Markewitz BA, Kohan DE, Michael JR: Endothelin-1 synthesis, receptors, and signal transduction in alveolar epithelium: evidence for an autocrine role. Am J Physiol 1995, 268:L192–200. 160. Kuebler WM, Parthasarathi K, Wang PM, Bhattacharya J: A novel signalling mechanism between gas and blood compartments of the lung. J Clin Invest 2000, 105:905–913. 123. Kasper M, Haroske G: Alterations in the alveolar epithelium after injury leading to pulmonary fibrosis. Histol Histopathol 1996, 11:463–483. 161. Lohmann-Matthes ML, Steinmuller C, Franke-Ullmann G: Pulmonary macrophages. Eur Respir J 1994, 7:1678–1689. 162. Mason RJ, Leslie CC, McCormick-Shannon K, Deterding RR, Nakamura T, Rubin JS, Shannon JM: Hepatocyte growth factor is a growth factor for rat alveolar type II cells. Am J Respir Cell Mol Biol 1994, 11:561–567. 163. Leslie CC, McCormick-Shannon K, Shannon JM, Garrick B, Damm D, Abraham JA, Mason RJ: Heparin-binding EGF-like growth factor is a mitogen for rat alveolar type II cells. Am J Respir Cell Mol Biol 1997, 16:379–387. 164. O’Brien AD, Standiford TJ, Christensen PJ, Wilcoxen SE, Paine R, 3rd: Chemotaxis of alveolar macrophages in response to signals derived from alveolar epithelial cells. J Lab Clin Med 1998, 131:417–424. 165. Blau H, Riklis S, Kravtsov V, Kalina M: Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A. Am J Physiol 1994, 266:L148–155. 166. Christensen PJ, Armstrong LR, Fak JJ, Chen GH, McDonald RA, Toews GB, Paine R III: Regulation of rat pulmonary dendritic cell immunostimulatory activity by alveolar epithelial cellderived granulocyte macrophage colony- stimulating factor. Am J Respir Cell Mol Biol 1995, 13:426–433. 167. Worgall S, Singh R, Leopold PL, Kaner RJ, Hackett NR, Topf N, Moore MA, Crystal RG: Selective expansion of alveolar macrophages in vivo by adenovirus-mediated transfer of the murine granulocyte-macrophage colony-stimulating factor cDNA. Blood 1999, 93:655–666. 168. Weissbach S, Neuendank A, Pettersson M, Schaberg T, Pison U: Surfactant protein A modulates release of reactive oxygen species from alveolar macrophages. Am J Physiol 1994, 267: L660–666. 169. Stamme C, Walsh E, Wright JR: Surfactant protein A differentially regulates IFN-g- and LPS-induced nitrite production by rat alveolar macrophages. Am J Respir Cell Mol Biol 2000, 23: 772–779. |
The author adopts on pp. 13-16 an uninterrupted review of some 30 articles from Fehrenbach without indicating this source. Continued from Fragment_014_01. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Graf Isolan, Zeitstempel: 20140310120636