Rabbit macrophages

DLA, DNA damage, rabbit (macrophage. Clara and type II) lung cells + NT 5 Becher et al. (1993)... 

Mathison JC, Virca GD, Wolfson E, Tobias PS, Glaser K, Ulevitch RJ. 1990. Adaptation to bacterial lipopolysaccharide controls lipopolysaccharide-induced tumor necrosis factor production in rabbit macrophages. J. Clin. Invest. 85 1108-18... 

Other toxins produced by Clostridium species have been shown to have immunomodulatory activities. The Type D toxin produced by Clostridium botulism inhibits the production of TNF-a by LPS stimulated human monocytes. Additionally, the Clostridium perfingens delta toxin has been shown to be cytotoxic to rabbit macrophages, but not to thymocytes. ... 

In the preterm Macaca nemestrina (130-156 days of gestation), the number of alveolar macrophages is low and increases rapidly after birth (Jacobs et al. 1985). In foetal rabbits, macrophage appearance coincides with maturation of the lung near term and in the first days after birth (Zeligs et al. 1977, Sieger 1978). 

Bafilomycin (10 pM, pH 7.4) caused shortening of microvilli, focal loss of surface ruffles, and marked cytoplasmic vacuolation in resident rabbit macrophages by 1 h incubation, with significant macrophage fragmentation and apoptosis at 48 h incubation (Haque et al. 1997). Amiloride (100 pM, pH 7.4) caused elongation of microvilli and significant apoptosis by 1 h incubation. 

Furthermore, it has been shown (Anderson et aL, 1987 Anderson and Lukey, 1987) that ascorbate can mediate efficient neutralization of extracellular phagocyte-derived oxidants without affecting the formation of bactericidal oxygen radicals within the intracellular phagosome. This appears to be a major role of ascorbate in phagocytic cells. In addition, ascorbate was shown to protect rabbit macrophages in vitro from injuries associated with phagocytosis (McKee and Myrvik, 1979). 

Fig. 16 Results of the vascular response to stent implantation at 6 weeks postoperatively. CLSM images show (a-c) re-endothelialization and (d-f) macrophage inhltration after stent implantation (a,d) the empty stent (b,e) the control stent and (c,f) the experimental stent. The immunofluorescence was performed with mouse anti-human CD31 (PECAM-1, blue-, arrows indicate sites of re-endothelialization), mouse anti-rabbit macrophages (RAMll, green) and propidium iodide (PI, red). The insets of (a-c) are the same sections stained with hematoxylin-eosin. Sites of stent struts. Because of histological preparation, stent struts have been lost or migrated slightly. Arrow in inset to (b) indicates site of thrombus-like substance deposition. From [166] reproduced by permission of Elsevier...

As briefly mentioned earlier in this chapter (see Section 3.1.1), several different strategies have been adopted for obtaining data for the heat production of cells attached to a substratum. Human keratinocytes were grown to confluency on the collagen coated hydrophilic membrane of a Petriperm dish [96], a piece was cut out and then inserted into the chamber of a large capacity Calvet calorimeter (see Reference [3] for details of it) to record the heat production. In another approach, rabbit macrophages were grown as two-tiered monolayers in the stainless steel vessels of a Thermometric TAM calorimeter... 

Carew, T.E., Schwenke, D.C. and Steinberg, D. (1987). Antiatherogenic effect of probucol unrelated to its hypocholesterolaemic effect evidence that antioxidants in vivo can selectively inhibit low density lipoprotein degradation in macrophage-rich fatty streaks and slow the progression of atherosclerosis in the Watanabe heritable hyperlipidaemic rabbit. Proc. Natl Acad. Sci. USA 84, 7725-7729. 

Romert, L. and Jenssen, D. (1983). Rabbit alveolar macrophage-mediated mutagenesis of polycyclic aromatic hydrocarbons in V79 Chinese hamster cells. Mutat. Res. Ill, 245-252. 

Robinson AV. 1982. Effect of in vitro exposure to hydrogen sulfide on rabbit alveolar macrophages cultured on gas-permeable membranes. Environ Res 27 491-500. 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

Nickel chloride, by inhalation in rabbits, produced a slight but significant increase in lung weight [354]. In addition, enlarged vacuolated macrophages... 

---