Lack of specificity of brain gangliosides in the modulation of lymphocyte activation

A potential role for glycolipid gangliosides to act as immunomodulating agents has been suggested. Most studies have employed brain gangliosides. We have systematically investigated highly purified murine brain gangliosides for their ability to modulate lymphocyte activation. All sialic acid classes of ganglioside inhibited lipopolysaccharide (LPS)-induced antibody secretion and all polysialated gangliosides inhibited LPS-induced DNA synthesis. Monosialated gangliosides had no effect on DNA synthesis induced by LPS. 8-BrcGMP-induced DNA synthesis was also inhibited, suggesting that a negative signal was delivered to B lymphocytes by co-cultivation with exogenous gangliosides. The lack of specificity with respect to sialic acid class observed in these studies suggests that further investigation of an immunomodulatory role for gangliosides focus on endogenous lymphocyte gangliosides.     

Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure

Interleukin (IL)-13, a key mediator of Th2-mediated immunity, contributes to the pathogenesis of asthma and other pulmonary diseases via its ability to generate fibrosis, mucus metaplasia, eosinophilic inflammation, and airway hyperresponsiveness. In these studies, we compared surfactant accumulation in wild-type mice and mice in which IL-13 was overexpressed in the lung. When compared with littermate controls, transgenic animals showed alveolar type II cell hypertrophy under light and electron microscopy. Over time, their alveoli also filled with surfactant in a pulmonary alveolar proteinosis pattern. At the same time, prominent interstitial fibrosis occurs. Bronchoalveolar lavage fluid from these mice had a three- to sixfold increase in surfactant phospholipids. Surfactant proteins (SP)-A, -B, and -C showed two- to threefold increases, whereas SP-D increased 70-fold. These results indicate that IL-13 is a potent stimulator of surfactant phospholipid and surfactant accumulation in the lung. IL-13 may therefore play a central role in the broad range of chronic pulmonary conditions in which fibrosis, type II cell hypertrophy, and surfactant accumulation occur.     

Effects of aluminium on growth and root reactions of phosphorus stressed Betula pendula seedlings

The impact of two constant non-toxic levels of Al stress (0.2 and 0.4 mM) on growth and ³²P uptake capacity on sub-optimal (P-limited) Betula pendula seedlings grown in sand culture was examined.Seedling growth was under optimum controlled conditions in a growth chamber where nutrient additions were made at a predetermined relative addition rate (R_A) of 10% day^-1. Three treatment groups of seedlings 0, 0.2 and 0.4 mM Al were harvested at 15, 29 and 42 days. The excised roots were exposed to a ³²P-labelled solution for 15 minutes to measure their capacity for P uptake. Growth was determined by weighing the roots, stems and leaves of the seedlings.Growth data showed that relative growth rate (R_G) should equal the R_A of P the most limiting nutrient, which was supplied at P/N 3% instead of an optimal 15%. Therefore, Ingestad's theory can also be used succesfully in sand culture and this may be particularly important for future studies of root and rhizosphere exudates. Low levels of Al (< 0.2 mM) in combination with low P supply significantly lowered the R_G of the birch seedlings by further reducing P supply. However, previous studies of birch seedling growth and nutrient uptake using Ingestad's solution culture technique with optimumal P supply did not show any effect of Al on growth untill the Al was in excess of 3 mM. Aluminium was not directly toxic to the plants and therefore roots could respond to the ³²P bioassay.     

Changes induced by the roots of Erica arborea L. to create a suitable environment in a soil developed from alkaline and fine-textured marine sediments

Background and aims

We report on the modifications induced by the roots of Erica arborea L. on a soil derived from alkaline and fine-textured marine sediments.

Methods

Physical, chemical, mineralogical and biochemical properties of bulk soil and of the rhizosphere of Erica were characterised to evaluate its role on soil development.

Results

Once the upper horizons had been decarbonated because of geomorphic and pedogenic processes, Erica colonised the soil and progressively modified it through the activity of roots. In the upper horizons, there was no difference between rhizosphere and bulk soil for pH, organic C and exchangeable Al and H. At depth, pH, organic C and exchangeable Al and H differed between rhizosphere and bulk soil. The weathering reactions induced by the Erica roots caused a relative quartz enrichment in the rhizosphere compared with the bulk soil. In the E, EB and Bw horizons, the microbial community of the rhizosphere appeared better adapted than in the underlying 2Bw horizons, where the rhizospheric microorganisms were poorly adapted as these horizons represented the boundary between acid and sub-alkaline soil environments.

Conclusions

The activity of Erica roots modified soil properties so to produce more favourable conditions for itself and the rhizosphere microflora.     

Numerical and experimental study of steady-state CO2 and inert gas washout

The predictions of a single-path trumpet-bell numerical model of steady-state CO2 and infused He and sulfur hexafluoride (SF6) washout were compared with experimental measurements on healthy human volunteers. The mathematical model used was a numerical solution of the classic airway convention-diffusion equation with the addition of a distributed source term at the alveolar end. In the human studies, a static sampling technique was used to measure the exhaled concentrations and phase III slopes of CO2, He, and SF6 during the intravenous infusion of saline saturated with a mixture of the two inert gases. We found good agreement between the experimentally determined normalized slopes (phase III slope divided by mixed expired concentration) and the numerically determined normalized slopes in the model with no free parameters other than the physiological ones of upper airway dead space, tidal volume, breathing frequency, and breathing pattern (sinusoidal). We conclude 1) that the single-path (Weibel) trumpet-bell anatomic model used in conjunction with the airway convection-diffusion equation with a distributed source term is adequate to describe the steady-state lung washout of CO2 and infused He and SF6 in normal lungs and 2) that the interfacial area separating the tidal volume fron from the functional residual capacity gas, through which gas diffusion into the moving tidal volume occurs, exerts a major effect on the normalized slopes of phase III.     

Regulation of SP-B and SP-C secretion in rat type II cells in primary culture

Secretion of lung surfactant phospholipids is a highly regulated process. A variety of physiological and pharmacological agents stimulate surfactant phospholipid secretion in isolated type II cells. Although the lipid and hydrophobic protein components of surfactant are believed to be secreted together by exocytosis of lamellar body contents, regulation of surfactant protein (SP) B and SP-C secretion has not previously been examined. To address the question of whether secretion of SP-B and SP-C is stimulated by the same agonists that stimulate phospholipid secretion, we measured secretion of all four SPs under the same conditions used to measure phosphatidylcholine secretion. Freshly isolated rat type II cells were cultured overnight and exposed to known surfactant phospholipid secretagogues for 2.5 h, after which the amounts of SP-A, SP-B, SP-C, and SP-D in the medium were measured with immunoblotting. Secretion of SP-B and SP-C was stimulated three- to fivefold by terbutaline, 5'-(N-ethylcarboxyamido)adenosine, ATP, 12-O-tetradecanoylphorbol 13-acetate, and ionomycin. Similar to their effects on phospholipid secretion, the stimulatory effects of the agonists were abolished by Ro 31-8220. Secretion of SP-A and SP-D was not stimulated by the secretagogues tested. We conclude that secretion of the phospholipid and hydrophobic protein components of surfactant is similarly regulated, whereas secretion of the hydrophilic proteins is regulated differently.     

Pulmonary surfactant secretion in briefly cultured mouse type II cells

There is little information on the regulation of surfactant secretion in mouse type II cells. We isolated type II cells from C57BL/6 and FVB mice, cultured them overnight, and then examined their response to known surfactant secretagogues. Secretion of phosphatidylcholine, surfactant protein (SP)-B and SP-C was stimulated by terbutaline, 5'-N-ethylcarboxyamidoadenosine (NECA), ATP, UTP, TPA, and ionomycin. Phosphatidylcholine secretion was increased approximately twofold by all agonists in both strains of mice. The response to terbutaline and NECA is the same as in rat type II cells, whereas the response to ATP, UTP, TPA, and ionomycin is considerably less. Secretion of SP-B and SP-C was increased sevenfold by terbutaline and threefold by ATP, effects similar to those in rat type II cells. The response to terbutaline was significantly decreased in type II cells from beta(2)-adrenergic receptor null mice. These data establish that briefly cultured type II cells provide a suitable model for investigation of surfactant secretion in normal and genetically altered mice.     

Adenosine and leukotrienes have a regulatory role in lung surfactant secretion in the newborn rabbit

Previous studies have shown that secretion of phosphatidylcholine in cultured adult rat type II pneumocytes is stimulated by purinoceptor agonists and leukotrienes. The objective of the present study was to determine if such agents have a physiological role in the regulation of surfactant secretion. We chose the newborn rabbit as the experimental model, since in this system there is a marked increase in surfactant secretion immediately after birth. We examined the effects of an inhibitor of leukotriene biosynthesis, nordihydroguaiaretic acid, two leukotriene antagonists, FPL-55712 and FPL-57231, and a P1 purinoceptor antagonist, 8-phenyltheophylline, on this increase. Newborn rabbits were delivered by Cesarean section at 30 days gestation. Some animals in each litter were killed immediately, while others were injected with test agents or solvent vehicle while still in the amniotic sacs. After breathing for 3 h in an incubator, these animals were also killed. The lungs were lavaged with saline and the phospholipid content and composition of the lung lavage liquid was measured. In control animals, there was a greater than 2-fold increase in the amounts of total phospholipid and phosphatidylcholine and in the phosphatidylcholine/sphingomyelin ratio during the 3 h period of breathing. The increases in total phospholipid and phosphatidylcholine were decreased 38-62% by the antagonists, while the increase in the phosphatidylcholine/sphingomyelin ratio was decreased 61-77%. These data show that the ventilation-induced increase in secretion of lung surfactant in the newborn rabbit is inhibited by leukotriene and P1 receptor antagonists and by an inhibitor of leukotriene biosynthesis and, when taken together with the data from the tissue culture system, support a role for leukotrienes and adenosine in the physiological regulation of surfactant secretion.     

Rhizospheric Processes Influencing the Biogeochemistry of Forest Ecosystems

In the rhizosphere, biotic and abiotic processes interact to create a zone distinct from the bulk soil that may strongly influence the biogeochemistry of forest ecosystems. This paper presents a conceptual model based upon three operationally defined soil-root compartments (bulk soil, rhizosphere and soil-root interface) to assess nutrient availability in the mineral soil-root system. The model is supported by chemical and mineralogical analyses from bulk and rhizosphere soils collected from a Norway spruce forest. The rhizosphere was more intensively weathered and had accumulated more acidity, base cations and phosphorus than the bulk soil. The quantity and quality of organic matter regulate the reciprocal relationships between soil and roots with their associated biota. However, the biogeochemical role of organic matter in the rhizosphere still remains as an area in which more future research is needed. The mechanisms that may regulate nutrient availability in the rhizosphere are also discussed and related to nutrient cycling and adaptation of forests growing under nutrient poor or perturbed conditions. We suggest that the rhizosphere is not an ephemeral environment in the soil, but persists over time and is resilient against perturbation as evinced by consistent differences between rhizosphere and bulk chemistry and mineralogy over wide range of field treatments.