ALPINE FARM SCALE INVESTIGATIONS OF THE RELATIONSHIPS BETWEEN PRODUCTIVE SYSTEM AND QUALITY OF DAIRY PRODUCTS

Alpine dairy farming is shifted from an extensive activity based on pasture and low genetic merit cow to an intensive system with specialized breeds and increasing level of concentrate as a supplement in the diet. As a main consequence, a lower echo-compatibility could determine adverse externalities on environment and quality of dairy products. Considering 18 dairy farming located in the mountain area of Veneto Region (Italy), the Environmental Summarizing Indicator (ESI) was estimated by using agronomic and dairying variables. Results indicated that variability of ESI was manly due to productive performance of dairy cows probably because there was a lack of information in the assessment of pasture characteristics. However, higher level of ESI were closely related to the increase of N-phile species and/or less attractive vegetation for grazing cows, even if the indicator seems to explain only a limited part of the variability of the phenomenon. The increase of ESI values seemed to lead to a loss of nutritive value of milk because of the incidence of health favourable fatty acids was reduced

Secreted phospholipases A(2): A proinflammatory connection between macrophages and mast cells in the human lung

Secretory phospholipases A(2) (sPLA(2)) are an emerging class of mediators of inflammation. These enzymes accumulate in plasma and other biological fluids of patients with inflammatory, autoimmune and allergic diseases. sPLA(2)s are secreted at low levels in the normal airways and tend to increase during inflammatory lung diseases (e.g. bronchial asthma, chronic obstructive pulmonary disease, interstitial lung fibrosis, and sarcoidosis) as the result of plasma extravasation and/or local production. Such immune resident cells as macrophages and mast cells can be a source of sPLA(2)s in the lung. However, these cells are also targets for sPLA(2)s that sustain the activation programs of macrophages and mast cells with mechanism related to their enzymatic activity as well as to their capacity to interact with surface molecules (e.g., heparan sulfate proteoglycans, M-type receptor, mannose receptor). Recent evidence suggests that mast cells are a better source of extracellular sPLA(2)s than macrophages. On the other hand, macrophages appear to be a preferential target for sPLA(2)s. Anatomical association between macrophages and mast cells in the airways suggest that sPLA(2)s released by mast cells may activate in a paracrine fashion several macrophage functions relevant to the modulation of lung inflammation. Thus, sPLA(2)s may play a major role in inflammatory lung diseases by acting as a proinflammatory connection between macrophages and mast cells

Human macrophages and monocytes express functional na(+)/ca (2+) exchangers 1 and 3

The Na(+)/Ca(2+) exchanger (NCX) is a plasma membrane protein that can switch Na(+) and Ca(2+) in either direction to maintain the homeostasis of intracellular Ca(2+). A family of three genes (NCX1, NCX2, and NCX3) has been identified in neurons and muscle cells. NCX activity has also been reported in certain immune cells (e.g., mast cells). We have examined the expression and function of these NCX isoforms in the human monocytes and lung macrophages. Monocytes were purified from peripheral blood of healthy donors. Macrophages (HLM) were isolated and purified from the lung parenchyma of patients undergoing thoracic surgery. NCX1 and NCX3, but not NCX2, were expressed in HLM and monocytes at both mRNA and protein level. Exposure to Na(+)-free medium induced a significant increase in intracellular calcium concentration ([Ca(2+)](i)) in both cell types, suggesting that NCX isoforms expressed on these cells were functionally active. This response was completely abolished by the NCX inhibitor 5-(N-4-chlorobenzyl)-20,40-dimethylbenzamil (CB-DMB). In addition, incubation of macrophages with Na(+)-free medium induced a marked release of TNF-??. Preincubation of HLM with CB-DMB and RNAi-mediated knockdown of NCX1 blocked TNF-?? release. Our results demonstrate that human macrophages and monocytes express NCX1 and NCX3 that operate in a bidirectional manner to restore [Ca(2+)](i) to generate Ca(2+) signals and to induce TNF-?? production. We suggest that NCX may modulate Ca(2+) homeostasis and proinflammatory functions in human macrophages and monocytes