20 research outputs found
Are Nested Networks More Robust to Disturbance? A Test Using Epiphyte-Tree, Comensalistic Networks
Recent research on ecological networks suggests that mutualistic networks are
more nested than antagonistic ones and, as a result, they are more robust
against chains of extinctions caused by disturbances. We evaluate whether
mutualistic networks are more nested than comensalistic and antagonistic
networks, and whether highly nested, host-epiphyte comensalistic networks fit
the prediction of high robustness against disturbance. A review of 59 networks
including mutualistic, antagonistic and comensalistic relationships showed that
comensalistic networks are significantly more nested than antagonistic and
mutualistic networks, which did not differ between themselves. Epiphyte-host
networks from old-growth forests differed from those from disturbed forest in
several topological parameters based on both qualitative and quantitative
matrices. Network robustness increased with network size, but the slope of this
relationship varied with nestedness and connectance. Our results indicate that
interaction networks show complex responses to disturbances, which influence
their topology and indirectly affect their robustness against species
extinctions
Distinct contributions of TNF receptor 1 and 2 to TNF-induced glomerular inflammation in mice
TNF is an important mediator of glomerulonephritis. The two TNF-receptors TNFR1 and TNFR2 contribute differently to glomerular inflammation in vivo, but specific mechanisms of TNFR-mediated inflammatory responses in glomeruli are unknown. We investigated their expression and function in murine kidneys, isolated glomeruli ex vivo, and glomerular cells in vitro. In normal kidney TNFR1 and TNFR2 were preferentially expressed in glomeruli. Expression of both TNFRs and TNF-induced upregulation of TNFR2 mRNA was confirmed in murine glomerular endothelial and mesangial cell lines. In vivo, TNF exposure rapidly induced glomerular accumulation of leukocytes. To examine TNFR-specific inflammatory responses in intrinsic glomerular cells but not infiltrating leukocytes we performed microarray gene expression profiling on intact glomeruli isolated from wildtype and Tnfr-deficient mice following exposure to soluble TNF ex vivo. Most TNF-induced effects were exclusively mediated by TNFR1, including induced glomerular expression of adhesion molecules, chemokines, complement factors and pro-apoptotic molecules. However, TNFR2 contributed to TNFR1-dependent mRNA expression of inflammatory mediators in glomeruli when exposed to low TNF concentrations. Chemokine secretion was absent in TNF-stimulated Tnfr1-deficient glomeruli, but also significantly decreased in glomeruli lacking TNFR2. In vivo, TNF-induced glomerular leukocyte infiltration was abrogated in Tnfr1-deficient mice, whereas Tnfr2-deficiency decreased mononuclear phagocytes infiltrates, but not neutrophils. These data demonstrate that activation of intrinsic glomerular cells by soluble TNF requires TNFR1, whereas TNFR2 is not essential, but augments TNFR1-dependent effects. Previously described TNFR2-dependent glomerular inflammation may therefore require TNFR2 activation by membrane-bound, but not soluble TNF