Lithology could affect benthic communities living below boulders

AbstractStructure and diversity of sessile zoobenthic assemblages seem to be driven not only by chemical-physical constraints and biological interactions but also by substrate lithology and its surface features. Nevertheless, broadly distributed crustose epilithic corallines could mask the role of substrate on animal settling. To evaluate the direct influence of different rocky substrates, occurrence and coverage of several sessile species, growing on the dark (i.e. coralline-free) face of sublittoral limestone and granite boulders were compared in the Tavolara MPA (Mediterranean Sea). The analysis of photographic samples demonstrated significant differences in terms of species composition and coverage, according to lithology. Moreover, limestone boulders were widely bare, while the cover per cent was almost total on granite. The leading cause of observed patterns could be the different level of dissolution of the two types of rocks, due to their different mineral composition and textural characteristics. Limestone has previously been shown to have higher dissolution compared with granite, and consequently, a more unstable surface. Our results suggest that, in dark habitats, the absence of the crustose coralline layer allows more rock dissolution and consequent lower stability of the limestone compared with granite, which, in turn, reduces the zoobenthos colonization

In Celiac Disease, a Subset of Autoantibodies against Transglutaminase Binds Toll-Like Receptor 4 and Induces Activation of Monocytes

BACKGROUND: Celiac disease is a small intestine inflammatory disorder with multiple organ involvement, sustained by an inappropriate immune response to dietary gluten. Anti-transglutaminase antibodies are a typical serological marker in patients with active disease, and may disappear during a gluten-free diet treatment. Involvement of infectious agents and innate immunity has been suggested but never proven. Molecular mimicry is one of the mechanisms that links infection and autoimmunity. METHODS AND FINDINGS: In our attempt to clarify the pathogenesis of celiac disease, we screened a random peptide library with pooled sera of patients affected by active disease after a pre-screening with the sera of the same patients on a gluten-free diet. We identified a peptide recognized by serum immunoglobulins of patients with active disease, but not by those of patients on a gluten-free diet. This peptide shares homology with the rotavirus major neutralizing protein VP-7 and with the self-antigens tissue transglutaminase, human heat shock protein 60, desmoglein 1, and Toll-like receptor 4. We show that antibodies against the peptide affinity-purified from the sera of patients with active disease recognize the viral product and self-antigens in ELISA and Western blot. These antibodies were able to induce increased epithelial cell permeability evaluated by transepithelial flux of [(3)H] mannitol in the T84 human intestinal epithelial cell line. Finally, the purified antibodies induced monocyte activation upon binding Toll-like receptor 4, evaluated both by surface expression of activation markers and by production of pro-inflammatory cytokines. CONCLUSIONS: Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry. Moreover, such antibodies recognize self-antigens and are functionally active, able to increase intestinal permeability and induce monocyte activation. We therefore provide evidence for the involvement of innate immunity in the pathogenesis of celiac disease through a previously unknown mechanism of engagement of Toll-like receptor 4

Endothelial Cells' Activation and Apoptosis Induced by a Subset of Antibodies against Human Cytomegalovirus: Relevance to the Pathogenesis of Atherosclerosis

Human cytomegalovirus (hCMV) is involved in the pathogenesis of atherosclerosis. We have previously shown in patients with atherosclerosis that antibodies directed against the hCMV-derived proteins US28 and UL122 are able to induce endothelial cell damage and apoptosis of non-stressed endothelial cells through cross-rection with normally expressed surface molecules. Our aim was to dissect the molecular basis of such interaction and to investigate mechanisms linking innate immunity to atherosclerosis.We analysed the gene expression profiles in endothelial cells stimulated with antibodies affinity-purified against either the UL122 or the US28 peptides using the microarray technology. Microarray results were validated by quantitative PCR and by detection of proteins in the medium. Supernatant of endothelial cells incubated with antibodies was analysed also for the presence of Heat Shock Protein (HSP)60 and was used to assess stimulation of Toll-Like Receptor-4 (TLR4). Antibodies against UL122 and US28 induced the expression of genes encoding for adhesion molecules, chemokines, growth factors and molecules involved in the apoptotis process together with other genes known to be involved in the initiation and progression of the atherosclerotic process. HSP60 was released in the medium of cells incubated with anti-US28 antibodies and was able to engage TLR4.Antibodies directed against hCMV modulate the expression of genes coding for molecules involved in activation and apoptosis of endothelial cells, processes known to play a pivotal role in the pathogenesis of atherosclerosis. Moreover, endothelial cells exposed to such antibodies express HSP60 on the cell surface and release HSP60 in the medium able to activate TLR4. These data confirm that antibodies directed against hCMV-derived proteins US28 and UL122 purified from patients with coronary artery disease induce endothelial cell damage and support the hypothesis that hCMV infection may play a crucial role in mediating the atherosclerotic process

Antibodies against Human Cytomegalovirus in the Pathogenesis of Systemic Sclerosis: A Gene Array Approach

Background Systemic sclerosis is an autoimmune disease characterized by immunological abnormalities, vascular damage, and fibroblast proliferation. We have previously shown that a molecular mimicry mechanism links antibodies against the human-cytomegalovirus-derived protein UL94 to the pathogenesis of systemic sclerosis. The UL94 epitope shows homology with NAG-2, a surface molecule highly expressed on endothelial cells. Anti-UL94 peptide antibodies purified from patients' sera induce apoptosis of endothelial cells upon engagement of the NAG-2-integrin complex. Methods and Findings We show here that NAG-2 is expressed on dermal fibroblasts and that anti-UL94 antibodies bind to fibroblasts. We have used the gene array strategy (Affimetrix oligonucleotide microarrays) to analyze the transcriptional profile in response to a 4-h and an 8-h treatment with antibodies against the UL94 peptide in endothelial cells and dermal fibroblasts. Exposure of endothelial cells to anti-UL94 antibodies had a profound impact on gene expression, resulting in the upregulation of 1,645 transcripts. Several gene clusters were upregulated including genes encoding adhesion molecules, chemokines, colony-stimulating factors (CSFs), growth factors, and molecules involved in apoptosis. Following antibody stimulation, dermal fibroblasts showed an upregulation of 989 transcripts and acquired a "scleroderma-like" phenotype. Indeed, genes involved in extracellular matrix deposition, growth factors, chemokines, and cytokines were upregulated. We confirmed the microarray results by real-time quantitative polymerase chain reaction and by measuring some of the corresponding proteins with ELISA and Western blotting. Conclusion Our results show that anti-human-cytomegalovirus antibodies may be linked to the pathogenesis of systemic sclerosis not only by inducing endothelial cell activation and apoptosis but also by causing activation of fibroblasts, one of the hallmarks of the disease

A predictive approach to benthic marine habitat mapping: Efficacy and management implications

The availability of marine habitats maps remains limited due to difficulty and cost of working at sea. Reduced light penetration in the water hampers the use of optical imagery, and acoustic methods require extensive sea-truth activities. Predictive spatial modelling may offer an alternative to produce benthic habitat maps based on complete acoustic coverage of the seafloor together with a comparatively low number of sea truths. This approach was applied to the coralligenous reefs of the Marine Protected Area of Tavolara - Punta Coda Cavallo (NE Sardinia, Italy). Fuzzy clustering, applied to a set of observations made by scuba diving and used as sea truth, allowed recognising five coralligenous habitats, all but one existing within EUNIS (European Nature Information System) types. Variable importance plots showed that the distribution of habitats was driven by distance from coast, depth, and lithotype, and allowed mapping their distribution over the MPA. Congruence between observed and predicted distributions and accuracy of the classification was high. Results allowed calculating the occurrence of the distinct coralligenous habitats in zones with different protection level. The five habitats are unequally protected since the protection regime was established when detailed marine habitat maps were not available. A SWOT (Strengths-Weaknesses-Opportunities-Threats) analysis was performed to identify critical points and potentialities of the method. The method developed proved to be reliable and the results obtained will be useful when modulating on-going and future management actions in the studied area and in other Mediterranean MPAs to develop conservation efforts at basin scale