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Barrios, M.

Publications and source records attributed to Barrios, M..

3 recordsLinked to original sources

A Common Agrochemical Mixture Increases Snail Hosts and Ecological Drivers of Schistosomiasis Risk

O_LIAgricultural intensification is accelerating across tropical regions, increasing fertilizer and pesticide inputs into freshwater ecosystems that regulate the transmission of many environmentally mediated diseases. For schistosomiasis, a major neglected tropical disease, transmission risk is strongly governed by the abundance of freshwater snail intermediate hosts and their aquatic habitat, yet most agrochemical studies have focused on single compounds rather than realistic mixtures. C_LIO_LIUsing replicated semi-natural aquatic microcosms, we experimentally tested how nitrogen- urea fertilizer and the widely used herbicide atrazine, applied alone and in combination at environmentally relevant concentrations, alter snail hosts (Biomphalaria glabrata), submerged aquatic vegetation (Ceratophyllum demersum), and algal resources that underpin schistosomiasis transmission. C_LIO_LIFertilizer and atrazine, both singly and together, increased snail habitat (C. demersum) and adult snail abundance. By reducing phytoplankton, atrazine likely alleviated shading on vegetation, thereby promoting habitat that supported snails through indirect bottom-up pathways. Agrochemical mixtures produced non-additive effects on host and habitat dynamics, indicating that transmission-relevant ecological responses cannot be predicted from single-compound exposures alone. Although parasite infection levels were low, the observed increases in snail hosts and habitat represent reliable ecological drivers of schistosomiasis risk. C_LIO_LISynthesis and applications. Our findings demonstrate that common agrochemical mixtures can restructure freshwater food webs in ways likely to elevate disease risk, highlighting the need to incorporate mixture-driven ecological responses into agrochemical risk assessment and agricultural management strategies in disease-endemic regions. C_LI

ecology↗

A necroptotic-to-apoptotic signaling axis underlies inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic condition caused by altered cytokine signaling, maladaptive immunity, dysbiosis, and intestinal barrier dysfunction. Patients with IBD receive therapy to correct these imbalances and achieve remission. However, most patients relapse, suggesting that pathological mechanisms persist during remission. Here, we show that excess epithelial cell death is an underlying feature of IBD that arises in patients in remission and on advanced therapy. Mechanistically, nascent inflammation reprograms epithelial cells into a macrophage-like state that promotes RIPK1-independent necroptotic signaling, then triggers iNOS-mediated mitochondrial apoptosis of absorptive epithelial cells and PUMA-mediated intestinal stem cell death. These findings reveal aberrant epithelial cell death signaling as a hallmark of IBD that occurs early in mucosal lesion development and persists despite current therapeutic approaches. One-Sentence SummaryEpithelial cell death is dysregulated in patients with inflammatory bowel disease.

cell biology↗

An immunohistochemical atlas of necroptotic pathway expression

Necroptosis is a lytic form of regulated cell death reported to contribute to inflammatory diseases of the gut, skin and lung, as well as ischemic-reperfusion injuries of the kidney, heart and brain. However, precise identification of the cells and tissues that undergo necroptotic cell death in vivo has proven challenging in the absence of robust protocols for immunohistochemical detection. Here, we provide automated immunohistochemistry protocols to detect core necroptosis regulators - Caspase-8, RIPK1, RIPK3 and MLKL - in formalin-fixed mouse and human tissues. We observed surprising heterogeneity in protein expression within tissues, whereby short-lived immune barrier cells were replete with necroptotic effectors, whereas long-lived cells lacked RIPK3 or MLKL expression. Local changes in the expression of necroptotic effectors occurred in response to insults such as inflammation, dysbiosis or immune challenge, consistent with necroptosis being dysregulated in disease contexts. These methods will facilitate the precise localisation and evaluation of necroptotic signaling in vivo. HighlightsO_LI13 automated immunohistochemistry protocols for detecting the necroptotic pathway C_LIO_LINecroptotic pathway expression is confined to fast-cycling immune barriers C_LIO_LINecroptotic pathway expression changes at sites of immunoinflammatory challenge C_LIO_LIImmunodetection of necrosomes in IBD patients is a putative new diagnostic tool C_LI

cell biology↗