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Adriouch, S.

Publications and source records attributed to Adriouch, S..

3 recordsLinked to original sources

Anti-PD-1/PD-L1 Therapy Triggers Cognitive Deficits and Anxiety-Like Behaviors Through Tumor-Initiated Neuroinflammatory Niches in Male Mice

Checkpoint inhibitors are promising immunotherapy to treat cancer patients, but their cognitive impact has not been evaluated despite several neurological adverse events. We studied the impact of immune desert or inflamed cancers when combined with immune checkpoint inhibitors (ICI) anti-PD-1/anti-PD-L1 on mouse behaviors and brain immune cells infiltration/homeostasis, and neuroinflammation in male mice. We showed that systemic inflammation, brain-barriers permeability accompanying meningeal infiltration of peripheral macrophages and neuroinflammation as well as deficits in cognition or emotional reactivity, depending on immuno-inflammatory or immune-desert cancer type. Combined with cancers, anti-PD-1 and PD-L1 treatments exacerbated the decline in executive functions and hippocampal vascular inflammation. PD-L1 specifically relayed the infiltration of the T{gamma}{delta} lymphocytes subpopulation in choroid plexus and leptomeninges implicated, whose systemic neutralization counteracted anti-PDL1-induced cognitive deficits and anxiety in mice bearing immune-inflamed cancer. Our findings highlight new systemic biomarkers of cold or hot cancer, treated with anti-PD-1/anti-PDL-1, and associated with cognitive and emotional alterations in mice; guiding ways of intervention to secure the cancer curation and improve patients quality of life under ICI treatment. Competing Interest StatementThe authors have declared no competing interest. One Sentence SummaryImpact of cancer and checkpoint inhibitors on cognitive functions

cancer biology↗

Spatial characterization of microbiota profiles along the gut in a widely used mouse model: effects of high-fat diet and fructooligosaccharides

The intestinal microbiota plays a pivotal role in regulating metabolic processes, and its imbalance is linked to metabolic disorders. Modulating the gut microbiota composition and function through prebiotic supplementation has been repeatedly shown to improve host metabolism. While most studies have focused on the fecal microbiota due to the ease of sampling, fecal samples do not reflect the microbial dynamics throughout the gastrointestinal tract, as regional environmental conditions shape distinct microbiota composition. Given the metabolic significance of the proximal intestine and the potential influence of microbiota on these processes, we characterized the microbiota composition along the gastrointestinal tract in a widely used model for studying host-microbiota interactions: C57Bl6J male mice fed a high-fat diet (HFD) with or without prebiotics supplementation (FOS, fructooligosaccharides). The microbiota composition, determined by long-read Nanopore sequencing, was markedly altered by HFD and FOS supplementation not only in feces but also in the jejunum, ileum and caecum. In contrast to previous observations made in humans, obesity in mice was associated with a decrease in microbiome diversity in the small intestine, highlighting species-specific microbial responses to metabolic challenges. Additionally, the pronounced bifidogenic effect of FOS supplementation in the ileum suggests FOS fermentation in the small intestine in mice, contrary to what has been previously described in humans. Finally, we report a relative homogeneity of microbiome composition along the digestive tract, possibly due to the coprophagic behavior of mice. These findings challenge the translational relevance of rodent models for studying the role of the small intestinal microbiota in human metabolic disease.

microbiology↗

Small-molecule P2RX7 activator sensitizes tumor to immunotherapy and vaccinates mouse against tumor re-challenge

Only a subpopulation of non-small cell lung cancer (NSCLC) patients responds to immunotherapies, highlighting the urgent need to develop new therapeutic strategies to improve patient outcome. We developed a new chemical positive modulator (HEI3090) of the purinergic P2RX7 receptor that potentiates PD-1 treatment to effectively control the growth of lung tumors in transplantable and oncogene-induced mouse models and triggers long lasting antitumor immune responses. Mechanistically, the molecule stimulates dendritic P2RX7 expressing cells to generate IL-18 which leads to the production of IFN-{gamma} by Natural Killer and CD4+ T cells within tumors. Combined with immune checkpoint inhibitor, the molecule induces a complete tumor regression in 80% of LLC tumor bearing mice. Cured mice are also protected against tumor re-challenge due to a CD8-dependent protective response. Hence, combination treatment of small-molecule P2RX7 activator followed by immune checkpoint inhibitor represents a promising novel strategy that may be active against NSCLC.

cancer biology↗