Stroke Alters the Function of Enteric Neurons to Impair Smooth Muscle Relaxation and Dysregulates Gut Transit.

Background: Gut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of muscle cells in the gut wall. More recently, studies of gut inflammation revealed interactions of macrophages with enteric neurons are also involved in modulating gut motility.

The interplay between the microbiota, diet and T regulatory cells in the preservation of the gut barrier in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is becoming more common in the Western world due to changes in diet-related microbial dysbiosis, genetics and lifestyle. Incidences of gut permeability can predate IBD and continued gut barrier disruptions increase the exposure of bacterial antigens to the immune system thereby perpetuating chronic inflammation. Currently, most of the approved IBD therapies target individual pro-inflammatory cytokines and pathways.

Sympathetic-Mediated Intestinal Cell Death Contributes to Gut Barrier Impairment After Stroke.

Tissue injury induced by stroke is traditionally thought to be localised to the brain. However, there is an accumulating body of evidence to demonstrate that stroke promotes pathophysiological consequences in peripheral tissues including the gastrointestinal system. In this study, we investigated the mechanisms underlying gut permeability after stroke.

Brain-associated innate leukocytes display diverse inflammatory states following experimental stroke.

Previous studies investigating innate leukocyte recruitment into the brain after cerebral ischemia have shown conflicting results. Using distinct cell surface and intracellular markers, the current study evaluated the contributions of innate immune cells to the poststroke brain following 1-h middle cerebral artery occlusion (tMCAO) or permanent MCAO (pMCAO), and assessed whether these cells ascribed to an inflammatory state. Moreover, we examined whether there is evidence for leukocyte infiltration into the contralateral (CL) hemisphere despite the absence of stroke infarct.

Deficiency of Dietary Fiber Modulates Gut Microbiota Composition, Neutrophil Recruitment and Worsens Experimental Colitis.

Ulcerative colitis is an inflammatory disease of the colon that is associated with colonic neutrophil accumulation. Recent evidence indicates that diet alters the composition of the gut microbiota and influences host-pathogen interactions. Specifically, bacterial fermentation of dietary fiber produces metabolites called short-chain fatty acids (SCFAs), which have been shown to protect against various inflammatory diseases.

Imbalance in the force: the dark side of the microbiota on stroke risk and progression.

The composition of the gut microbiota depends on many factors, including our lifestyle, diet, metabolism, antibiotic use and hygiene. The contribution of these factors in shaping the gut microbiota and the subsequent effects on the prevention and development of stroke has been under intense investigation. Furthermore, several reports have uncovered the impact of stroke on intestinal dysfunction and gut dysbiosis, highlighting the delicate interplay between the brain, gut and microbiome following this acute brain injury.

Advanced age promotes colonic dysfunction and gut-derived lung infection after stroke.

Bacterial infection a leading cause of death among patients with stroke, with elderly patients often presenting with more debilitating outcomes. The findings from our retrospective study, supported by previous clinical reports, showed that increasing age is an early predictor for developing fatal infectious complications after stroke. However, exactly how and why older individuals are more susceptible to infection after stroke remains unclear.

Distinct contributions of hyperglycemia and high-fat feeding in metabolic syndrome-induced neuroinflammation.

Background: High-fat feeding and hyperglycemia, key risk factors for the development of metabolic syndrome (MetS), are emerging to associate with increased risk of developing dementia and cognitive decline. Despite this, clinical and experimental studies have yet to elucidate the specific contributions of either high-fat feeding or hyperglycemia to potential neuroinflammatory components. In this study, we delineate these individual components of MetS in the development of neuroinflammation.

Invariant Natural Killer T Cells Shape the Gut Microbiota and Regulate Neutrophil Recruitment and Function During Intestinal Inflammation.

Invariant natural killer T (iNKT) cells and neutrophils play an increasingly important part in the pathogenesis of inflammatory diseases, but their precise roles in modulating colitis remain unclear. Previous studies have shown important interplays between host immune system and the gut microbiota, and the resulting modulation of inflammation. However, the interactions between iNKT cells, neutrophil and gut microbiota in regulating colitis pathology are poorly understood.

Partners in crime: neutrophils and monocytes/macrophages in inflammation and disease.

Neutrophils are becoming recognized as highly versatile and sophisticated cells that display de novo synthetic capacity and potentially prolonged lifespan. Emerging concepts such as neutrophil heterogeneity and plasticity have revealed that, under pathological conditions, neutrophils may differentiate into discrete subsets defined by distinct phenotypic and functional characteristics. Indeed, these newly described neutrophil subsets will undoubtedly add to the already complex interactions between neutrophils and other immune cell types for an effective immune response.