Mucosal immunity to pathogenic intestinal bacteria

Pérez-López, Araceli; Behnsen, Judith; Nuccio, Sean Paul; Raffatellu, Manuela

doi:10.1038/nri.2015.17

Cited by 295 publications

(183 citation statements)

References 157 publications

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“…Traditional antimicrobial peptides are directly microbicidal (defensins (α and β), cathelicidins); other peptides regulate microbes by sequestering nutrients (e.g. iron, zinc, manganese) necessary for growth (calprotectin, REG3γ) 188 . For the purposes of this review, we will limit our discussion to the first group.…”

Section: Physical Barriers Protecting the Gi Tractmentioning

confidence: 99%

Pathogenesis of NEC: Role of the innate and adaptive immune response

Denning

Bhatia

Kane

et al. 2017

Seminars in Perinatology

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Necrotizing enterocolitis (NEC) is a devastating disease in premature infants with high case fatality and significant morbidity among survivors. Immaturity of intestinal host defenses predisposes the premature infant gut to injury. An abnormal bacterial colonization pattern with a deficiency of commensal bacteria may lead to a further breakdown of these host defense mechanisms, predisposing the infant to NEC. Here, we review the role of the innate and adaptive immune system in the pathophysiology of NEC.

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Section: Physical Barriers Protecting the Gi Tractmentioning

confidence: 99%

Pathogenesis of NEC: Role of the innate and adaptive immune response

Denning

Bhatia

Kane

et al. 2017

Seminars in Perinatology

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“…The intestinal epithelium is inhabited by trillions of microbes that are kept in check by diverse epithelial and cellular immune responses 35– 37 . The activity of the immune system, however, has to be tightly controlled to prevent inflammatory disorders and maintain homeostatic regeneration of tissues.…”

Section: Tgfβ Signaling In Immune Regulationmentioning

confidence: 99%

Recent advances in understanding contextual TGFβ signaling

2017

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The appearance of the first animal species on earth coincides with the emergence of transforming growth factor β (TGFβ) pathways. The evolution of these animals into more complex organisms coincides with a progressively increased TGFβ repertoire through gene duplications and divergence, making secreted TGFβ molecules the largest family of morphogenetic proteins in humans. It is therefore not surprising that TGFβ pathways govern numerous aspects of human biology from early embryonic development to regeneration, hematopoiesis, neurogenesis, and immunity. Such heavy reliance on these pathways is reflected in the susceptibility to minor perturbations in pathway components that can lead to dysregulated signaling and a diverse range of human pathologies such as cancer, fibrosis, and developmental disorders. Attempts to comprehensively resolve these signaling cascades are complicated by the long-recognized paradoxical role the pathway plays in cell biology. Recently, several groups have probed examples of the disparate aspects of TGFβ biology in a variety of animal models and uncovered novel context-dependent regulatory mechanisms. Here, we briefly review recent advancements and discuss their overall impact in directing future TGFβ research.

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“…Most of what is known of classical adaptive immunology relates to the immune system of the bowel, but there are in addition some specialised features unique to the intestinal mucosa 16– 18 .…”

Section: General Introductionmentioning

confidence: 99%

Making sense of the cause of Crohn’s – a new look at an old disease

Segal

2016

F1000Res

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The cause of Crohn’s disease (CD) has posed a conundrum for at least a century. A large body of work coupled with recent technological advances in genome research have at last started to provide some of the answers. Initially this review seeks to explain and to differentiate between bowel inflammation in the primary immunodeficiencies that generally lead to very early onset diffuse bowel inflammation in humans and in animal models, and the real syndrome of CD. In the latter, a trigger, almost certainly enteric infection by one of a multitude of organisms, allows the faeces access to the tissues, at which stage the response of individuals predisposed to CD is abnormal. Direct investigation of patients’ inflammatory response together with genome-wide association studies (GWAS) and DNA sequencing indicate that in CD the failure of acute inflammation and the clearance of bacteria from the tissues, and from within cells, is defective. The retained faecal products result in the characteristic chronic granulomatous inflammation and adaptive immune response. In this review I will examine the contemporary evidence that has led to this understanding, and look for explanations for the recent dramatic increase in the incidence of this disease.

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Mucosal immunity to pathogenic intestinal bacteria

Cited by 295 publications

References 157 publications

Pathogenesis of NEC: Role of the innate and adaptive immune response

Pathogenesis of NEC: Role of the innate and adaptive immune response

Recent advances in understanding contextual TGFβ signaling

Making sense of the cause of Crohn’s – a new look at an old disease

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