Erratum: Corrigendum: S100-alarmin-induced innate immune programming protects newborn infants from sepsis

Ulas, Thomas; Pirr, Sabine; Fehlhaber, Beate; Bickes, Marie S; Loof, Torsten G.; Vogl, Thomas J.; Mellinger, Lara; Heinemann, Anna S.; Burgmann, Johanna; Schöning, Jennifer; Schreek, Sabine; Pfeifer, Sandra; Reuner, Friederike; Völlger, Lena; Stanulla, Martin; Köckritz-Blickwede, Maren von; Glander, Shirin; Barczyk-Kahlert, Katarzyna; Kaisenberg, Constantin S. von; Friesenhagen, Judith; Fischer-Riepe, Lena; Zenker, Stefanie; Schultze, Joachim L.; Röth, Jürgen; Viemann, Dorothee

doi:10.1038/ni1017-1173b

Cited by 2 publications

(1 citation statement)

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“…However, this concept is challenged by clinical observations of hyper-inflammatory courses of neonatal sepsis 42 . Recent work suggested that neonatal immune responses are not impaired, but rather determined by a tightly regulated physiological immune programming preventing harmful hyper-inflammation in combination with sufficient immunological protection 43 . The potency of the neonatal immune system to elicit a strong reaction to dangerous stimuli is also demonstrated by the fact that neonatal peripheral immune cells participate in sterile tissue inflammation induced by perinatal brain injury 44 , indicating a complex interplay between the peripheral immune and the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

Peripheral immune cells and perinatal brain injury: a double-edged sword?

2021

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Perinatal brain injury is the leading cause of neurological mortality and morbidity in childhood ranging from motor and cognitive impairment to behavioural and neuropsychiatric disorders. Various noxious stimuli, including perinatal inflammation, chronic and acute hypoxia, hyperoxia, stress and drug exposure contribute to the pathogenesis. Among a variety of pathological phenomena, the unique developing immune system plays an important role in the understanding of mechanisms of injury to the immature brain. Neuroinflammation following a perinatal insult largely contributes to evolution of damage to resident brain cells, but may also be beneficial for repair activities. The present review will focus on the role of peripheral immune cells and discuss processes involved in neuroinflammation under two frequent perinatal conditions, systemic infection/inflammation associated with encephalopathy of prematurity (EoP) and hypoxia/ischaemia in the context of neonatal encephalopathy (NE) and stroke at term. Different immune cell subsets in perinatal brain injury including their infiltration routes will be reviewed and critical aspects such as sex differences and maturational stage will be discussed. Interactions with existing regenerative therapies such as stem cells and also potentials to develop novel immunomodulatory targets are considered. Impact Comprehensive summary of current knowledge on the role of different immune cell subsets in perinatal brain injury including discussion of critical aspects to be considered for development of immunomodulatory therapies.

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Section: Introductionmentioning

confidence: 99%

Peripheral immune cells and perinatal brain injury: a double-edged sword?

2021

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Codevelopment of Microbiota and Innate Immunity and the Risk for Group B Streptococcal Disease

Kolter

Henneke

2017

Front. Immunol.

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The pathogenesis of neonatal late-onset sepsis (LOD), which manifests between the third day and the third month of life, remains poorly understood. Group B Streptococcus (GBS) is the most important cause of LOD in infants without underlying diseases or prematurity and the third most frequent cause of meningitis in the Western world. On the other hand, GBS is a common intestinal colonizer in infants. Accordingly, despite its adaption to the human lower gastrointestinal tract, GBS has retained its potential virulence and its transition from a commensal to a dangerous pathogen is unpredictable in the individual. Several cellular innate immune mechanisms, in particular Toll-like receptors, the inflammasome and the cGAS pathway, are engaged by GBS effectors like nucleic acids. These are likely to impact on the GBS-specific host resistance. Given the long evolution of streptococci as a normal constituent of the human microbiota, the emergence of GBS as the dominant neonatal sepsis cause just about 50 years ago is remarkable. It appears that intensive usage of tetracycline starting in the 1940s has been a selection advantage for the currently dominant GBS clones with superior adhesive and invasive properties. The historical replacement of Group A by Group B streptococci as a leading neonatal pathogen and the higher frequency of other β-hemolytic streptococci in areas with low GBS prevalence suggests the existence of a confined streptococcal niche, where locally competing streptococcal species are subject to environmental and immunological selection pressure. Thus, it seems pivotal to resolve neonatal innate immunity at mucous surfaces and its impact on microbiome composition and quality, i.e., genetic heterogeneity and metabolism, at the microanatomical level. Then, designer pro- and prebiotics, such as attenuated strains of GBS, and oligonucleotide priming of mucosal immunity may unfold their potential and facilitate adaptation of potentially hazardous streptococci as part of a beneficial local microbiome, which is stabilized by mucocutaneous innate immunity.

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Erratum: Corrigendum: S100-alarmin-induced innate immune programming protects newborn infants from sepsis

Cited by 2 publications

References 1 publication

Peripheral immune cells and perinatal brain injury: a double-edged sword?

Peripheral immune cells and perinatal brain injury: a double-edged sword?

Codevelopment of Microbiota and Innate Immunity and the Risk for Group B Streptococcal Disease

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