A novel synthetic lipopeptide is allergy‐protective by the induction of <scp>LPS</scp>‐tolerance

Stiehm, Matthias; Peters, Karin; Wiesmüller, Karl‐Heinz; Bufe, Albrecht; Peters, Marcus

doi:10.1111/cea.12116

Cited by 19 publications

(17 citation statements)

References 49 publications

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“…Increased activation of this cytokine also upregulates pseudokinase IRAK-M (Pan et al 2010; Srivastav et al 2015; Standiford et al 2011). This is significant because IRAK-M would appear to be the ‘master regulator’ of the TLR pathway suppression characteristic of the state of endotoxin tolerance in PMBCs (del Fresno et al 2007; Escoll et al 2003; Stiehm et al 2013; van’t Veer et al 2007; Wiersinga et al 2009). Indeed, the weight of evidence suggests that increased activity of this enzyme alone is sufficient to maintain an LPS-induced hypo-inflammatory state in human macrophages and monocytes (van’t Veer et al 2007).…”

Section: Iandons and The Development Of Endotoxin Tolerance Via Ido Uprmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

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Section: Iandons and The Development Of Endotoxin Tolerance Via Ido Uprmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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“…Bacteria found in farm cowshed, including Acinetobacter iwoffii and Lactococcus lactis , prime the DCs to induce a Th1 polarization, thus protecting from allergies [60]. Cowshed dust extracts containing molecules such as synthetic lipopeptide from Bacillus cereus , LPGerD, induces TLR-2/IRAK-M signaling in bone marrow-derived DCs [61]. Such activation of TLR-2 nullifies the LPS stimulus leading to a tolerant immune response.…”

Section: Effect Of Microbiome On DC Phenotypementioning

confidence: 99%

Clinical view on the importance of dendritic cells in asthma

Gaurav

Agrawal

2013

Expert Review of Clinical Immunology

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Summary Allergic asthma is characterized by airway hyperresponsiveness and inflammation and may lead to airway remodeling in uncontrolled cases. Genetic predisposition to an atopic phenotype plays a major component in the pathophysiology of asthma. However, with tremendous role of epigenetic factors and environmental stimuli in precipitating an immune response, the underlying pathophysiological mechanisms are complicated. Dendritic cells are principal antigen presenting cells and initiators of the immune response in allergic asthma. Their phenotype, guided by multiple factors may dictate the immune reaction to an allergic or tolerogenic response. Involvement of the local cytokine milieu, microbiome and interplay between immune cells add dimension to the fate of immune response. In addition to allergen exposure, these factors modulate DC phenotype and function. In this article, integration of many factors and pathways associated with the recruitment and activation of DCs in the pathophysiology of allergic asthma is presented in a clinical and translational manner.

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“…The pseudokinase IRAK-M could be considered a ‘master regulator’ of ET because it is one of the genes that is consistently induced into ET [46,47] and has been implicated in a number of human pathologies – such as sepsis [6], cancer [34], ACS [8], and asthma [48] – during which ET manifests. This protein belongs to the four-member interleukin-1 receptor-associated kinase (IRAK) family.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of endotoxin tolerance: mechanisms and clinical consequences

López-Collazo¹,

2013

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Endotoxin tolerance was first described in a study that exposed animals to a sublethal dose of bacterial endotoxin. The animals subsequently survived a lethal injection of endotoxin. This refractory state is associated with the innate immune system and, in particular, with monocytes and macrophages, which act as the main participants. Several mechanisms are involved in the control of endotoxin tolerance; however, a full understanding of this phenomenon remains elusive. A number of recent reports indicate that clinical examples of endotoxin tolerance include not only sepsis but also diseases such as cystic fibrosis and acute coronary syndrome. In these pathologies, the risk of new infections correlates with a refractory state. This review integrates the molecular basis and clinical implications of endotoxin tolerance in various pathologies.

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A novel synthetic lipopeptide is allergy‐protective by the induction of LPS‐tolerance

Cited by 19 publications

References 49 publications

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Clinical view on the importance of dendritic cells in asthma

Pathophysiology of endotoxin tolerance: mechanisms and clinical consequences

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