NOD1 sensing of house dust mite–derived microbiota promotes allergic experimental asthma

Yahia, Saliha Ait; Audousset, Camille; Álvarez-Simón, Daniel; Vorng, Han; Togbé, Dieudonnée; Marquillies, Philippe; Delacre, Myriam; Rose, Stéphanie; Bouscayrol, Hélène; Rifflet, Aline; Quesniaux, Valérie; Boneca, Ivo Gomperts; Chamaillard, Mathias; Tsicopoulos, Anne

doi:10.1016/j.jaci.2020.12.649

Cited by 11 publications

(16 citation statements)

References 43 publications

(49 reference statements)

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“…In accordance with these results, our group has shown that both NOD1 deficient and RIPK2 deficient mice, when subjected to an HDM asthma protocol, present reduced asthma features including reduced AHR, eosinophil, and neutrophil recruitment. In agreement, the levels of IL5, IL13, and IL33 among other cytokines, coincided with reduced asthma histopathology features in their lungs, indicating that NOD1 aggravates HDM-induced asthma through RIPK2 ( 114 ). Similar to the NOD1 deficient mice, the NOD2 deficient mice displayed decreased eosinophil and neutrophil recruitment.…”

Section: Nlrs In Asthmasupporting

confidence: 55%

“…Importantly, we have also shown using NOD1 deficient bone marrow transplants that epithelial cells play a more relevant role in the reduced asthmatic response in the NOD1 deficient mice than the bone marrow derived cell subsets. Moreover, the HDM in vitro stimulation of NOD1 knockdown human bronchial epithelial cells further supported the higher relevance of NOD1 compared with NOD2, in the aggravation of asthma most likely via the differential expression of agonist transporters at the respiratory epithelium ( 114 ).…”

Section: Nlrs In Asthmamentioning

confidence: 72%

“…It has been shown that the stimulation of human bronchial epithelial cells with a NOD1 agonist induces the release of IL8 and CCL2 among other down stream mediators, while NOD2 activation does not result in changes in either IL8 or CCL2 production ( 113 ). Accordingly, although, our group has shown that the stimulation of human bronchial epithelial cells with HDM induces NOD1 and NOD2 gene expression and IL8 production ( 114 ), only NOD1 knockdown in human bronchial epithelial cells reduced significantly IL8 production ( 114 ). NOD2 (as well as NLRC5) gene expression has also been shown to be increased in influenza-stimulated primary bronchial epithelial cells from asthmatic patients ( 115 ).…”

Section: Nlrs In Asthmamentioning

confidence: 98%

“…These findings indicate that the sensing of NOD1 specific ligands present in HDM extracts is most likely the underlying cause of the NOD1 linked HDM asthma aggravation. It highlights an unprecedented interaction between NOD1 and HDM, unveiling a new mechanism whereby HDM-derived microbiota potentiates disease severity through NOD1 and RIPK2 signaling ( 114 ).…”

Section: Nlrs In Asthmamentioning

confidence: 99%

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NOD-like receptors in asthma

et al. 2022

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Asthma is an extremely prevalent chronic inflammatory disease of the airway where innate and adaptive immune systems participate collectively with epithelial and other structural cells to cause airway hyperresponsiveness, mucus overproduction, airway narrowing, and remodeling. The nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are a family of intracellular innate immune sensors that detect microbe-associated molecular patterns and damage-associated molecular patterns, well-recognized for their central roles in the maintenance of tissue homeostasis and host defense against bacteria, viruses and fungi. In recent times, NLRs have been increasingly acknowledged as much more than innate sensors and have emerged also as relevant players in diseases classically defined by their adaptive immune responses such as asthma. In this review article, we discuss the current knowledge and recent developments about NLR expression, activation and function in relation to asthma and examine the potential interventions in NLR signaling as asthma immunomodulatory therapies.

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Section: Nlrs In Asthmasupporting

confidence: 55%

Section: Nlrs In Asthmamentioning

confidence: 72%

Section: Nlrs In Asthmamentioning

confidence: 98%

Section: Nlrs In Asthmamentioning

confidence: 99%

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NOD-like receptors in asthma

et al. 2022

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“…Since the murine strain and the MDP dose administered were in complete concordance, the differences between our results and those of the aforementioned study might be related to the allergen, the model design, or the chosen timing of MDP administration, i.e., the sensitization phase in our study. In this context, we have recently shown that, despite the existence of MDP in house dust mite (HDM) extracts, the lack of NOD2 hindered eosinophil BAL cell recruitment but did not alter the lung cytokine profile, the humoral response, or the AHR in a model of HDM-induced asthma exhibiting a predominant Th2 profile [ 40 ]. In contrast, NOD1, as well as RIPK2 adaptor deficiency, strongly downregulated all the features of HDM-induced asthma [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

NOD2 Signaling Circuitry during Allergen Sensitization Does Not Worsen Experimental Neutrophilic Asthma but Promotes a Th2/Th17 Profile in Asthma Patients but Not Healthy Subjects

Bouté

Yahia

Fan

et al. 2022

IJMS

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Nucleotide-binding oligomerization domain 2 (NOD2) recognizes pathogens associated with the development of asthma. Moreover, NOD2 adjuvants are used in vaccine design to boost immune responses. Muramyl di-peptide (MDP) is a NOD2 ligand, which is able to promote Th2/Th17 responses. Furthermore, polymorphisms of the NOD2 receptor are associated with allergy and asthma development. This study aimed to evaluate if MDP given as an adjuvant during allergen sensitization may worsen the development of Th2/Th17 responses. We used a mouse model of Th2/Th17-type allergic neutrophil airway inflammation (AAI) to dog allergen, with in vitro polarization of human naive T cells by dendritic cells (DC) from healthy and dog-allergic asthma subjects. In the mouse model, intranasal co-administration of MDP did not modify the AAI parameters, including Th2/Th17-type lung inflammation. In humans, MDP co-stimulation of allergen-primed DC did not change the polarization profile of T cells in healthy subjects but elicited a Th2/Th17 profile in asthma subjects, as compared with MDP alone. These results support the idea that NOD2 may not be involved in the infection-related development of asthma and that, while care has to be taken in asthma patients, NOD2 adjuvants might be used in non-sensitized individuals.

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NOD1 mediated D. pteronyssinus-induced allergic airway inflammation through RIP2/NF-κB

Liu

Luo

et al. 2023

Immunobiology

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NOD1 sensing of house dust mite–derived microbiota promotes allergic experimental asthma

Cited by 11 publications

References 43 publications

NOD-like receptors in asthma

NOD-like receptors in asthma

NOD2 Signaling Circuitry during Allergen Sensitization Does Not Worsen Experimental Neutrophilic Asthma but Promotes a Th2/Th17 Profile in Asthma Patients but Not Healthy Subjects

NOD1 mediated D. pteronyssinus-induced allergic airway inflammation through RIP2/NF-κB

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