Gene Variants, mRNA and NOD1/2 Protein Levels in Tunisian Childhood Asthma

Belhaj, R; Kaabachi, Wajih; Khalfallah, I.; Hamdi, B.; Hamzaoui, Kamel; Hamzaoui, A.

doi:10.1007/s00408-019-00209-4

Cited by 5 publications

(3 citation statements)

References 47 publications

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“… 25 In addition, the rs2075820 variant in NOD1 was closely associated with high risk of childhood asthma, and both the mRNA and protein levels of NOD1 were significantly increased in asthma patients. 26 The above studies demonstrated the potential correlation between NOD1 and COPD progression. However, little is known about the role of NOD1 in COPD, or whether it is involved in the occurrence and development of the disease.…”

Section: Introductionmentioning

confidence: 78%

Nucleotide-Oligomerizing Domain-1 Activation Exaggerates Cigarette Smoke-Induced Chronic Obstructive Pulmonary-Like Disease in Mice

Han¹,

Li²,

Du³

et al. 2021

COPD

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Introduction: Chronic obstructive pulmonary disease (COPD) is a progressive condition related to abnormal inflammatory responses. As an inflammatory driver, nucleotide-binding oligomerizing domain-1 (NOD1) is highly expressed in pulmonary inflammatory cells; however, the roles of NOD1 in COPD are unknown. Methods: A COPD mouse model was established by lipopolysaccharides tracheal instillation plus cigarette smoke (CS) exposure. NOD1 activation was induced by C12-iE-DAP (iE) treatment in both control and COPD mice. Inflammatory infiltration, pulmonary histological damage and gene expression were measured to evaluate the lung function of treated mice. Results: The results showed that NOD1 was up-regulated in COPD mice, which significantly exaggerated CS-induced impairment of lung function, demonstrated by increased airway resistance, functional residual capacity and pulmonary damages. Mechanistically, NOD1 activation strongly activated the TLR4/NF-κB signaling pathway and then increased inflammatory responses and promoted the secretion of inflammatory cytokines. Discussion: This study demonstrates that NOD1 is an important risk factor in the progression of COPD; therefore, targeting NOD1 in lung tissues is a potential strategy for COPD treatment.

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Section: Introductionmentioning

confidence: 78%

Nucleotide-Oligomerizing Domain-1 Activation Exaggerates Cigarette Smoke-Induced Chronic Obstructive Pulmonary-Like Disease in Mice

Han¹,

Li²,

Du³

et al. 2021

COPD

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“…More recently, Belhaj et al. found an association between the NOD1 rs2075820 variant and childhood asthma in a Tunisian cohort ( 104 ). Most likely, these polymorphisms may affect bacterial sensing and hence modify the downstream signaling pathways that normally would be triggered by NOD1 ( 45 ).…”

Section: Nlrs In Asthmamentioning

confidence: 99%

“…Following these studies, other authors have explored the role of NOD2 polymorphisms in asthma predisposition in different cohorts reporting conflicting results. While some have failed to show any significant association between NOD2 genetic polymorphisms and asthma ( 104 ), more recent studies have provided data backing up the existence of a link between NOD2 polymorphisms and asthma. For example, Cai et al.…”

Section: Nlrs In Asthmamentioning

confidence: 99%

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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