The role of nucleotide-binding oligomerization domain 1 during cytokine production by macrophages in response to Mycobacterium tuberculosis infection

Lee, Jun Young; Hwang, Eun Ha; Kim, Dong Jae; Oh, Sang Muk; Lee, Kyung Bok; Shin, Sung Jae; Park, Jong Hwan

doi:10.1016/j.imbio.2015.07.020

Cited by 19 publications

(12 citation statements)

References 34 publications

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“…Both NOD1 and NOD2 signal through the adaptor protein RIPK2 to reach NF-κB and MAPK pathways. Few reports have been published on an important role for NOD1 during Mtb infection, one showing NOD1 plays a role in cytokine production only in the absence of NOD2 or after LPS-pretreatment of BMDMs ( 82 ). Mycobacteria do possess the iE-DAP moiety in their peptidoglycan ( 83 ).…”

Section: Prrs and Their Functions Against Mtb At The Cellular Levelmentioning

confidence: 99%

Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance to Mycobacterium tuberculosis

et al. 2021

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Human genetic control is thought to affect a considerable part of the outcome of infection with Mycobacterium tuberculosis (Mtb). Most of us deal with the pathogen by containment (associated with clinical “latency”) or sterilization, but tragically millions each year do not. After decades of studies on host genetic susceptibility to Mtb infection, genetic variation has been discovered to play a role in tuberculous immunoreactivity and tuberculosis (TB) disease. Genes encoding pattern recognition receptors (PRRs) enable a consistent, molecularly direct interaction between humans and Mtb which suggests the potential for co-evolution. In this review, we explore the roles ascribed to PRRs during Mtb infection and ask whether such a longstanding and intimate interface between our immune system and this pathogen plays a critical role in determining the outcome of Mtb infection. The scientific evidence to date suggests that PRR variation is clearly implicated in altered immunity to Mtb but has a more subtle role in limiting the pathogen and pathogenesis. In contrast to ‘effectors’ like IFN-γ, IL-12, Nitric Oxide and TNF that are critical for Mtb control, ‘sensors’ like PRRs are less critical for the outcome of Mtb infection. This is potentially due to redundancy of the numerous PRRs in the innate arsenal, such that Mtb rarely goes unnoticed. Genetic association studies investigating PRRs during Mtb infection should therefore be designed to investigate endophenotypes of infection – such as immunological or clinical variation – rather than just TB disease, if we hope to understand the molecular interface between innate immunity and Mtb.

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Section: Prrs and Their Functions Against Mtb At The Cellular Levelmentioning

confidence: 99%

Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance to Mycobacterium tuberculosis

et al. 2021

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“…The significance of this was demonstrated in vivo in which Nod1 ‐/‐ Nod2 ‐/‐ mice previously infected with E coli had decreased bacterial clearance and mouse survival after subsequent infection with Listeria monocytogenes , which contains both NOD1 and NOD2 ligands. Similarly, although activation of NF‐κB and MAPK and production of inflammatory cytokines in BMDMs to M tuberculosis were not dependent on NOD1, immune responses to M tuberculosis were partly mediated by NOD1 signaling after tolerization of TLRs by LPS pretreatment 136 . These results demonstrate the importance of NOD1 and NOD2 signaling in host defense especially in the setting of secondary bacterial infections when TLR responses are impaired as a result of tolerization 135 …”

Section: Role Of Nod1 and Nod2 In Host Defensementioning

confidence: 74%

NOD1 and NOD2 in inflammatory and infectious diseases

Trindade

Chen

2020

Immunological Reviews

106

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It has been long recognized that NOD1 and NOD2 are critical players in the host immune response, primarily by their sensing bacterial peptidoglycan‐conserved motifs. Significant advances have been made from efforts that characterize their upstream activators, assembly of signaling complexes, and activation of downstream signaling pathways. Disruption in NOD1 and NOD2 signaling has also been associated with impaired host defense and resistance to the development of inflammatory diseases. In this review, we will describe how NOD1 and NOD2 sense microbes and cellular stress to regulate host responses that can affect disease pathogenesis and outcomes.

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“…Члены семейства NOD-подобного рецептора (NLR) играют важную роль во врожденном иммунитете, индуцируя воспалительный ответ и регулируя пути гибели/выживания клеток. Они относятся к внутриклеточным рецепторам и представляют собой вторую линию распознавания патогенов M. tuberculosis, индуцируя провоспалительный ответ в макрофагах [23,56]. NLR в основном экспрессируются на антигенпрезентирующих клетках: дендритных клетках, макрофагах, а также на эпителиальных клетках.…”

Section: Nod-рецепторыunclassified

Innate immune receptors in development of Mycobacterium tuberculosis infection

Лапштаева

Живечкова

Сычев

et al. 2020

Russian Journal of Infection and Immunity

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According to the World Health Organization, over 10 million new tuberculosis cases are reported annually worldwide. According to the 2017 Federal State Statistics Service Report, incidence rate for active TB infection in the Russian Federation was 109.8 cases per 100,000 population, of which 41.3% accounted for chronic disease form. Regardless of climatic conditions, high prevalence of TB infection, is not only due to high Mycobacterium tuberculosis viability, but also its ability for long persistence in human body and reactivation after an unlimited period of dormancy. The outcome of infection is largely determined by host immunoreactivity and its ability to develop protective immune response. In addition, status of immune system also underlies tuberculosis course after the onset: either as a localized form, or as a form with extensive damage to the lungs and even other organs observed in generalized infection. In recent decades, a great attention was paid to examining mechanisms of adaptive cell immunity played in pathogenesis of TB infection. No doubt, adaptive immunity is a powerful defense system providing a targeted specific immune response, but now it is becoming clear that it represents solely an effector arm of innate immunity. Innate immunity is a phylogenetically more ancient, inherited system largely aimed at ensuring rapid pathogen elimination and preventing development of infection at early stages when adaptive immunity ongoing antigen-specific maturation. Mechanisms of innate immunity mediated by cells, diverse receptors, molecules and their complexes, found on various cells. Activation of innate immunity begins with recognition of conserved molecular groups present in various pathogens called pathogen-associated molecular patterns (PAMPs), which are sensed by pathogen recognition receptors (PRRs). Here, we review current data on the role of innate receptors in recognizing M. tuberculosis-derived PAMPs, production of immunoregulatory cytokines and activation of signaling pathways playing a crucial role in the regulation of necroptosis, apoptosis and autophagy of infected macrophages. Significance of innate mucosal factors in implementing immune response to M. tuberculosis is discussed. In particular, Toll-like receptors, scavenger-receptors, mannose receptor, DC-SIGN etc. were described to participate in development of M. tuberculosis immunity. The data on single nucleotide polymorphic variants for innate genes are shown, which predispose to developing tuberculosis and affecting its course.

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The role of nucleotide-binding oligomerization domain 1 during cytokine production by macrophages in response to Mycobacterium tuberculosis infection

Cited by 19 publications

References 34 publications

Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance to Mycobacterium tuberculosis

Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance to Mycobacterium tuberculosis

NOD1 and NOD2 in inflammatory and infectious diseases

Innate immune receptors in development of Mycobacterium tuberculosis infection

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