The crosstalk between TLR2 and NOD2 in Aspergillus fumigatus keratitis

Wu, Jiayin; Zhang, Yuting; Xin, Zhaoting; Wu, Xinyi

doi:10.1016/j.molimm.2014.11.021

Cited by 36 publications

(23 citation statements)

References 32 publications

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“…Further, there exists a cooperative regulation of NOD2-and TLR2-specific ligands for mediating immune cytokines (8,36,37). NOD2-TLR2 synergy was also found in different cellular contexts (38,39). Thus, the present study underscores the fact that though multiple PAMPs recognize a single PRR, there exist regulatory mechanisms to orchestrate the ligand-specific immune responses.…”

Section: Discussionsupporting

confidence: 62%

Ac2PIM-responsive miR-150 and miR-143 Target Receptor-interacting Protein Kinase 2 and Transforming Growth Factor Beta-activated Kinase 1 to Suppress NOD2-induced Immunomodulators

Prakhar¹,

Holla²,

Ghorpade³

et al. 2015

Journal of Biological Chemistry

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Background: Ac 2 PIM signals via TLR2 to direct both pro-and anti-inflammatory responses. Results: Ac 2 PIM induces miR-150/143 via SRC-FAK-PYK2-CREB-P300 signaling to target RIP2 and TAK1 and subdues MDPstimulated PI3K-PKC-MAPK-␤-catenin axis. Conclusion: Ac 2 PIM-mediated TLR2 signaling suppresses the NOD2-induced immunomodulators viz. COX-2, SOCS-3, and MMP-9. Significance: TLR2-NOD2 crosstalk accentuated the utilities of Ac 2 PIM and MDP as vaccine adjuvant.

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Section: Discussionsupporting

confidence: 62%

Ac2PIM-responsive miR-150 and miR-143 Target Receptor-interacting Protein Kinase 2 and Transforming Growth Factor Beta-activated Kinase 1 to Suppress NOD2-induced Immunomodulators

Prakhar¹,

Holla²,

Ghorpade³

et al. 2015

Journal of Biological Chemistry

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“…Likewise, we have also shown that mice devoid of type I IFN receptors (ie, thus devoid of downstream signaling from IFNs resulting from TLR2 activation) are similarly protected by L. plantarum . Among several interpretations, it is conceivable that there may be substantial cross-talk between TLR2 and NOD2 pathways in this setting (Wu et al, 2015; Zeuthen et al, 2008; Borm et al, 2008; Netea et al, 2005; Pavot et al, 2014; Watanabe et al, 2006), a possibility that requires further consideration.…”

Section: Discussionmentioning

confidence: 99%

Immunobiotic Lactobacillus administered post-exposure averts the lethal sequelae of respiratory virus infection

Percopo¹,

Rice²,

Brenner³

et al. 2015

Antiviral Research

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We reported previously that priming of the respiratory tract with immunobiotic Lactobacillus prior to virus challenge protects mice against subsequent lethal infection with pneumonia virus of mice (PVM). We present here the results of gene microarray which document differential expression of proinflammatory mediators in response to PVM infection alone and those suppressed in response to Lactobacillus plantarum. We also demonstrate for the first time that intranasal inoculation with live or heat-inactivated L. plantarum or Lactobacillus reuteri promotes full survival from PVM infection when administered within 24 h after virus challenge. Survival in response to L. plantarum administered after virus challenge is associated with suppression of proinflammatory cytokines, limited virus recovery, and diminished neutrophil recruitment to lung tissue and airways. Utilizing this post-virus challenge protocol, we found that protective responses elicited by L. plantarum at the respiratory tract were distinct from those at the gastrointestinal mucosa, as mice devoid of the anti-inflammatory cytokine, interleukin (IL)-10, exhibit survival and inflammatory responses that are indistinguishable from those of their wild-type counterparts. Finally, although L. plantarum interacts specifically with pattern recognition receptors TLR2 and NOD2, the respective gene-deleted mice were fully protected against lethal PVM infection by L. plantarum, as are mice devoid of type I interferon receptors. Taken together, L. plantarum is a versatile and flexible agent that is capable of averting the lethal sequelae of severe respiratory infection both prior to and post-virus challenge via complex and potentially redundant mechanisms.

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“…The PRRs TLR2 and NOD2 have been reported to cross-talk and play a role in immune regulation as well as to influence the expression of one another [49]. TNF-α production has been shown to be enhanced upon simultaneous activation of NOD2 and TLR2, which could in part explain the increased TNF-α production by moDCs observed for ACV-strains compared to Introd-Vac strains [50].…”

Section: Discussionmentioning

confidence: 99%

Emerging Bordetella pertussis Strains Induce Enhanced Signaling of Human Pattern Recognition Receptors TLR2, NOD2 and Secretion of IL-10 by Dendritic Cells

et al. 2017

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Vaccines against pertussis have been available for more than 60 years. Nonetheless, this highly contagious disease is reemerging even in countries with high vaccination coverage. Genetic changes of Bordetella pertussis over time have been suggested to contribute to the resurgence of pertussis, as these changes may favor escape from vaccine-induced immunity. Nonetheless, studies on the effects of these bacterial changes on the immune response are limited. Here, we characterize innate immune recognition and activation by a collection of genetically diverse B. pertussis strains isolated from Dutch pertussis patients before and after the introduction of the pertussis vaccines. For this purpose, we used HEK-Blue cells transfected with human pattern recognition receptors TLR2, TLR4, NOD2 and NOD1 as a high throughput system for screening innate immune recognition of more than 90 bacterial strains. Physiologically relevant human monocyte derived dendritic cells (moDC), purified from peripheral blood of healthy donors were also used. Findings indicate that, in addition to inducing TLR2 and TLR4 signaling, all B. pertussis strains activate the NOD-like receptor NOD2 but not NOD1. Furthermore, we observed a significant increase in TLR2 and NOD2, but not TLR4, activation by strains circulating after the introduction of pertussis vaccines. When using moDC, we observed that the recently circulating strains induced increased activation of these cells with a dominant IL-10 production. In addition, we observed an increased expression of surface markers including the regulatory molecule PD-L1. Expression of PD-L1 was decreased upon blocking TLR2. These in vitro findings suggest that emerging B. pertussis strains have evolved to dampen the vaccine-induced inflammatory response, which would benefit survival and transmission of this pathogen. Understanding how this disease has resurged in a highly vaccinated population is crucial for the design of improved vaccines against pertussis.

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The crosstalk between TLR2 and NOD2 in Aspergillus fumigatus keratitis

Cited by 36 publications

References 32 publications

Ac2PIM-responsive miR-150 and miR-143 Target Receptor-interacting Protein Kinase 2 and Transforming Growth Factor Beta-activated Kinase 1 to Suppress NOD2-induced Immunomodulators

Ac2PIM-responsive miR-150 and miR-143 Target Receptor-interacting Protein Kinase 2 and Transforming Growth Factor Beta-activated Kinase 1 to Suppress NOD2-induced Immunomodulators

Immunobiotic Lactobacillus administered post-exposure averts the lethal sequelae of respiratory virus infection

Emerging Bordetella pertussis Strains Induce Enhanced Signaling of Human Pattern Recognition Receptors TLR2, NOD2 and Secretion of IL-10 by Dendritic Cells

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