Hyperactivation of the NLRP3 inflammasome protects mice against influenza A virus infection via IL-1β mediated neutrophil recruitment

Niu, Jianlou; Wu, Shuangyan; Chen, Mingkuan; Xu, Ke; Guo, Qiuhong; Lu, Ailing; Zhao, Liping; Sun, Bing; Meng, Guangxun

doi:10.1016/j.cyto.2019.04.019

Cited by 35 publications

(46 citation statements)

References 43 publications

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“…GSDMD forms pores in the membrane of infected cells, facilitating the secretion of IL-1β/IL-18 and inducing the inflammation-associated cell death known as pyroptosis (15). The secretion of IL-1β subsequently recruits neutrophils to the inflammatory site to aid in the elimination of invading viruses (16). Moreover, both IL-1β and IL-18 are responsible for the subsequent induction of the adaptive immune response (17,18).…”

Section: The Activation Of the Nlrp3 Inflammasomementioning

confidence: 99%

NLRP3 Inflammasome—A Key Player in Antiviral Responses

2020

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The NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome is an oligomeric complex comprised of the NOD-like receptor NLRP3, the adaptor ASC, and caspase-1. This complex is crucial to the host's defense against microbes as it promotes IL-1β and IL-18 secretion and induces pyroptosis. NLRP3 recognizes variety of pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) generated during viral replication that triggers the NLRP3 inflammasome-dependent antiviral immune responses and facilitates viral eradication. Meanwhile, several viruses have evolved elaborate strategies to evade the immune system by targeting the NLRP3 inflammasome. In this review, we will focus on the crosstalk between the NLRP3 inflammasome and viruses, provide an overview of viral infection-induced NLRP3 inflammasome activation, and the immune escape strategies of viruses through their modulation of the NLRP3 inflammasome activity.

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Section: The Activation Of the Nlrp3 Inflammasomementioning

confidence: 99%

NLRP3 Inflammasome—A Key Player in Antiviral Responses

2020

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“…The fine balance of neutrophilic inflammation in response to respiratory tract viral infections is exemplified by a variety of findings that may appear contradictory. For example, a recent study demonstrated that activation of the NOD-, LRR-and pyrin domain-containing protein 3 (NLRP3) inflammasome improves survival during influenza A virus (IAV) infection in mice by recruiting neutrophils via interleukin-1β [89]. However, neutrophils do not provide a universal protective effect during influenza infection.…”

Section: Viral Infectionsmentioning

confidence: 99%

Neutrophil Adaptations upon Recruitment to the Lung: New Concepts and Implications for Homeostasis and Disease

Giacalone

Margaroli

Mall

et al. 2020

IJMS

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Neutrophils have a prominent role in all human immune responses against any type of pathogen or stimulus. The lungs are a major neutrophil reservoir and neutrophilic inflammation is a primary response to both infectious and non-infectious challenges. While neutrophils are well known for their essential role in clearance of bacteria, they are also equipped with specific mechanisms to counter viruses and fungi. When these defense mechanisms become aberrantly activated in the absence of infection, this commonly results in debilitating chronic lung inflammation. Clearance of bacteria by phagocytosis is the hallmark role of neutrophils and has been studied extensively. New studies on neutrophil biology have revealed that this leukocyte subset is highly adaptable and fulfills diverse roles. Of special interest is how these adaptations can impact the outcome of an immune response in the lungs due to their potent capacity for clearing infection and causing damage to host tissue. The adaptability of neutrophils and their propensity to influence the outcome of immune responses implicates them as a much-needed target of future immunomodulatory therapies. This review highlights the recent advances elucidating the mechanisms of neutrophilic inflammation, with a focus on the lung environment due to the immense and growing public health burden of chronic lung diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD), and acute lung inflammatory diseases such as transfusion-related acute lung injury (TRALI).

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“…The activated caspase 1 proteolytically processes and activates pro-IL-1β, pro-IL-18, and the pyroptotic factor GSDMD [ 94 , 140 , 141 ]. Both IL-1β and IL-18 subsequently induce an adaptive immune response against pathogens whereas the activated GSDMD induces cell death by pyroptosis [ 142 , 143 , 144 ]. Of note, NEK7 is also shown to oligomerize specifically with activated NLRP3 into a complex which is essential for ASC speck formation and caspase 1 activation and thus appears to be an integral part of NLRP3 inflammasome [ 145 , 146 ].…”

Section: Nod- Lrr- and Pyrin Domain-containing Protein 3 (Nlrp3)mentioning

confidence: 99%

Innate Immune Sensing of Influenza A Virus

Malik

Zhou

2020

Viruses

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Influenza virus infection triggers host innate immune response by stimulating various pattern recognition receptors (PRRs). Activation of these PRRs leads to the activation of a plethora of signaling pathways, resulting in the production of interferon (IFN) and proinflammatory cytokines, followed by the expression of interferon-stimulated genes (ISGs), the recruitment of innate immune cells, or the activation of programmed cell death. All these antiviral approaches collectively restrict viral replication inside the host. However, influenza virus also engages in multiple mechanisms to subvert the innate immune responses. In this review, we discuss the role of PRRs such as Toll-like receptors (TLRs), Retinoic acid-inducible gene I (RIG-I), NOD-, LRR-, pyrin domain-containing protein 3 (NLRP3), and Z-DNA binding protein 1 (ZBP1) in sensing and restricting influenza viral infection. Further, we also discuss the mechanisms influenza virus utilizes, especially the role of viral non-structure proteins NS1, PB1-F2, and PA-X, to evade the host innate immune responses.

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Hyperactivation of the NLRP3 inflammasome protects mice against influenza A virus infection via IL-1β mediated neutrophil recruitment

Cited by 35 publications

References 43 publications

NLRP3 Inflammasome—A Key Player in Antiviral Responses

NLRP3 Inflammasome—A Key Player in Antiviral Responses

Neutrophil Adaptations upon Recruitment to the Lung: New Concepts and Implications for Homeostasis and Disease

Innate Immune Sensing of Influenza A Virus

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