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Cited by 51Inflammasome and immune disordersCOVID-19 Clinical Research StudiesSARS-CoV-2 and COVID-19 Research

NLRP3 inflammasome activation in COVID-19: an interlink between risk factors and disease severity

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Amin, Saiful, Aktar, Salma, Rahman, Md. Mijanur, Chowdhury, Mohammed Mehadi Hassan·2022·Microbes and Infection
DOI 10.1016/j.micinf.2021.104913PMC PMC8613976
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Abstract

NLRP3 inflammasome is a critical immune component that plays a crucial role in mounting innate immune responses. The deleterious effects of inflammasome activation have been correlated with the COVID-19 disease severity. In the presence of several underlying disorders, the immune components of our bodies are dysregulated, creating conditions that could adversely affect us other than providing a required level of protection. In this review, we focused on the occurrence of NLRP3 inflammasome activation in response to SARS-COV-2 infection, dysregulation of NLRP3 activation events in the presence of several comorbidities, the contribution of activated NLRP3 inflammasome to the severity of COVID-19, and available therapeutics for the treatment of such NLRP3 inflammasome related diseases based on current knowledge. The primed state of immunity in individuals with comorbidities (risk factors) could accelerate many deaths and severe COVID-19 cases via activation of NLRP3 inflammasome and the release of downstream inflammatory molecules. Therefore, a detailed understanding of the host-pathogen interaction is needed to clarify the pathophysiology and select a potential therapeutic approach.

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  • SARS-CoV-2 infection strongly activates complement and other innate immune pathways such as TLR4 and the inflammasome, leading to increased IL-1β and IL-18 levels.

    “SARS-CoV-2 infection has been documented to strongly activate complement and to activate other innate immune pathways such as TLR4 and the inflammasome, which leads to increased IL-1 β and IL-18 levels. 137-142”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [141]

    The sections on complement cascade activation and inflammasome activation describe SARS-CoV-2-associated complement activity, NLRP3 activation, and elevated IL-1β and IL-18 in severe COVID-19. But section 2.1 identifies TLR7 and TLR8—not TLR4—as the receptors activated by viral RNA, so the specific TLR4 attribution is not supported by this paper. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Other key innate cytokines elevated during COVID-19 include TNFα and IL-6, which is increased by IL-1β.

    “Other key innate cytokines that are elevated during COVID-19 include TNF α and IL-6, which is increased by IL-1 β . 137-142”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [141]

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Cited by

Sorted by citations

Authors
Amin, S., Aktar, S., Rahman, M. M., & Chowdhury, M. M. H.
Affiliations
  • Chittagong Medical University (BD)
  • Noakhali Science and Technology University (BD)
Corresponding author
Aktar, Salma
ORCID
Venue
Microbes and Infection
Publisher
Elsevier BV
Published
2022-02
Volume
24
Issue
1
Pages
104913
ISSN
1286-4579 (ISSN-L)
DOI
10.1016/j.micinf.2021.104913
PMC
PMC8613976
OpenAlex
W3216239167
Cited by
51
References
11
Citations by year
2026: 6 · 2025: 9 · 2024: 6 · 2023: 17 · 2022: 13
FWCI
0.94
Type
journal article
Language
en
Open access
Licence
Locations
  • Microbes and Infection (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
  • Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
Keywords
NLRP3 inflammasome, COVID-19 pandemic, SARS-CoV-2, disease severity, comorbidities, risk factors, innate immunity, inflammatory cytokines, host-pathogen interaction
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, COVID-19, SARS-CoV-2, Humans, Risk Factors, Severity of Illness Index, Inflammasomes

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