Insights into inflammasome regulation: cellular, molecular, and pathogenic control of inflammasome activation

Challagundla, Naveen; Saha, Bhaskar; Agrawal-Rajput, Reena

doi:10.1007/s12026-022-09286-9

Cited by 12 publications

(7 citation statements)

References 270 publications

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“…IL-1α and IL1β act through the IL-1 receptor. The biological activity of IL-1 is modulated by its natural soluble inhibitors: sIL-1R1, sIL-1RII and IL1-RA [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

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Role of Innate and Adaptive Cytokines in the Survival of COVID-19 Patients

Monserrat

Gómez-Lahoz

Ortega

et al. 2022

IJMS

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SARS-CoV-2 is a new coronavirus characterized by a high infection and transmission capacity. A significant number of patients develop inadequate immune responses that produce massive releases of cytokines that compromise their survival. Soluble factors are clinically and pathologically relevant in COVID-19 survival but remain only partially characterized. The objective of this work was to simultaneously study 62 circulating soluble factors, including innate and adaptive cytokines and their soluble receptors, chemokines and growth and wound-healing/repair factors, in severe COVID-19 patients who survived compared to those with fatal outcomes. Serum samples were obtained from 286 COVID-19 patients and 40 healthy controls. The 62 circulating soluble factors were quantified using a Luminex Milliplex assay. Results. The patients who survived had decreased levels of the following 30 soluble factors of the 62 studied compared to those with fatal outcomes, therefore, these decreases were observed for cytokines and receptors predominantly produced by the innate immune system—IL-1α, IL-1α, IL-18, IL-15, IL-12p40, IL-6, IL-27, IL-1Ra, IL-1RI, IL-1RII, TNFα, TGFα, IL-10, sRAGE, sTNF-RI and sTNF-RII—for the chemokines IL-8, IP-10, MCP-1, MCP-3, MIG and fractalkine; for the growth factors M-CSF and the soluble receptor sIL2Ra; for the cytokines involved in the adaptive immune system IFNγ, IL-17 and sIL-4R; and for the wound-repair factor FGF2. On the other hand, the patients who survived had elevated levels of the soluble factors TNFβ, sCD40L, MDC, RANTES, G-CSF, GM-CSF, EGF, PDGFAA and PDGFABBB compared to those who died. Conclusions. Increases in the circulating levels of the sCD40L cytokine; MDC and RANTES chemokines; the G-CSF and GM-CSF growth factors, EGF, PDGFAA and PDGFABBB; and tissue-repair factors are strongly associated with survival. By contrast, large increases in IL-15, IL-6, IL-18, IL-27 and IL-10; the sIL-1RI, sIL1RII and sTNF-RII receptors; the MCP3, IL-8, MIG and IP-10 chemokines; the M-CSF and sIL-2Ra growth factors; and the wound-healing factor FGF2 favor fatal outcomes of the disease.

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“…IL-1α and IL1β act through the IL-1 receptor. The biological activity of IL-1 is modulated by its natural soluble inhibitors: sIL-1R1, sIL-1RII and IL1-RA [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…The production of IL-1 through inflammasome activation is associated with that of IL-18 that favors IL-6, IL-8 and TNFα production [ 40 , 41 ]. IL-6 is considered pivotal for the onset of innate immune-inflammatory responses [ 16 , 17 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Innate and Adaptive Cytokines in the Survival of COVID-19 Patients

Monserrat

Gómez-Lahoz

Ortega

et al. 2022

IJMS

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“…The mechanisms underlying the activation of protein complexes and the expression of IL-1β neutrophils remain unclear. It is essential to understand the activation mechanism of inflammasomes and their role in various clinical entities, as they could be significant therapeutic targets with the potential to reduce inflammation in numerous diseases [ 112 ].…”

Section: Summary and Future Prospectsmentioning

confidence: 99%

Neutrophils in Health and Disease: From Receptor Sensing to Inflammasome Activation

Iwaniuk

Jabłońska

2023

IJMS

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Neutrophils—polymorphonuclear cells (PMNs) are the cells of the initial immune response and make up the majority of leukocytes in the peripheral blood. After activation, these cells modify their functional status to meet the needs at the site of action or according to the agent causing injury. They receive signals from their surroundings and “plan” the course of the response in both temporal and spatial contexts. PMNs dispose of intracellular signaling pathways that allow them to perform a wide range of functions associated with the development of inflammatory processes. In addition to these cells, some protein complexes, known as inflammasomes, also have a special role in the development and maintenance of inflammation. These complexes participate in the proteolytic activation of key pro-inflammatory cytokines, such as IL-1β and IL-18. In recent years, there has been significant progress in the understanding of the structure and molecular mechanisms behind the activation of inflammasomes and their participation in the pathogenesis of numerous diseases. The available reports focus primarily on macrophages and dendritic cells. According to the literature, the activation of inflammasomes in neutrophils and the associated death type—pyroptosis—is regulated in a different manner than in other cells. The present work is a review of the latest reports concerning the course of inflammasome activation and inflammatory cytokine secretion in response to pathogens in neutrophils, as well as the role of these mechanisms in the pathogenesis of selected diseases.

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“…Inflammasomes are protein complexes that play a central role in innate immunity (Man and Kanneganti, 2016;Gasteiger et al, 2017;Challagundla et al, 2022;Dong et al, 2022). Inflammasome signals have been reported to cause the activation of caspase-1 and increase the secretion of TNF-α and IL-1β, which are inflammatory cytokines in microglia and may be associated with depressive symptoms (Zhu et al, 2017;Slusarczyk et al, 2018;Li et al, 2021;Rao et al, 2021;.…”

Section: Inflammasomementioning

confidence: 99%

Involvement of inflammatory responses in the brain to the onset of major depressive disorder due to stress exposure

Miyata

Ishino

Shimizu

et al. 2022

Front. Aging Neurosci.

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Major depressive disorder (MDD) is a multifactorial disease affected by several environmental factors. Although several potential onset hypotheses have been identified, the molecular mechanisms underlying the pathogenesis of this disorder remain unclear. Several recent studies have suggested that among many environmental factors, inflammation and immune abnormalities in the brain or the peripheral tissues are associated with the onset of MDDs. Furthermore, several stress-related hypotheses have been proposed to explain the onset of MDDs. Thus, inflammation or immune abnormalities can be considered stress responses that occur within the brain or other tissues and are regarded as one of the mechanisms underlying the stress hypothesis of MDDs. Therefore, we introduce several current advances in inflammation studies in the brain that might be related to the pathophysiology of MDD due to stress exposure in this review.

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Insights into inflammasome regulation: cellular, molecular, and pathogenic control of inflammasome activation

Cited by 12 publications

References 270 publications

Role of Innate and Adaptive Cytokines in the Survival of COVID-19 Patients

Role of Innate and Adaptive Cytokines in the Survival of COVID-19 Patients

Neutrophils in Health and Disease: From Receptor Sensing to Inflammasome Activation

Involvement of inflammatory responses in the brain to the onset of major depressive disorder due to stress exposure

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