Macrophage Meets the Circadian Clock: Implication of the Circadian Clock in the Role of Macrophages in Acute Lower Respiratory Tract Infection

Shirato, Ken; Sato, Shogo

doi:10.3389/fcimb.2022.826738

Cited by 14 publications

(17 citation statements)

References 162 publications

(212 reference statements)

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“…The infiltrating macrophages are plastic cells, which differentiated from the monocytes into two subtypes of polarized macrophages in response to microenvironmental change, including classical macrophages (M1) and alternative macrophages (M2) (Gayer et al, 2022; Shirato & Sato, 2022). Usually, the monocytes are Toll‐like receptor (TLR) responsive to differentiate into inflammatory macrophages during inflammation, whereas intestinal resident macrophages are unresponsive to TLR and so presented with anti‐inflammatory feature (Kim et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

NF‐κB inactivation attenuates the M1 macrophage polarization in experimental necrotizing enterocolitis by glutaredoxin‐1 deficiency

Luo

Guo

et al. 2022

Cell Biology International

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The pathogenesis of necrotizing enterocolitis (NEC) is severe inflammatory injury in preterm infants, which resulted from macrophage polarization. Nuclear factor‐κB (NF‐κB) is implicated to be involved in macrophage polarization. We here evaluated the essential role of NF‐κB in macrophage polarization in NEC in human samples from neonates with NEC and the mouse experimental NEC model. Enhanced intestinal macrophage (IM) infiltration was presented in human neonates with NEC, the majority of which were M1 macrophages. Meanwhile, NF‐κB was activated in the IMs in human NEC samples. NF‐κB inhibition by BAY promoted the M1 to M2 macrophage polarization. Furthermore, glutaredoxin‐1 (Grx1) deficiency promoted M2 polarization via NF‐κB inactivation from the lipopolysaccharide‐induced proinflammatory macrophages. The IMs isolated from Grx1−/− mice presented with decreases in total numbers and less macrophage differentiation. Grx1−/− derived IM were effective in the increased survival in experimental NEC through inflammation blocking. Our study provides evidence that NF‐κB inactivation by Grx1 depletion contributed to the alleviation of NEC via inhibiting M1 macrophage polarization. The modulation to alternative macrophages in the intestines may provide a promising benefits for NEC treatment.

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Section: Introductionmentioning

confidence: 99%

NF‐κB inactivation attenuates the M1 macrophage polarization in experimental necrotizing enterocolitis by glutaredoxin‐1 deficiency

Luo

Guo

et al. 2022

Cell Biology International

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“…Li et al, 2017). We emphasize the importance of research in Mφ because they are implicated in diseases associated with spaceflight, such as atherosclerosis-where plaque-associated Mφ overexpress MRTF-A (An et al, 2019)-as well as circadian clock disruption (Shirato and Sato, 2022)-where Mφ circadian clock components that regulate the timing of phagocytosis and motility are promoted by MRTF-A (Kitchen et al, 2020;Xiong et al, 2021).…”

Section: Mrtf-a Transduces Mφ Pro-inflammatory Signalsmentioning

confidence: 99%

MRTF May Be the Missing Link in a Multiscale Mechanobiology Approach toward Macrophage Dysfunction in Space

2022

Preprint

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Macrophages exhibit impaired phagocytosis, adhesion, migration, and cytokine production in space, hindering their ability to elicit immune responses. Considering that the combined effect of spaceflight microgravity and radiation is multiscale and multifactorial in nature, it is expected that contradictory findings are common in the field. This theory paper reanalyzes research on the macrophage spaceflight response across multiple timescales from seconds to weeks, and spatial scales from the molecular, intracellular, extracellular, to the physiological. Key findings include time-dependence of both pro-inflammatory activation and integrin expression. Here, we introduce the time-dependent, intracellular localization of MRTF-A as a hypothetical confounder of macrophage activation. We discuss the mechanosensitive MRTF-A/SRF pathway dependence on the actin cytoskeleton/nucleoskeleton, microtubules, membrane mechanoreceptors, hypoxia, oxidative stress, and intracellular/extracellular crosstalk. By adopting a multiscale perspective, this paper provides the first mechanistic answer for a three-decade-old question regarding impaired cytokine secretion in microgravity—and strengthens the connection between the recent advances in mechanobiology, microgravity, and the spaceflight immune response. Finally, we hypothesize MRTF involvement and complications in treating spaceflight-induced cardiovascular, skeletal, and immune disease.

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“…Specifically, RORα and REV‐REBα play opposing roles and finely regulate the transcription of Bmal1 and E4bp4 , by binding to ROR responsive elements that are located in the promoters of these genes 20 . REV‐ERBs repress the transcription of Bmal1 , while RORs activate their transcription 21 . RORs activate the expression of E4bp4 , whereas REV‐REBs inhibit its transcription 22 .…”

Section: Introductionmentioning

confidence: 99%

The role of circadian clock in regulating cell functions: implications for diseases

Lin,

He,

Cai

et al. 2024

MedComm

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The circadian clock system orchestrates daily behavioral and physiological rhythms, facilitating adaptation to environmental and internal oscillations. Disruptions in circadian rhythms have been linked to increased susceptibility to various diseases and can exacerbate existing conditions. This review delves into the intricate regulation of diurnal gene expression and cell function by circadian clocks across diverse tissues. . Specifically, we explore the rhythmicity of gene expressions, behaviors, and functions in both immune and non‐immune cells, elucidating the regulatory effects and mechanisms imposed by circadian clocks. A detailed discussion is centered on elucidating the complex functions of circadian clocks in regulating key cellular signaling pathways. We further review the circadian regulation in diverse diseases, with a focus on inflammatory diseases, cancers, and systemic diseases. By highlighting the intimate interplay between circadian clocks and diseases, especially through clock‐controlled cell function, this review contributes to the development of novel disease intervention strategies. This enhanced understanding holds significant promise for the design of targeted therapies that can exploit the circadian regulation mechanisms for improved treatment efficacy.

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Macrophage Meets the Circadian Clock: Implication of the Circadian Clock in the Role of Macrophages in Acute Lower Respiratory Tract Infection

Cited by 14 publications

References 162 publications

NF‐κB inactivation attenuates the M1 macrophage polarization in experimental necrotizing enterocolitis by glutaredoxin‐1 deficiency

NF‐κB inactivation attenuates the M1 macrophage polarization in experimental necrotizing enterocolitis by glutaredoxin‐1 deficiency

MRTF May Be the Missing Link in a Multiscale Mechanobiology Approach toward Macrophage Dysfunction in Space

The role of circadian clock in regulating cell functions: implications for diseases

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