Blockade of CD38 diminishes lipopolysaccharide-induced macrophage classical activation and acute kidney injury involving NF-κB signaling suppression

Shu, Bingyan; Feng, Yan; Gui, Yuan; Lu, Qingmiao; Wei, Wei; Xue, Xiang; Sun, Xiaoli; He, Weichun; Yang, Junwei; Dai, Chunsun

doi:10.1016/j.cellsig.2017.10.014

Cited by 67 publications

(58 citation statements)

References 51 publications

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“…Quercetin reduced the infiltration of neutrophils and macrophages in the liver. In line with the role of CD38 in maintenance of a pro-inflammatory phenotype, macrophages that had recovered from quercetin-treated mice had lower levels of NF-kB signaling and inflammatory markers as compared to macrophages from vehicle-treated mice [36]. Flavonoids, however, may also use protective mechanisms that are independent of CD38 inhibition, as the contributing role of CD38 in tissue damage was not confirmed in CD38-deficient mice [76].…”

Section: Cd38 In Sepsismentioning

confidence: 88%

“…Furthermore, the lack of functional CD38 expression or the selective interference with its receptor or enzymatic activities in myeloid cells resulted in reduced production of pro-inflammatory mediators in response to LPS [35,36] or to bacterial [27] or viral infection [37]. In macrophages, these effects correlated with inhibition of the activation of the NFκB signaling pathway [36].…”

Section: Cd38 Contributes To Pro-inflammatory Phenotypes In Innate Immentioning

confidence: 99%

“…In some cases, the host response to an invading pathogen leads to the development of sepsis, a pathological syndrome with a hyperreactive phase in which exacerbated inflammation causes organ dysfunction followed by immunosuppression [73]. A role for CD38 in LPS-induced acute kidney injury [36] was suggested using quercetin, a dietary flavonoid that inhibits the NADase activity of CD38 [74,75]. Quercetin reduced the infiltration of neutrophils and macrophages in the liver.…”

Section: Cd38 In Sepsismentioning

confidence: 99%

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Roles of CD38 in the Immune Response to Infection

Glaría

Valledor

2020

Cells

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CD38 is a multifunctional protein widely expressed in cells from the immune system and as a soluble form in biological fluids. CD38 expression is up-regulated by an array of inflammatory mediators, and it is frequently used as a cell activation marker. Studies in animal models indicate that CD38 functional expression confers protection against infection by several bacterial and parasitic pathogens. In addition, infectious complications are associated with anti-CD38 immunotherapy. Although CD38 displays receptor and enzymatic activities that contribute to the establishment of an effective immune response, recent work raises the possibility that CD38 might also enhance the immunosuppressive potential of regulatory leukocytes. This review integrates the current knowledge on the diversity of functions mediated by CD38 in the host defense to infection.

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Section: Cd38 In Sepsismentioning

confidence: 88%

Section: Cd38 Contributes To Pro-inflammatory Phenotypes In Innate Immentioning

confidence: 99%

Section: Cd38 In Sepsismentioning

confidence: 99%

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Roles of CD38 in the Immune Response to Infection

Glaría

Valledor

2020

Cells

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“…Okamoto's group has also described a mutation in exon 4 of CD38 in some subjects with type II diabetes mellitus [ 33 ]. CD38 is implicated in the oxytocin signaling pathway, and single nucleotide polymorphisms in this gene have been associated with low serum oxytocin levels in autism spectrum disorder (ASD) patients [ 19 , 34 , 35 ]. Disruption of oxytocin signaling has been associated with features of ASD, including impaired communication and social behavior, based on animal studies.…”

Section: Cd38 Gene Organization Polymorphisms and Human Diseasesmentioning

confidence: 99%

“…These findings implicate CD38 in the pathophysiology of asthma. CD38 has been implicated in other human pathologies including in neuroinflammatory diseases, renal dysfunctions, neoplastic disorders, and viral infections (respiratory syncytial virus) [ 19 – 22 ].…”

Section: Introductionmentioning

confidence: 99%

CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms

Deshpande

Guedes

Graeff

et al. 2018

Mediators of Inflammation

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Asthma is an inflammatory disease in which proinflammatory cytokines have a role in inducing abnormalities of airway smooth muscle function and in the development of airway hyperresponsiveness. Inflammatory cytokines alter calcium (Ca2+) signaling and contractility of airway smooth muscle, which results in nonspecific airway hyperresponsiveness to agonists. In this context, Ca2+ regulatory mechanisms in airway smooth muscle and changes in these regulatory mechanisms encompass a major component of airway hyperresponsiveness. Although dynamic Ca2+ regulation is complex, phospholipase C/inositol tris-phosphate (PLC/IP3) and CD38-cyclic ADP-ribose (CD38/cADPR) are two major pathways mediating agonist-induced Ca2+ regulation in airway smooth muscle. Altered CD38 expression or enhanced cyclic ADP-ribosyl cyclase activity associated with CD38 contributes to human pathologies such as asthma, neoplasia, and neuroimmune diseases. This review is focused on investigations on the role of CD38-cyclic ADP-ribose signaling in airway smooth muscle in the context of transcriptional and posttranscriptional regulation of CD38 expression. The specific roles of transcription factors NF-kB and AP-1 in the transcriptional regulation of CD38 expression and of miRNAs miR-140-3p and miR-708 in the posttranscriptional regulation and the underlying mechanisms of such regulation are discussed.

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Ultrasmall Nanoparticles Regulate Immune Microenvironment by Activating IL‐33/ST2 to Alleviate Renal Ischemia‐Reperfusion Injury

Xu,

Xing,

Yuan

et al. 2024

Adv Healthcare Materials

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Renal ischemia‐reperfusion injury (IRI) is a common disease with high morbidity and mortality. Renal IRI can cause the disorder of immune microenvironment and reprograming the immune microenvironment to alleviate excessive inflammatory response is crucial for its treatment. Cytokine IL‐33 can improve the immune inflammatory microenvironment by modulating both innate and adaptive immune cells, and serve as an important target for modulating immune microenvironment of renal IRI. Herein, we report that bilobetin‐functionalized ultra‐small Cu2‐xSe nanoparticles (i.e., CSPB NPs) can activate the PKA/p‐CREB/IL‐33/ST2 signaling pathway to regulate innate and adaptive immune cells for reprograming the immune microenvironment of IRI‐induced acute kidney injury (AKI). The biocompatible CSPB NPs can promote the polarization of M1‐like macrophages into M2‐like macrophages, and the expansion of ILC2 and Treg cells by activating IL‐33/ST2 to modulate the excessive immune inflammatory response of renal IRI. More importantly, they can rapidly accumulate at the injured kidney to significantly alleviate IRI. This work demonstrates that modulating the expression of cytokines to reprogram immune microenvironment has great potential in the treatment of renal IRI and other ischemic diseases.This article is protected by copyright. All rights reserved

show abstract

Blockade of CD38 diminishes lipopolysaccharide-induced macrophage classical activation and acute kidney injury involving NF-κB signaling suppression

Cited by 67 publications

References 51 publications

Roles of CD38 in the Immune Response to Infection

Roles of CD38 in the Immune Response to Infection

CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms

Ultrasmall Nanoparticles Regulate Immune Microenvironment by Activating IL‐33/ST2 to Alleviate Renal Ischemia‐Reperfusion Injury

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