Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury

Uchida, Takahiro; Itô, Seigo; Kumagai, Hiroo; Oda, Takashi; Nakashima, Hiroyuki; Seki, Shu

doi:10.3390/ijms20102487

Cited by 22 publications

(24 citation statements)

References 75 publications

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“…Studies have shown that sepsis induced AKI is accompanied by destruction of the immune system [23], and unconscionable apoptosis of immune cells can exacerbate sepsis and increase the mortality rate of patients. A grave inflammatory response induced by LPS stimulates neutrophils to emancipate numerous of pro-inflammatory cytokines, which have been reported to play pivotal roles in the pathogenesis of AKI [24].…”

Section: Discussionmentioning

confidence: 99%

Protopine Protects Mice against LPS-Induced Acute Kidney Injury by Inhibiting Apoptosis and Inflammation via the TLR4 Signaling Pathway

Zhang

Zeng

et al. 2019

Molecules

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Corydalis humosa Migo is a traditional Chinese medicine that clears away damp heat, relieves sore. Protopine (PRO) is an alkaloid component isolated from C. humosa Migo. However, the role of protopine in acute kidney injury (AKI) has not yet been reported. This study aims to investigate the effect and mechanism of protopine isolated from C. humosa Migo on lipopolysaccharide (LPS)-induced AKI in mice. Inflammation accumulation was assessed by small animal living imaging. The blood urea nitrogen (BUN), and serum creatinine (Scr) were measured to assess the effects of protopine on renal function in LPS-induced AKI. The levels of tumor necrosis factor (TNF), interleukin-2 (IL-2), interferon-γ (IFN-γ), and (interleukin-10) IL-10 in serum were detected by cytometric bead array. Flow cytometry was used to detect the levels of reactive oxygen species (ROS) in primary kidney cells. The proportions of granulocytes, neutrophils, and macrophages in peripheral blood were examined to evaluate the effect of protopine on immune cells in mice with AKI. Toll-like receptor (TLR4) and apoptotic signaling pathway were detected by Western blot analysis. The results showed that protopine markedly improved the renal function, relieve inflammation, reversed inflammatory cytokines, transformed apoptosis markers, and regulated the TLR4 signaling pathway in mice with AKI induced by LPS. The protopine isolated from C. humosa Migo protected mice against LPS-induced AKI by inhibiting apoptosis and inflammation via the TLR4 signaling pathway, thus providing a molecular basis for a novel medical treatment of AKI.

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Section: Discussionmentioning

confidence: 99%

Protopine Protects Mice against LPS-Induced Acute Kidney Injury by Inhibiting Apoptosis and Inflammation via the TLR4 Signaling Pathway

Zhang

Zeng

et al. 2019

Molecules

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“…Meanwhile, CD4+ T cells and CD4+ T cells secreting interferon-gamma (IFN-γ) positive lymphocytes could participate in immune response of HIV infection and mycoplasmal infection [ 5 – 7 ]. Similarly, the accumulation of multifarious immune cells including NKT cells, CD4+ T cells, B cells and IFN-γ-producing neutrophils are closely associated with the pathogenesis of AKI [ 8 – 10 ]. Lipopolysaccharide (LPS)-induced sepsis is a primary cause of AKI in critically ill patients [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of circ-FANCA alleviates LPS-induced HK2 cell injury via targeting miR-93-5p/OXSR1 axis in septic acute kidney injury

Li¹,

Zhang

Wang

et al. 2021

Diabetol Metab Syndr

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Background Sepsis is life-threatening disease with systemic inflammation and can lead to various diseases, including septic acute kidney injury (AKI). Recently, diverse circular RNAs (circRNAs) are considered to be involved in the development of this disease. In this study, we aimed to elucidate the role of circ-FANCA and the potential action mechanism in sepsis-induced AKI. Methods HK2 cells were treated with lipopolysaccharide (LPS) to establish septic AKI cell model. The expression of circ-FANCA, microRNA-93-5p (miR-93-5p) and oxidative stress responsive 1 (OXSR1) mRNA was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was assessed using cell counting kit-8 (CCK-8) assay. Cell apoptosis and cell cycle distribution were measured by flow cytometry. The inflammatory response was monitored according to the release of pro-inflammatory cytokines via enzyme-linked immunosorbent assay (ELISA). The activities of oxidative indicators were examined using the corresponding kits. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to validate the interaction between miR-93-5p and circ-FANCA or OXSR1. Protein analysis was conducted through western blot. Results Circ-FANCA was upregulated in septic AKI serum specimens and LPS-treated HK2 cells. Functionally, circ-FANCA knockdown facilitated cell proliferation and restrained apoptosis, inflammation and oxidative stress in LPS-triggered HK2 cells. Further mechanism analysis revealed that miR-93-5p was a target of circ-FANCA and circ-FANCA modulated LPS-induced cell damage by targeting miR-93-5p. Meanwhile, miR-93-5p overexpression repressed LPS-treated HK2 cell injury by sponging OXSR1. Furthermore, circ-FANCA regulated OXSR1 expression by sponging miR-93-5p. Besides, exosome-derived circ-FANCA was upregulated in LPS-induced HK2 cells, which was downregulated by GW4869. Conclusion Circ-FANCA knockdown attenuated LPS-induced HK2 cell injury by regulating OXSR1 expression via targeting miR-93-5p.

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“…Limited NK cell research exists in other major organs such as kidneys, heart, and others [ 70 , 71 ], but they show that NK cells play substantial roles in both immune protection and/or tissue injury in the inflammatory pathogenesis of renal and cardiovascular diseases. While the peripheral immune responses and parameters are useful in generating disease outcome predictors for COVID-19, knowledge of immune cell responses at the local and mucosal tissue microenvironment are even more critical for viral control and limiting severity of disease.…”

Section: Nk Cells At Sites Of Sars-cov-2 Infectionmentioning

confidence: 99%

Friends or foes? The knowns and unknowns of natural killer cell biology in COVID-19 and other coronaviruses in July 2020

2020

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The COVID-19 pandemic has caused more than 575,000 deaths worldwide as of mid-July 2020 and still continues globally unabated. Immune dysfunction and cytokine storm complicate the disease, which in turn leads to the question of whether stimulation or suppression of the immune system would curb the disease. Given the varied antiviral and regulatory functions of natural killer (NK) cells, they could be potent and powerful immune allies in this global fight against COVID-19. Unfortunately, there is somewhat limited knowledge of the role of NK cells in SARS-CoV-2 infections and even in the related SARS-CoV-1 and MERS-CoV infections. Several NK cell therapeutic options already exist in the treatment of tumor and other viral diseases and could be repurposed against COVID-19. In this review, we describe the current understanding and potential roles of NK cells and other Fc receptor (FcR) effector cells in SARS-CoV-2 infection, advantages of using animals to model COVID-19, and NK cell–based therapeutics that are being investigated for COVID-19 therapy.

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Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury

Cited by 22 publications

References 75 publications

Protopine Protects Mice against LPS-Induced Acute Kidney Injury by Inhibiting Apoptosis and Inflammation via the TLR4 Signaling Pathway

Protopine Protects Mice against LPS-Induced Acute Kidney Injury by Inhibiting Apoptosis and Inflammation via the TLR4 Signaling Pathway

Knockdown of circ-FANCA alleviates LPS-induced HK2 cell injury via targeting miR-93-5p/OXSR1 axis in septic acute kidney injury

Friends or foes? The knowns and unknowns of natural killer cell biology in COVID-19 and other coronaviruses in July 2020

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