Involvement of nuclear factor erythroid 2‑related factor�2 in�neonatal intestinal interleukin‑17D expression in hyperoxia

Liu, Xuying; Zhang, Dongyang; Cai, Qing-Qing; Liu, Dongyan; Sun, Siyu

doi:10.3892/ijmm.2020.4697

Cited by 4 publications

(4 citation statements)

References 39 publications

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“…IL-17D is expressed by CD4 + T cells, CD19 + B cells, and villous epithelial cells in the small intestine. Under stimulation by hyperoxia, the expression of IL-17D in CD4 + T cells and CD19 + B cells gradually increased with prolongation of hyperoxia exposure, while the expression of IL-17D in intestinal epithelial cells reached a peak at 7 days and then gradually decreased [ 32 ]. Nrf2 is an important transcription factor regulating the IL-17D expression, and Nrf2 is inhibited by Keap1 in the cytoplasm under the resting state.…”

Section: Immune Barriermentioning

confidence: 99%

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Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Liu

2022

Journal of Immunology Research

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High concentration oxygen is widely used in the treatment of neonates, which has a significant effect on improving blood oxygen concentration in neonates with respiratory distress. The adverse effects of hyperoxia therapy on the lung, retina, and neurodevelopment of newborns have been extensively studied, but less attention has been paid to intestinal damage caused by hyperoxia therapy. In this review, we focus on the physical, immune, and microorganism barriers of the intestinal tract and discuss neonatal intestinal tract damage caused by hyperoxia therapy and analyze the molecular mechanism of intestinal damage caused by hyperoxia in combination with necrotizing enterocolitis.

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Section: Immune Barriermentioning

confidence: 99%

“…In the immune barrier, high oxygen increased SIgA content in the mucus layer by stimulating the SC expression [ 16 , 25 ]. In addition, high oxygen also increases IL-17D, IL-10, and IFN- γ , resulting in a disturbance of cytokine levels [ 12 , 32 ].…”

Section: Figurementioning

confidence: 99%

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Liu

2022

Journal of Immunology Research

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“…The Effect of NAC and APO on Cell Survival. In our previous studies, ROS was speculated to play a key role in hyperoxia [5,7]. Therefore, in this study, the ROS inhibitor, NAC, which clears ROS from cells, and APO, which inhibits the production of cellular ROS, were used.…”

Section: Hyperoxia Affects the Levels Of Neonatal Rat Intestinalmentioning

confidence: 99%

“…Cytokines often possess overlapping biological activities and exert different effects at different concentrations [4]. And many cytokines play key roles during hyperoxia [4,5].…”

Section: Introductionmentioning

confidence: 99%

ROS Plays a Role in the Neonatal Rat Intestinal Barrier Damages Induced by Hyperoxia

Liu

Zhang

Sun

2020

BioMed Research International

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Background. Hyperoxia treats a subset of critical neonatal illnesses but induces intestinal damage in neonatal pups. In this process, the intestinal flora and mucosal epithelium might be altered by hyperoxia. So the changes of the intestinal flora and mucosal epithelium were studied. Methods. Neonatal rats were randomized into the model group that was exposed to hyperoxia and the control group that was maintained under normoxic conditions; then, intestinal lavage fluid and intestinal tissues were harvested. ELISA was used to detect D-lactic acid (D-LA), endotoxin (ET), diamine oxidase (DAO), intestinal fatty acid binding protein (i-FABP), liver-type fatty acid binding protein (L-FABP) and cytokines in the intestinal lavage of neonatal rats during hyperoxia. The intestinal zonula occluden-1 (ZO-1), occlusion protein (Occludin), and closure protein-4 (Claudin-4) of neonatal pups were detected by immunohistochemistry, western blotting, and real-time Polymerase chain reaction (RT-PCR) during hyperoxia. NCM460 cell survival rates were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) during hyperoxia and administration of N-acetyl-L-cysteine (NAC). The expression levels of ZO-1, Occludin, and Claudin-4 in NCM460 cells were detected by immunohistochemistry, western blotting, and RT-PCR during hyperoxia and NAC. Results. D-LA, ET, L-FABP, i-FABP, DAO, TNF-α, IL-10, and IFN-γ were significantly increased by hyperoxia, while ZO-1, Occludin, and Claudin-4 were clearly decreased in the hyperoxia group compared with the control group. NAC promoted cell survival, which was inhibited by hyperoxia. The cellular expression levels of ZO-1, Occludin, and Claudin-4, which were lowered by hyperoxia, were increased by NAC. Conclusion. Hyperoxia causes injury of the intestinal mucosa, and ROS plays a role in this intestinal damage during hyperoxia.

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Interleukin-17D produced by alveolar epithelial type II cells alleviates LPS-induced acute lung injury via the Nrf2 pathway

Dong,

Liu,

Gao

et al. 2023

Clinical Science

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Background: Sepsis engenders an imbalance in the body's inflammatory response, with cytokines assuming a pivotal role in its progression. A relatively recent addition to the interleukin-17 family, denominated Interleukin-17D (IL-17D), is notably abundant within pulmonary confines. Nevertheless, its implication in sepsis remains somewhat enigmatic. This study endeavors to scrutinize the participation of IL-17D in sepsis-induced acute lung injury (ALI). Methods: The levels of IL-17D in the serum and bronchoalveolar lavage fluid(BALF) of both healthy cohorts and septic patients were ascertained through an ELISA protocol. For the creation of a sepsis-induced ALI model, intraperitoneal lipopolysaccharide(LPS) injections were administered to male C57/BL6 mice. Subsequently, we examined the fluctuations and repercussions associated with IL-17D in sepsis-induced ALI, probing its interrelation with nuclear factor erythroid 2-related factor 2(Nrf2), alveolar epithelial permeability, and heme oxygenase-1. Results: IL-17D levels exhibited significant reduction both in the serum and BALF of septic patients. Similar observations manifested in mice subjected to LPS-induced acute lung injury (ALI). Intraperitoneal administration of recombinant Interleukin 17D protein(rIL-17D) prompted increased expression of claudin18 and concomitant enhancement of alveolar epithelial permeability, thus, culminating in improved lung injury. Alveolar epithelial type Ⅱ(ATⅡ) cells were identified as the source of IL-17D, regulated by Nrf2. Furthermore, a deficiency in HO-1 yielded elevated IL-17D levels, albeit administration of rIL-17D ameliorated the exacerbated pulmonary damage resulting from HO-1 deficiency. Conclusion: Nrf2 fosters IL-17D production within ATⅡ cells, thereby conferring a protective role in sepsis-induced ALI. Keywords: acute lung injury; alveolar epithelial type Ⅱ cells; heme oxygenase-1; interleukin-17D; nuclear factor erythroid 2-related factor 2; sepsis

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Involvement of nuclear factor erythroid 2‑related factor�2 in�neonatal intestinal interleukin‑17D expression in hyperoxia

Cited by 4 publications

References 39 publications

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

ROS Plays a Role in the Neonatal Rat Intestinal Barrier Damages Induced by Hyperoxia

Interleukin-17D produced by alveolar epithelial type II cells alleviates LPS-induced acute lung injury via the Nrf2 pathway

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