Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Zhang, Yuan; Zhang, Jiuli; Bao, Jun; Tang, Chaohua; Zhang, Ziwei

doi:10.1002/jcp.29836

Cited by 24 publications

(10 citation statements)

References 69 publications

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“…Selenoproteins are involved in the regulation of cellular redox homeostasis, and the protection of oxidative stress ( Schomburg and Schweizer, 2009 ). Besides, the study has shown that Se deficiency can change the distribution and steady-state of other minerals, which had been confirmed again in our experiment ( Zhang et al., 2021 ). In this study, we established the Se deficiency model in swine and IPEC-J2 cells, in which results showed that Se deficiency caused a downward trend in the overall selenoproteins expressions and disrupted the balance of intestinal trace elements.…”

Section: Discussionsupporting

confidence: 85%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

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Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1 , microtubule-associated proteins 1A ( LC3-1 ), microtubule-associated proteins 1B ( LC3-2 ), autophagy-related protein 5 ( ATG5 ), autophagy-related protein 12 ( ATG12 ), autophagy-related protein 16 ( ATG16 ), mammalian target of rapamycin ( mTOR ), calmodulin-dependent protein kinase kinase β ( CAMKK-β ), adenosine 5′-monophosphate-activated protein kinase ( AMPK ), sarco(endo)plasmic reticulum Ca 2+ -ATPase ( SERCA ), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro ( P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine.

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Section: Discussionsupporting

confidence: 85%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

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“…Besides, our previous research also showed that selenium de ciency did cause in ammation of swine intestinal tissue and IPEC-J2 cells [46]. In our present experiment, it was observed that ROS production in IPEC-J2 cells increased due to selenium de ciency stimulation.…”

Section: Discussionsupporting

confidence: 68%

Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine

Zheng¹,

Guan²,

Yang³

et al. 2020

Preprint

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Background:Selenium deficiency can seriously affect the intestinal status of swine, and cause diarrhea in swine. However, the specific mechanism of selenium intestinal injury caused by selenium deficiency is rarely reported.Methods:Here, to explore the damage of selenium deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal selenium deficiency were established. The intestinal model of swine intestine was established by feeding different selenium concentrations. Besides, selenium-deficient medium and normal medium were used to culture IPEC-J2 cells to establish in vitro models. Morphological observation and cell staining were used to determine the way of intestinal injury, and gene expression was quantitatively detected by qPCR and WB.Results:Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. MDC staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. Also, according to the ROS test results, the percentage of ROS in the Se-deficiency group is higher than the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy and calcium-related genes (Beclin1, LC3-1, LC3-2, ATG5, ATG12, ATG16, mTOR, CAMKK-β, AMPK, SERCA, calpain) in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro. Under the influence of selenium deficiency, the mRNA expression level of selenoproteins decreased significantly, and the steady-state content of some elements was also destroyed. Conclusion:Altogether, our results indicated that selenium deficiency could destroy the calcium homeostasis and antioxidant homeostasis of swine intestine to trigger cell autophagy. Moreover, selenium deficiency reduces the overall expression of selenoproteins and affects the content of elements in the intestine.

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“…Necroptosis may also support the effector activity of Th17 cells following recognition of fungi. A special case of this is when necroptosis of macrophages in a process called metaphorosis can lead to calcineurin-dependent lateral transfer of A. fumigates to live macrophages to downregulate fungal germination [ 100 , 101 ]. Selenium deficiency induced accelerated cell necroptosis in IPEC-J2 cells, resulting in increased expression of IL-1β, IL-6, IL-7 and IL-17, while the expression of IFNγ, IL-10 and IL-4 is down-regulated indicating a Th17 polarization of helper T cells [ 100 ].…”

Section: Immunological Decision-making Ii: How Do the Different Necro...mentioning

confidence: 99%

“…A special case of this is when necroptosis of macrophages in a process called metaphorosis can lead to calcineurin-dependent lateral transfer of A. fumigates to live macrophages to downregulate fungal germination [ 100 , 101 ]. Selenium deficiency induced accelerated cell necroptosis in IPEC-J2 cells, resulting in increased expression of IL-1β, IL-6, IL-7 and IL-17, while the expression of IFNγ, IL-10 and IL-4 is down-regulated indicating a Th17 polarization of helper T cells [ 100 ]. Intestinal epithelial cell necroptosis, which results in the recruitment and activation of ILC3s and IL-22 production, also enhances Th17 responses [ 102 ].…”

Section: Immunological Decision-making Ii: How Do the Different Necro...mentioning

confidence: 99%

Types of necroinflammation, the effect of cell death modalities on sterile inflammation

et al. 2022

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Distinct types of immune responses are activated by infections, which cause the development of type I, II, or III inflammation, regulated by Th1, Th2, Th17 helper T cells and ILC1, ILC2 and ILC3 cells, respectively. While the classification of immune responses to different groups of pathogens is widely accepted, subtypes of the immune response elicited by sterile inflammation have not yet been detailed. Necroinflammation is associated with the release of damage-associated molecular patterns (DAMP) from dying cells. In this review, we present that the distinct molecular mechanisms activated during apoptosis, necroptosis, pyroptosis, and ferroptosis lead to the release of different patterns of DAMPs and their suppressors, SAMPs. We summarize the currently available data on how regulated cell death pathways and released DAMPs and SAMPs direct the differentiation of T helper and ILC cells. Understanding the subtypes of necroinflammation can be crucial in developing strategies for the treatment of sterile inflammatory diseases caused by cell death processes.

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Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Cited by 24 publications

References 69 publications

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine

Types of necroinflammation, the effect of cell death modalities on sterile inflammation

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