Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 May;24(4):221-230.
doi: 10.1177/1753425918769372. Epub 2018 Apr 11.

LPS challenge increased intestinal permeability, disrupted mitochondrial function and triggered mitophagy of piglets

Affiliations

LPS challenge increased intestinal permeability, disrupted mitochondrial function and triggered mitophagy of piglets

Shuting Cao et al. Innate Immun. 2018 May.

Abstract

Here we investigated the influence of LPS-induced gut injury on antioxidant homeostasis, mitochondrial (mt) function and the level of mitophagy in piglets. The results showed that LPS-induced intestinal injury decreased the transepithelial electrical resistance, increased the paracellular permeability of F1TC dextran 4 kDa, and decreased the expression of claudin-1, occludin and zonula occludens-1 in the jejunum compared with the control group. LPS decreased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and increased the content of malondialdehyde in the jejunum. Meanwhile, the expression of SOD-related genes ( Cu/Zn-SOD, Mn-SOD) and GSH-Px-related genes ( GPX-1, GPX-4) declined in LPS-challenged pigs compared with the control. LPS also increased TNF-α, IL-6, IL-8 and IL-1β mRNA expression. LPS induced mt dysfunction, as demonstrated by increased reactive oxygen species production and decreased membrane potential of intestinal mitochondria, intestinal content of mt DNA and activities of the intestinal mt respiratory chain. Furthermore, LPS induced an increase in expression of mitophagy related proteins, PTEN-induced putative kinase (PINK1) and Parkin in the intestinal mitochondria, as well as an enhancement of the ratio of light chain 3-II (LC3-II) to LC3-I content in the jejunal mucosa. These results suggested that LPS-induced intestinal injury accompanied by disrupted antioxidant homeostasis, caused mt dysfunction and triggered mitophagy.

Keywords: LPS; intestinal injury; mitochondrial function; mitophagy; piglets.

PubMed Disclaimer

Conflict of interest statement

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Effect of LPS injection on the expression of tight junction (TJ) proteins of piglets in jejunal mucosa. (a) Representative blots of claudin-1, occludin, ZO-1 and β-actin in the jejunal mucosa of piglets. (b) Summary of Western blots for n = 6 pigs per treatment in LPS-injected pigs and control pigs. Values are means and SD represented by vertical bars. Control group (black bars), injected with 0.9% (w/v) NaCl solution. LPS group (gray bars), injected with LPS at 100 µg/kg BM. The protein expression of all samples is shown.
Figure 2.
Figure 2.
(a) Effect of LPS injection on intestine mitochondrial (mt) reactive oxygen species (ROS) production of piglets. (b) Effect of LPS injection on intestinal mt membrane potential change (△Ψm) of piglets. Values are means and SD represented by vertical bars. Control group (black bars), injected with 0.9% (w/v) NaCl solution. LPS group (gray bars), injected with LPS at 100 µg/kg BM. The ROS production and mt △Ψm were expressed as fold changes, calculated relative to the control group.
Figure 3.
Figure 3.
(a) Effect of LPS injection on intestine content of mtDNA of piglets. (b) Effect of LPS injection on intestinal mt complex activity of piglets. Values are means and SD represented by vertical bars. Control group (black bars), injected with 0.9% (w/v) NaCl solution. LPS group (gray bars), injected with LPS at 100 µg/kg BM.
Figure 4.
Figure 4.
Effect of LPS injection on the level of mitophagy-related protein of piglets. (a) Representative blots of PINK1, Parkin in the intestinal mitochondria. (b) Shows relative PINK1 and Parkin expression. (c) Representative blots of LC3-I and LC3-II in the jejunum mucosa. (d) Shows relative LC3-I and LC3-II expression. Values are means and SD represented by vertical bars. Control group (black bars), injected with 0.9% (w/v) NaCl solution. LPS group (gray bars), injected with LPS at 100 µg/kg BM. The protein expression of all samples was expressed as fold changes, calculated relative to the control group.

Similar articles

Cited by

References

    1. Xiao K, Song ZH, Jiao LF, et al. Developmental changes of TGF-beta 1 and Smads signaling pathway in intestinal adaption of weaned pigs. PloS one 2014; 9: e104589. - PMC - PubMed
    1. Hu CH, Xiao K, Luan ZS, et al. Early weaning increases intestinal permeability, alters expression of cytokine and tight junction proteins, and activates mitogen-activated protein kinases in pigs. J Anim Sci 2013; 91: 1094–1101. - PubMed
    1. Pi DA, Liu YL, Shi HF, et al. Dietary supplementation of aspartate enhances intestinal integrity and energy status in weanling piglets after lipopolysaccharide challenge. J Nutr Biochem 2014; 25: 456–462. - PubMed
    1. Marcu R, Zheng Y, Hawkins BJ. Mitochondria and angiogenesis. Adv Exp Med Biol 2017; 982: 371–406. - PubMed
    1. Jeong EM, Chung J, Liu H, et al. Role of mitochondrial oxidative stress in glucose tolerance, insulin resistance, and cardiac diastolic dysfunction. J Am Heart Assoc 2016; 5: pii: e00304. - PMC - PubMed

Publication types

MeSH terms

LinkOut - more resources