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• W3134894512 abstract "Several Gram-negative bacteria, including Actinobacillus pleuropneumoniae and Haemophilus parasuis, are responsible for respiratory diseases and cause huge economic losses to the swine industry worldwide. Lipopolysaccharide (LPS) is a cell outer membrane component of Gram-negative bacteria and serves as a major pro-inflammatory stimulus binding to pattern recognition receptor Toll-like receptor 4 (TLR4) (Ciesielska et al., 2020). LPS is ubiquitous in nature and exists in high concentrations in air pollution, soil, and organic dust. Inhalation of LPS is involved in the pathogenesis of lung inflammation (Kaelberer et al., 2020).Alveolar macrophages (AMs) are the predominant immune cells located at the air-surface interface of alveoli. Resident AMs that arise during embryogenesis and recruited AMs that originate postnatally from circulating monocytes coexist in the inflamed lung. Once infection occurs, AMs move between alveoli to sense and phagocytose inhaled bacteria before they can induce harmful lung inflammation (Neupane et al., 2020). Meanwhile, the Gram-negative bacterial LPS binding to the TLR4 of AMs initiates multiple intracellular signaling pathways and induces the production of some pro-inflammatory cytokines, such as interleukin 1β (IL-1β) (Li et al., 2017). These pro-inflammatory cytokines induce superfluous neutrophil recruitment, leading to continuous lung inflammation and injury. The activation states of AMs are divided into classically activated (M1) and alternatively activated (M2). M1-type AMs generally induced by TLR signaling and interferon-gamma (IFN-γ) secrete pro-inflammatory cytokines, and M2-type AMs generally induced by interleukin-4 (IL-4) are anti-inflammatory and typically express the transforming growth factor-β (TGF-β) (Hussell and Bell, 2014). However, the gene reprogramming and polarization states of macrophages are also affected by stimulation intensity and tissue origin. A meta-analysis of in vitro differentiated macrophages showed that macrophages display distinguishing activation states even after early (2–4 h) or late (18–24 h) LPS infection (Chen et al., 2019). In M1-type AMs, increased levels of reactive oxygen species, such as hydrogen peroxide, superoxide, and hydroxyl, are implicated in DNA damage and membrane dysfunction (Riazanski et al., 2020). Therefore, the cellular antioxidant capacity of AMs is indispensable for controlling the homeostasis of intracellular oxidative stress and maintaining immune defense.Selenium (Se) is considered as a functional element of thioredoxin reductase, glutathione peroxidase, and other Se-containing enzymes and protects against oxidative injury (Silvestrini et al., 2020). LPS infection impairs Se metabolism and leads to dysregulation of selenoprotein expression in the spleen, thymus, and lymph node of pigs (Sun et al., 2017). An animal study using a chicken model of Se deficiency has demonstrated the negative correlation between Se deficiency and inflammation-related gene expression in skeletal muscles (Wu et al., 2014). Se supplementation can attenuate inflammatory response and lung injury induced by a variety of stimuli, including virus (Liu et al., 2015), bacteria (Xu et al., 2020), and heavy metal (Ghorbel et al., 2017). It was also reported that supplementation of Se to macrophages ameliorates the pro-inflammatory response induced by LPS (Vunta et al., 2008). However, the potential molecular mechanism of the anti-inflammatory function of Se is still unclear. Transcriptome sequencing is proven to be a powerful tool to comprehensively view the immune response of porcine AMs (PAMs) to bacterial or viral infection (Kim et al., 2019; Park et al., 2020). In this study, we performed transcriptome sequencing to deepen the understanding of the mechanism of Se protecting PAMs against LPS infection." @default.
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• W3134894512 date "2021-03-04" @default.
• W3134894512 modified "2023-09-23" @default.
• W3134894512 title "Transcriptome Analysis of Selenium-Treated Porcine Alveolar Macrophages Against Lipopolysaccharide Infection" @default.
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• W3134894512 doi "https://doi.org/10.3389/fgene.2021.645401" @default.
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