Increased expression of the peroxisome proliferator-activated receptor γ in the immune system of weaned pigs after Escherichia coli lipopolysaccharide injection

Liu, Yulan; Lu, Joan; Shi, Jianzhong; Hou, Yongqing; Zhu, Huiling; Zhao, Shengjun; Hongming, Liu; Ding, Biao; Yin, Yulong; Yi, G. F.

doi:10.1016/j.vetimm.2008.02.014

Cited by 21 publications

(20 citation statements)

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“…5). These findings are in line with a recent report demonstrating that E. coli LPS up-regulated PPARγ expression in the immune system of pigs by inducing the generation of endogenous PPARγ agonists such as 15d PGJ (2) [49]. Thus, while enterobacterial and Ft LPS differ in molecular targets (i.e., TLR4 versus TLR2, respectively) and their ability to induce inflammatory cytokines, both types of LPS may induce the generation of endogenous PPAR agonists as a mechanism of down-regulating inflammation.…”

Section: Discussionsupporting

confidence: 91%

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection

et al. 2010

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BackgroundIt has been shown previously that administration of Francisella tularensis (Ft) Live Vaccine Strain (LVS) lipopolysaccharide (LPS) protects mice against subsequent challenge with Ft LVS and blunts the pro-inflammatory cytokine response.MethodsTo further investigate the molecular mechanisms that underlie Ft LVS LPS-mediated protection, we profiled global hepatic gene expression following Ft LVS LPS or saline pre-treatment and subsequent Ft LVS challenge using Affymetrix arrays.ResultsA large number of genes (> 3,000) were differentially expressed at 48 hours post-infection. The degree of modulation of inflammatory genes by infection was clearly attenuated by pre-treatment with Ft LVS LPS in the surviving mice. However, Ft LVS LPS alone had a subtle effect on the gene expression profile of the uninfected mice. By employing gene set enrichment analysis, we discovered significant up-regulation of the fatty acid metabolism pathway, which is regulated by peroxisome proliferator activated receptors (PPARs).ConclusionsWe hypothesize that the LPS-induced blunting of pro-inflammatory response in mouse is, in part, mediated by PPARs (α and γ).

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Section: Discussionsupporting

confidence: 91%

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection

et al. 2010

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“…Interestingly, this included downregulation of peroxisome proliferator-activated receptor gamma (PPARG) (Fig. 7B, blue box), which has been reported to be expressed in immune cells of weaned pigs and plays a role in mediating the inflammatory response and the function of immune cells, including dendritic cells (28,29). In contrast, many molecules within this network, including PPARG, were unchanged or upregulated in pH1N1-infected pigs.…”

Section: Ii) Ph1n1 Virus Infection Results In Higher Expression Of Cementioning

confidence: 99%

“…The increase in lipid-related genes in the pH1N1-infected animals may reflect compensatory late reprogramming of cellular metabolism to restore membrane damage incurred during early immune and inflammatory responses. Differences in the early immune responses to the pH1N1 and IA30 viruses may also account for the relative downregulation of PPARG in IA30 infection as PPARG is expressed in the immune cells of pigs, and its activation in immune cells plays a role in the mediation of the host response to immunological stress (28,29). As such, the observed decreases in PPARG in IA30-infected but not pH1N1-infected cells may be related to the relative absence of an early immune response in the IA30 infection and could indicate virus-specific differences in immune cell populations in the lungs of infected pigs.…”

Section: Vol 85 2011 Pandemic H1n1 Virus Causes Gene Upregulation Imentioning

confidence: 99%

2009 Pandemic H1N1 Influenza Virus Causes Disease and Upregulation of Genes Related to Inflammatory and Immune Responses, Cell Death, and Lipid Metabolism in Pigs

Belisle

Mosier

et al. 2011

J Virol

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“…The purified mycobacterial cell wall lipoprotein P19 is well-defined as a TLR2 agonist (23). PPARγ is a prime candidate for an intracellular molecular switch based on its central role in controlling the inflammatory response in macrophages (24), and although PPARγ has been extensively investigated in other diseases (25), its immunoregulatory role in infectious diseases (particularly tuberculosis) is just beginning to be recognized (8,26,27). In the present study, the expression of PPARγ in human macrophages was enhanced by M.tb H37Rv and P19, but not M. smegmatis.…”

Section: A B C D Discussionmentioning

confidence: 99%

Mycobacterium tuberculosis 19-kDa lipoprotein induces Toll-like receptor 2-dependent peroxisome proliferator-activated receptor γ expression and promotes inflammatory responses in human macrophages

Liu

Niu

et al. 2014

Molecular Medicine Reports

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Abstract. Mycobacterium tuberculosis (M.tb) enhances its survival in macrophages by suppressing immune responses, in part through its complex cell wall structures. M.tb 19-kDa lipoprotein (P19), a component of the complex cell wall structures of M.tb, is a Toll-like receptor (TLR) agonist, and may induce immune responses through TLR2. Furthermore, the activation of peroxisome proliferator-activated receptor γ (PPARγ) is also involved in M.tb-induced immune responses in macrophages. In the present study, specific agonists/antagonists and siRNA were used to investigate the role of PPARγ in P19-induced immune responses in human macrophages, including TLR2 activation, p38 phosphorylation and cytokine production. In the present study, PPARγ expression, p38 phosphorylation and cytokine production were upregulated following M.tb H37Rv infection or P19 treatment. By pretreating macrophages with a specific PPARγ agonist or antagonist, it was demonstrated that phosphorylation and IL-6 production are modulated in macrophages by PPARγ activity. Following TLR2 knockdown in macrophages, the expression of PPARγ was significantly decreased in the presence or absence of P19 treatment. Furthermore, p38 phosphorylation and cytokine production were significantly reduced in TLR2 knockdown macrophages following P19 treatment. It was demonstrated in the current study that PPARγ was induced and activated by M.tb infection and that P19-induced PPARγ expression, p38 phosphorylation and cytokine production in macrophages are dependent on TLR2. These findings suggest a role for PPARγ and TLR2 in P19-induced p38 phosphorylation and cytokine production, thereby potentially influencing M.tb pathogenesis.

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Increased expression of the peroxisome proliferator-activated receptor γ in the immune system of weaned pigs after Escherichia coli lipopolysaccharide injection

Cited by 21 publications

References 50 publications

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection

2009 Pandemic H1N1 Influenza Virus Causes Disease and Upregulation of Genes Related to Inflammatory and Immune Responses, Cell Death, and Lipid Metabolism in Pigs

Mycobacterium tuberculosis 19-kDa lipoprotein induces Toll-like receptor 2-dependent peroxisome proliferator-activated receptor γ expression and promotes inflammatory responses in human macrophages

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