LPS- and LTA-Induced Expression of IL-6 and TNF-αin Neonatal and Adult Blood: Role of MAPKs and NF-κB

Koch, Lutz; Frommhold, David; Buschmann, Kirsten; Kuß, Navina; Poeschl, Johannes; Ruef, Peter

doi:10.1155/2014/283126

Cited by 38 publications

(23 citation statements)

References 28 publications

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“…Previous studies have indicated that aLTA can induce the phosphorylation of p65, thereby activating the NF-B signaling pathway, upregulating the expression of TNF-␣, and subsequently inducing inflammatory responses in host cells [27,28]. We found that aLTA induced p65 mRNA expression, significantly enhanced p65 phosphorylation, and upregulated the expression of TNF-␣ in HT-29 cells.…”

Section: Discussionsupporting

confidence: 47%

Different effects of lipoteichoic acid from C. butyricum and S. aureus on inflammatory responses of HT-29 cells

Wang

et al. 2016

International Journal of Biological Macromolecules

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Section: Discussionsupporting

confidence: 47%

Different effects of lipoteichoic acid from C. butyricum and S. aureus on inflammatory responses of HT-29 cells

Wang

et al. 2016

International Journal of Biological Macromolecules

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“…When activated by external stimuli, p38, JNK, and ERK phosphorylation is increased and related proinflammatory cytokines will begin to be expressed [30]. Furthermore, the present study explores the anti-inflammatory mechanism of Andrographolide regarding the NF- κ B and MAPKs pathways.…”

Section: Discussionmentioning

confidence: 99%

Andrographolide Inhibits Inflammatory Cytokines Secretion in LPS-Stimulated RAW264.7 Cells through Suppression of NF-κB/MAPK Signaling Pathway

Tang

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Andrographolide, the main active component extracted from Andrographis paniculata (Burm.f.) Wall. ex Nees, exerts anti-inflammatory effects; however, the principal molecular mechanisms remain unclear. The objective of this study was to investigate the molecular mechanisms of Andrographolide in modifying lipopolysaccharide- (LPS-) induced signaling pathway in RAW264.7 cells. An in vitro model of inflammation was induced by LPS in mouse RAW264.7 cells in the presence of Andrographolide. The concentration and expression levels of proinflammatory cytokines were determined by an enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. The nuclear level of NF-κB was measured by an electrophoretic mobility shift assay (EMSA). The expression levels of NF-κB, p38, ERK, and JNK were determined by western blot. Andrographolide dose-dependently inhibited the release and mRNA expression of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 cells. The nuclear level of p65 protein was decreased in Andrographolide treatment group. Western blot analysis showed that Andrographolide suppressed LPS-induced NF-κB activation and the phosphorylation of IkBa, ERK1/2, JNK, and p38. These results suggest that Andrographolide exerts an anti-inflammatory effect by inhibiting the activation of NF-κB/MAPK signaling pathway and the induction of proinflammatory cytokines.

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“…ref. [411][412][413][414]. This too is inflammatory and itself induces further changes in NF-kB expression.…”

Section: Lps Induction Of Apoptotic Programmed Necrotic and Pyroptotmentioning

confidence: 99%

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

Kell

Pretorius

2015

Integrative Biology

140

178

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We have recently highlighted (and added to) the considerable evidence that blood can contain dormant bacteria. By definition, such bacteria may be resuscitated (and thus proliferate). This may occur under conditions that lead to or exacerbate chronic, inflammatory diseases that are normally considered to lack a microbial component. Bacterial cell wall components, such as the endotoxin lipopolysaccharide (LPS) of Gram-negative strains, are well known as potent inflammatory agents, but should normally be cleared. Thus, their continuing production and replenishment from dormant bacterial reservoirs provides an easy explanation for the continuing, low-grade inflammation (and inflammatory cytokine production) that is characteristic of many such diseases. Although experimental conditions and determinants have varied considerably between investigators, we summarise the evidence that in a great many circumstances LPS can play a central role in all of these processes, including in particular cell death processes that permit translocation between the gut, blood and other tissues. Such localised cell death processes might also contribute strongly to the specific diseases of interest. The bacterial requirement for free iron explains the strong co-existence in these diseases of iron dysregulation, LPS production, and inflammation. Overall this analysis provides an integrative picture, with significant predictive power, that is able to link these processes via the centrality of a dormant blood microbiome that can resuscitate and shed cell wall components.

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LPS- and LTA-Induced Expression of IL-6 and TNF-αin Neonatal and Adult Blood: Role of MAPKs and NF-κB

Cited by 38 publications

References 28 publications

Different effects of lipoteichoic acid from C. butyricum and S. aureus on inflammatory responses of HT-29 cells

Different effects of lipoteichoic acid from C. butyricum and S. aureus on inflammatory responses of HT-29 cells

Andrographolide Inhibits Inflammatory Cytokines Secretion in LPS-Stimulated RAW264.7 Cells through Suppression of NF-κB/MAPK Signaling Pathway

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

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