Upregulation of mouse CD14 expression in Kupffer cells by lipopolysaccharide.

Matsuura, Keiko; Ishida, Tetsuya; Setoguchi, Mihoko; Higuchi, Yasunori; Akizuki, Shin’ichiro; Yamamoto, Shunsuke

doi:10.1084/jem.179.5.1671

Cited by 119 publications

(101 citation statements)

References 27 publications

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“…Thus, in this respect liver differs from other organs belonging to the reticuloendothelial system, such as spleen or lung, which exhibit readily detectable tlr4 expression. Similarly, CD14, another LPS-recognition molecule intimately involved in the LPS-receptor complex, was also not detectable in liver of healthy mice [31,32]. Thus, under physiological conditions, the LPSreceptor and accessory molecules of the receptor complex seem to be strongly down-regulated in mouse liver.…”

Section: Discussionmentioning

confidence: 95%

Toll‐like receptor 4 expression levels determine the degree of LPS‐susceptibility in mice

et al. 2003

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C57BL/10ScCr (Cr) mice carry a deletion of the Toll-like receptor 4 (tlr4) gene (i.e. they are tlr4 0/0 ) and are thus refractory to LPS effects. Insertion of wild-type tlr4 transgene into the tlr4 0/0 Cr germ line endowed LPS susceptibility in the two transgenic lines created, indicating that TLR4 is the only limiting factor for LPS responsiveness in Cr mice. The absolute levels of tlr4 mRNA expressed by the heterozygous transgenic (tlr4 Tr/0 ), wild-type C57BL/10ScSn (Sn) (tlr4 +/+ ) and heterozygous F1 (Sn × Cr) (tlr4 +/0 ) mice varied markedly. However, the pattern of distribution of expression in the different organs was the same in all strains. In different biological assays (B cell mitogenicity, cytokine induction and lethal toxicity) the degree of LPS response obtained in the different strains of mice correlated with the levels of tlr4 mRNA expression. In macrophages, investigation of the LPS-induced cytokine (IL-6) response revealed a linear relationship between the response and the logarithm of TLR4-MD-2 levels.

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Section: Discussionmentioning

confidence: 95%

Toll‐like receptor 4 expression levels determine the degree of LPS‐susceptibility in mice

et al. 2003

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“…A high abundance of CD14 receptors have been identified in rat peritoneal macrophages but, surprisingly, isolated KCs do not posses a large number of these receptors. 34,54 However, CD14 expression in KCs is upregulated after LPS exposure. 54 Under our experimental conditions we observed that the absence of serum (i.e., LBP) did not affect LPS-induced iNOS mRNA levels in KCs.…”

Section: Discussionmentioning

confidence: 99%

Suppression of lipopolysaccharide-induced nitric oxide synthase expression by platelet-activating factor receptor antagonists in the rat liver and cultured rat kupffer cells

1999

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Excessive nitric oxide (NO) generated by hepatic cells in response to lipopolysaccharide (LPS) and inflammatory substances (e.g., platelet-activating factor [PAF]) is a key contributor to the pathophysiological outcomes observed in the liver during sepsis. In rats subjected to liver-focused endotoxemia, inducible nitric oxide synthase (iNOS) levels in the intact liver were elevated by 6 hours; cell-specific expression of iNOS messenger RNA (

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“…3A, mCD14 was not detectable on murine MC. Further, treatment with LPS, which was shown to enhance mCD14 expression in macrophages [35,36], also failed to induce detectable mCD14 expression on MC (see Supplementary Fig. 3 online).…”

Section: Activation Of MC By R-form Lps Is Independent Of Lbp and Cd14mentioning

confidence: 99%

R‐form LPS, the master key to the activation ofTLR4/MD‐2‐positive cells

et al. 2006

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Lipopolysaccharide (endotoxin, LPS) is a major recognition marker for the detection of gram-negative bacteria by the host and a powerful initiator of the inflammatory response to infection. Using S-and R-form LPS from wild-type and R-mutants of Salmonella and E. coli, we show that R-form LPS readily activates mouse cells expressing the signaling receptor Toll-like receptor 4/myeloid differentiation protein 2 (TLR4/MD-2), while the S-form requires further the help of the LPS-binding proteins CD14 and LBP, which limits its activating capacity. Therefore, the R-form LPS under physiological conditions recruits a larger spectrum of cells in endotoxic reactions than S-form LPS. We also show that soluble CD14 at high concentrations enables CD14-negative cells to respond to S-form LPS. The presented in vitro data are corroborated by an in vivo study measuring TNF-a levels in response to injection of R-and S-form LPS in mice. Since the R-form LPS constitutes ubiquitously part of the total LPS present in all wild-type bacteria its contribution to the innate immune response and pathophysiology of infection is much higher than anticipated during the last half century.Supporting information for this article is available at http://www.wiley-vch.de/contents/jc_2040/2006/35593_pdf IntroductionThe interaction of highly conserved microbial constituents with the innate immune system forms the basis of recognition of and reaction against intruding pathogens in mammals. One such constituent is lipopolysaccharide (endotoxin, LPS), a major recognition marker common to gram-negative bacteria [1][2][3], a large group comprising important human pathogens as well as commensals. Thus, the interaction of LPS with cells of the innate immune system leads to the formation and release of endogenous mediators initiating inflammatory and immune responses essential for an antibacterial defense [3,4]. This primarily protective mechanism may become overshadowed by an acute pathophysiological response with the typical clinical symptoms of septic shock that frequently follows the release of inflammatory mediators, such as tumor necrosis factor (TNF)-a during infection [5][6][7].Innate immunity * Both authors contributed equally to this work. [10]. Binding of allergen to its specific IgE on the surface of MC results in an immediate release of preformed pro-inflammatory mediators (e.g., histamine, TNF-a and proteases) from cytoplasmic granules (degranulation) [11] and a later release of de novo synthesized arachidonic acid metabolites and various cytokines like interleukin 6 (IL-6), TNF-a, and chemokines [10,11]. Unlike allergens, LPS induces no degranulation of MC, but like allergens, it stimulates the de novo synthesis and release of cytokines in these cells [9].Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLR, which are specialized in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness [12]. For functional interaction with LP...

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Upregulation of mouse CD14 expression in Kupffer cells by lipopolysaccharide.

Cited by 119 publications

References 27 publications

Toll‐like receptor 4 expression levels determine the degree of LPS‐susceptibility in mice

Toll‐like receptor 4 expression levels determine the degree of LPS‐susceptibility in mice

Suppression of lipopolysaccharide-induced nitric oxide synthase expression by platelet-activating factor receptor antagonists in the rat liver and cultured rat kupffer cells

R‐form LPS, the master key to the activation ofTLR4/MD‐2‐positive cells

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