Recombinant human lactoferrin has preventive effects on lipopolysaccharide-induced preterm delivery and production of inflammatory cytokines in mice

Otsuki, Katsufumi; Yakuwa, Kyoko; Sawada, Masamichi; Hasegawa, Akitoshi; Sasaki, Yasushi; Mitsukawa, Kaori; Chiba, Hiroshi; Nagatsuka, Masaaki; Saitô, Hiroshi; Okai, Takashi

doi:10.1515/jpm.2005.057

Cited by 24 publications

(27 citation statements)

References 22 publications

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“…In our study, LF was found to inhibit TNF-α secretion at 12 h after LPS challenge in the BALF. Previous reports also demonstrated the production of TNF-α by LPS intraperitoneal injection was inhibited by prophylactic administration of LF [19,20].…”

Section: Discussionmentioning

confidence: 78%

Lactoferrin protects against lipopolysaccharide-induced acute lung injury in mice

Xijing

Dapeng

Chen

et al. 2012

International Immunopharmacology

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Section: Discussionmentioning

confidence: 78%

Lactoferrin protects against lipopolysaccharide-induced acute lung injury in mice

Xijing

Dapeng

Chen

et al. 2012

International Immunopharmacology

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“…10 Lactoferrin is able to bind and buffer several pathogen associated molecular patterns, such as lipopolysaccharide (LPS), viral components and soluble components of the extracellular matrix. 11 This ability is associated with the putative lactoferrin anti-inflammatory activity, as shown in several studies. 12 Lactoferrin administration led to decreased release of tumor necrosis factor-a and IL-6 in mice, [13][14][15] to downregulated pro-inflammatory cytokine production in different cell lines acting via nuclear factor-kB, 16 and to decreased LPSinduced binding of nuclear factor-kB to the tumor necrosis factor-a promoter.…”

Section: Introductionmentioning

confidence: 76%

Lactoferrin increases 172ThrAMPK phosphorylation and insulin-induced p473SerAKT while impairing adipocyte differentiation

et al. 2009

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Objective: Lactoferrin is a pleiotropic glycoprotein of the innate immune system with known effects on immunomodulation and cell differentiation. To gain an insight into the interaction among obesity, inflammation and insulin action, we aimed to examine the effects of lactoferrin on adipogenesis and the response to insulin in human hepatocarcinoma (HepG2) and 3T3-L1 cell lines. Design: The cells were cultured with increasing lactoferrin concentration under non-inflammatory, inflammatory and standard conditions. The response to insulin was evaluated through 473Ser AKT phosphorylation. The effects of lactoferrin on adipogenesis were studied through the expression of different lipogenic markers, AMP-activated protein kinase (AMPK) activation, retinoblastoma (Rb) activity and Oil Red O staining in 3T3-L1 cells. Results: Lactoferrin increased dose-dependent insulin-induced 473Ser AKT phosphorylation in both cell lines. Inflammationinduced decreased 473Ser AKT phosphorylation was also rescued by lactoferrin. In addition, lactoferrin led to increased p172Thr AMPK during 3T3-L1 differentiation and to decreased adipogenesis (as shown by decreased expression of fatty acid synthase, acetyl-coenzyme A carboxylase-a and peroxisome proliferator-activated receptor-g in parallel with decreased formation of lipid droplets). Lactoferrin also increased dose-dependent Rb activity (expression and hypophosphorylation) during 3T3-L1 differentiation. Conclusion: Lactoferrin administration increased insulin-induced 473Ser AKT phosphorylation, even in those conditions wherein the response to insulin was downregulated, and led to blunted adipogenesis in the context of increased p172Thr AMPK and Rb activity.

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“…The protective role of Lf in LPS-induced pathologies has been further evaluated in other disease models. Indeed, mice were protected by hLf from hepatitis (Yamaguchi et al 2001), by bLf from arthritis (Hayashida et al 2004) and diarrhoea (Talukder and Harada 2007), and by both Lfs against preterm delivery (Mitsuhashi et al 2000;Otsuki et al 2005;Sasaki et al 2004) after LPS challenge. The exact mechanisms by which Lf exerts preventive and/or therapeutic potential are not yet known, however, some of the effects could be due to Lf intrinsic capacity to bind LPS or to subvert LPS triggered pathways.…”

Section: Lf-mediated Anti-inflammatory Mechanismsmentioning

confidence: 99%

Immunoregulatory role of lactoferrin-lipopolysaccharide interactions

et al. 2010

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Lactoferrin (Lf) is a mammalian exclusive protein widely distributed in milk and exocrine secretions exhibiting multifunctional properties. Many of the proven or proposed functions of Lf, apart from its iron binding activity, depend on its capacity to bind to other macromolecules. Lf can bind and sequester lipopolysaccharide (LPS), thus preventing pro-inflammatory pathway activation, sepsis and tissue damage. However, the interplay between Lf and LPS is complex, and may result in different outcomes, including both suppression of the inflammatory response and immune activation. These findings are critically relevant in the development of Lf-based therapeutic interventions in humans. Understanding the molecular basis and functional consequences of Lf-LPS interaction will provide insights for determining its role in health and disease.

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Recombinant human lactoferrin has preventive effects on lipopolysaccharide-induced preterm delivery and production of inflammatory cytokines in mice

Abstract: Rh-LF may prolong gestation in LPS-induced preterm delivery in mice, by suppressing LPS-induced plasma IL-6 and TNF-alpha augmentation.

Cited by 24 publications

References 22 publications

Lactoferrin protects against lipopolysaccharide-induced acute lung injury in mice

Lactoferrin protects against lipopolysaccharide-induced acute lung injury in mice

Lactoferrin increases 172ThrAMPK phosphorylation and insulin-induced p473SerAKT while impairing adipocyte differentiation

Immunoregulatory role of lactoferrin-lipopolysaccharide interactions

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