Lactoferrin works as a new LPS-binding protein in inflammatory activation of macrophages

Na, Yong Joo; Han, Sang Bae; Kang, Jong Soon; Yoon, Yeo Dae; Park, Song‐Kyu; Kim, Hwan Mook; Yang, Kyu Hwan; Joe, Cheol O.

doi:10.1016/j.intimp.2004.05.009

Cited by 73 publications

(70 citation statements)

References 41 publications

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“…Addition of Lactoferrin to macrophages stimulated with suboptimal LPS (1 ng/ mL) increased production of IL-12 and decreased production of IL-10. This stimulatory activity may be attributed to Lactoferrin forming a complex with LPS to facilitate macrophage activation through CD14 (LPS co-stimulatory molecule) or the TLR-4 (LPS receptor) [36]. Previous studies on LPS activated macrophages and models of sepsis also reported this inhibitory effect of Lactoferrin to moderate other proinflammatory mediators [9,37].…”

Section: Discussionmentioning

confidence: 95%

Lactoferrin modulation of IL-12 and IL-10 response from activated murine leukocytes

Hwang¹,

Wilk²,

Bangale³

et al. 2007

Med Microbiol Immunol

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Lactoferrin possesses a wide range of immunomodulatory activities, including promotion of the delayed type hypersensitivity response (DTH) towards BCG (Bacillus Calmette Guerin) antigens. Addition of Lactoferrin as an adjuvant to the BCG vaccine was previously demonstrated to augment protection against subsequent mycobacterial challenge, with concomitant development of a strong T cell helper type 1 (T H 1) immunity. Because generation of T H 1 immunity is in large part dependent on the balance of monocytic pro-and anti-inflammatory cytokines, the effect of Lactoferrin on leukocytes was investigated. Lactoferrin enhanced proinflammatory responses in a dose-dependant manner from splenocyte and adherent (F4/80 + ) splenocyte populations, bone marrow derived monocytes (BMM), and J774A.1 cultured cells. In all scenarios tested, Lactoferrin induced a strong increase in the ratio of IL-12:IL-10 production from LPS stimulated cells. Examination of Lactoferrin effects on BCG infected J774A.1 cells and on BMM revealed similar immunomodulatory effects, with particularly strong increase in IL-12 production. Furthermore, immunization of mice with BCG admixed with Lactoferrin led to increased generation of CD4+ cells expressing IFN-γ upon restimulation with BCG antigens. These results provide molecular evidence to support the role of Lactoferrin as an adjuvant candidate to augment development of DTH response to vaccine antigens.

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Section: Discussionmentioning

confidence: 95%

Lactoferrin modulation of IL-12 and IL-10 response from activated murine leukocytes

Hwang¹,

Wilk²,

Bangale³

et al. 2007

Med Microbiol Immunol

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“…Physiologically, it is thought that breast milk provides protective anti-inflammatory factors containing the propensity of the immature human small intestine to respond to commensal colonizing bacteria by an excessive inflammatory response [27]. In preterm infants breast milk limits the incidence of necrotizing enterocolitis [28].…”

Section: Discussionmentioning

confidence: 99%

“…EPO also reduces the susceptibility to IFN-γ-induced experimental neonatal necrotizing lesions [7]. Lactoferrin reduces the production of inflammatory cytokines by monocytes by inhibiting activation through NF-κB [27]. Milk stasis is classically considered as the primary cause of mastitis and may progress to infection [8,9].…”

Section: Discussionmentioning

confidence: 99%

Subclinical mastitis occurs frequently in association with dramatic changes in inflammatory/anti-inflammatory breast milk components

et al. 2016

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“…Downregulation of TNF-a by bLF possibly can be partially related to bLF binding to LPS, and this may inhibit LPS binding to CD14 by competing with binding of LPS-binding protein to CD14. [29][30][31] In this study, extracellular free bLF was removed by washing with PBS before LPS stimulation to avoid formation of bLF-LPS complex. Therefore, we considered that response of OB to LPS may be affected by bLF pretreatment.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

Yamano

Miyauchi

Furusyo

et al. 2010

Laboratory Investigation

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Bovine lactoferrin (bLF) modulates the production of proinflammatory cytokines including tumor necrosis factor (TNF)-a, and may thus control alveolar bone destruction associated with periodontitis. In this study, the effects of bLF on mRNA expression in lipopolysaccharide (LPS)-stimulated osteoblasts (OBs) and on LPS-induced osteoclastogenesis were examined. The inhibitory effects of oral administration of liposomal-bLF (L-bLF), which improved the robustness of bLF to digestive enzymes, on alveolar bone resorption using LPS-induced periodontitis rat model are also reported. Three groups of 7-week-old male Wistar rats were treated with L-bLF (L-bLF group), bLF (bLF group), or the vehicle (control group) in drinking water (n ¼ 6 in each group). On day 7, LPS was topically applied into the gingival sulcus. Number of osteoclasts and immunoexpression of TNF-a were analyzed. The bLF inhibited the upregulation of TNF-a-mRNA-and upregulation of receptor activator of NFkB (RANKL)-mRNA expression and eliminated downregulation of osteoprotegerin (OPG)-mRNA expression in LPS-stimulated OBs and reduced LPS-induced osteoclastogenesis in co-culture with primary OBs and bone marrow cells. In the control group, the number of osteoclasts increased after LPS treatment. The number of osteoclasts that appeared along the alveolar bone margin was significantly reduced (Po0.01) in the L-bLF but not in the bLF group. Furthermore, L-bLF suppressed upregulation of TNF-a immunoexpression in periodontal tissue and TNF-a and interleukin (IL)-1b-mRNA level in gingival tissue. The results of this study indicate that oral administration of L-bLF significantly reduces alveolar bone resorption induced by LPS stimulation through inhibition of TNF-a production and modulation of RANKL/OPG balance in OBs. It is suggested that L-bLF could be a potent therapeutic and preventive agent for attenuating alveolar bone destruction in periodontitis patients.

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Lactoferrin works as a new LPS-binding protein in inflammatory activation of macrophages

Cited by 73 publications

References 41 publications

Lactoferrin modulation of IL-12 and IL-10 response from activated murine leukocytes

Lactoferrin modulation of IL-12 and IL-10 response from activated murine leukocytes

Subclinical mastitis occurs frequently in association with dramatic changes in inflammatory/anti-inflammatory breast milk components

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

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