Bovine lactoferrin induces both mucosal and systemic immune 
response in mice

Debbabi, Hajer; Dubarry, M; Rautureau, M; Tomé, Daniel

doi:10.1017/s0022029997002732

Cited by 116 publications

(80 citation statements)

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“…36,37) It has also been reported that oral administration of bLF to mice increased the secretion of anti-bLF IgA and IgG in the intestinal fluid but made no difference in the serum, and it is suggested that bLF could act as an immunostimulating factor of the mucosal immune system. 38) On the other hand, it has been demonstrated that a portion of bLF is transported into blood circulation through the intestine 32,33) as previously noted. In addition, bLF is known to be comparatively robust to digestive enzymes such as pepsin or trypsin.…”

Section: Resultsmentioning

confidence: 89%

Liposomalization of Lactoferrin Enhanced It's Anti-inflammatory Effects via Oral Administration

Ishikado

Imanaka

Takeuchi

et al. 2005

Biological & Pharmaceutical Bulletin

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It is known that lactoferrin is one of the functional proteins contained in mammalian milk and that it plays an important role in the immune system. In this study, we prepared multi-lamellar liposomal bovine lactoferrin composed of egg yolk phosphatidylcholine and phytosterol for oral delivery, and examined any resulting anti-inflammatory effects. Oral pretreatment of liposomal lactoferrin exhibited more suppressive effects than did nonliposomal lactoferrin on CCl 4 -induced hepatic injury in rats as well as on lipopolysaccharide-induced TNF-alpha production from mouse peripheral blood mononuclear leukocytes. Further investigation revealed that the liposomalization did not exert influence on the absorbability of lactoferrin to the venous blood or lymph following an intraduodenal administration in rats. Furthermore, there was no significant difference exhibited between the antigenicity of liposomal and non-liposomal lactoferrin, which was measured using the passive cutaneous anaphylaxis reaction following oral sensitization to them in guinea pigs. These results suggest that liposomal lactoferrin might act more effectively than conventional lactoferrin in the intestinal site, which is regarded as an active site of orally administered lactoferrin, although the biological mechanism is not fully understood yet. Consequently we propose that liposomal lactoferrin could be a novel active constituent useful for preventive and therapeutic treatment of inflammatory diseases.

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Section: Resultsmentioning

confidence: 89%

Liposomalization of Lactoferrin Enhanced It's Anti-inflammatory Effects via Oral Administration

Ishikado

Imanaka

Takeuchi

et al. 2005

Biological & Pharmaceutical Bulletin

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“…In these studies, bovine lactoferrin was used to significantly enhance the current BCG vaccine. There is antigenic variation between human, bovine and murine lactoferrins (approximately 70-77% direct protein sequence match between all three molecules), which may impact responses in mice [68]. Future studies should examine responses using human or humanized lactoferrins.…”

Section: Discussionmentioning

confidence: 99%

Lactoferrin enhanced efficacy of the BCG vaccine to generate host protective responses against challenge with virulent Mycobacterium tuberculosis

Hwang

Wilk

Budnicka

et al. 2007

Vaccine

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Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), is a disease with world wide consequences, affecting nearly a third of the world's population. The established vaccine for TB, an attenuated strain of Mycobacterium bovis Calmette Guerin (BCG), has existed since 1921. Lactoferrin, an iron binding protein found in mucosal secretions and granules of neutrophils was hypothesized to be an ideal adjuvant to enhance the efficacy of the BCG vaccine, specifically because of previous reports of lactoferrin enhancement of IL-12 production from macrophages infected with BCG. Different vaccination protocols were investigated for generation of host protective responses against MTB infection using lactoferrin admixed to the BCG vaccine. Resulting effects demonstrate that BCG/lactoferrin increased host protection against MTB infection by decreasing organ bacterial load and reducing lung histopathology; significant reduction in tissue CFUs and pathology were observed post challenge compared to those seen with BCG alone. Addition of lactoferrin to the vaccine led to reduced pathological damage upon subsequent infection with virulent MTB, with positive results demonstrated when admixed in oil-based vehicle (incomplete Freund's adjuvant; IFA) or when given with BCG in saline. The observed post-challenge results paralleled increasing production of IFN-γ and IL-6, but only limited changes to proinflammatory mediators TNF-α or IL-1β from BCG stimulated splenocytes. Overall, these studies indicate that lactoferrin is a useful and effective adjuvant to improve efficacy of the BCG vaccine, with potential to reduce related tissue damage and pulmonary histopathology.

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“…19,20) Other functions might relate to host primary defense mechanisms. [21][22][23] Among them, the anti-bacterial action of LF is considered to be caused through sequestra-tion of iron required for microbial growth. 24) Recently, chemopreventive ability of bovine LF (bLF) was demonstrated in chemically induced carcinogenesis in colon, [25][26][27] esophagus 28) and lung.…”

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confidence: 99%

Chemopreventive Effect of Bovine Lactoferrin on 4‐Nitroquinoline 1‐Oxide‐induced Tongue Carcinogenesis in Male F344 Rats

Tanaka

Kawabata

Kohno

et al. 2000

Japanese Journal of Cancer Research

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The modifying effects of dietary feeding of bovine lactoferrin (bLF) on tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. The activities of phase II detoxifying enzymes, glutathione S-transferase (GST) and quinone reductase (QR), polyamine content and ornithine decarboxylase (ODC) activity in the tongue were also examined for mechanistic analysis of possible modifying effects of bLF on carcinogenesis. At 7 weeks of age, all animals except those treated with bLF alone and untreated rats were given 20 ppm 4-NQO in drinking water for 8 weeks to induce tongue neoplasms. Starting 7 days before 4-NQO exposure, experimental groups were fed experimental diets containing bLF (0.2% and 2%) for 10 weeks ("initiation feeding"). Starting 1 week after the cessation of exposure to 4-NQO, the other experimental groups given 4-NQO and a basal diet were fed the experimental diets for 22 weeks ("postinitiation feeding"). At week 32, the incidence and multiplicity of tongue neoplasms in the "initiation feeding" groups of 0.2% and 2% bLF and the "post-initiation feeding" group of 0.2% bLF were lower than those of the 4-NQO alone group, but without statistical significance. However, "post-initiation feeding" of 2% bLF caused a significant reduction in the incidence (20% vs. 55%, P = = = =0.02418) and multiplicity (0.25± ± ± ±0.54 vs. 0.70 ± ± ± ±0.71, P< < < <0.05) of tongue squamous cell carcinoma (by 64%, P = = = =0.02418). bLF treatment elevated liver and tongue GST activities and liver QR activity. The "post-initiation feeding" with 2% bLF significantly decreased QR activity, proliferating cell nulcear antigen-positive index and ODC activity in the tongue. In addition, feeding with bLF decreased tongue polyamine content. These results suggest that bLF, when given at the 2% dose level during the post-initiation phase, exerts chemopreventive action against tongue tumorigenesis through modification of cell proliferation activity and/or the activities of detoxifying enzymes.

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Bovine lactoferrin induces both mucosal and systemic immune response in mice

Cited by 116 publications

References 0 publications

Liposomalization of Lactoferrin Enhanced It's Anti-inflammatory Effects via Oral Administration

Liposomalization of Lactoferrin Enhanced It's Anti-inflammatory Effects via Oral Administration

Lactoferrin enhanced efficacy of the BCG vaccine to generate host protective responses against challenge with virulent Mycobacterium tuberculosis

Chemopreventive Effect of Bovine Lactoferrin on 4‐Nitroquinoline 1‐Oxide‐induced Tongue Carcinogenesis in Male F344 Rats

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