Colostrinin delays the onset of proliferative senescence of diploid murine fibroblast cells

Bácsi, Attila; Woodberry, Mitchell W.; Kruzel, Marian L.; Boldogh, István

doi:10.1016/j.npep.2006.12.004

Cited by 16 publications

(21 citation statements)

References 44 publications

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“…In CLN-conditioned mice, the extent of IgE/IgG1 production, cutaneous reactions and airway inflammation was significantly more decreased in RWE-challenged animals than in HDME-exposed mice. CLN-mediated decreases in inflammatory responses to RWE may be explained by the fact that CLN-treated cells have an increased ability to cope with oxidative stress [8, 11, 46]. To a lesser degree, CLN conditioning also decreased HDME-mediated inflammatory responses, although HDME contains proteases to invade the site of exposure and potentiate allergic immune responses [36, 47].…”

Section: Discussionmentioning

confidence: 99%

“…CLN protects neuroblastoma cells from β-amyloid-induced apoptosis by inhibiting amyloid aggregation [10]. CLN delays the onset of proliferative senescence of diploid murine fibroblast cells [11]. Moreover, CLN administration to Alzheimer’s disease patients has resulted in stabilization of cognitive functions and improvement in the ability to perform routine domestic functions [12,13,14].…”

Section: Introductionmentioning

confidence: 99%

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Colostrinin Decreases Hypersensitivity and Allergic Responses to Common Allergens

Boldogh¹,

Aguilera-Aguirre²,

Bácsi³

et al. 2008

Int Arch Allergy Immunol

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Background: Colostrinin™ (CLN), isolated from mothers’ pre-milk fluid (colostrum), is a uniform mixture of low-molecular-weight, proline-rich polypeptides. CLN induces neurite outgrowth of pheochromocytoma cells, extends the lifespan of diploid fibroblast cells, inhibits β-amyloid-induced apoptosis and improves cognitive functions when administered to Alzheimer’s disease patients. Objective: The aim of this study was to investigate potential allergic responses to CLN and its impact on allergic sensitization and inflammation caused by common allergens. Methods: We used a well-characterized mouse model of allergic airway inflammation. Changes in IgE/IgG1 and mucin levels, airway eosinophilia and hyperreactivity to methacholine were determined by ELISA, differential cell counting and whole-body plethysmography, respectively. Results: CLN did not increase IgE/IgG1 levels or induce cutaneous hypersensitivity reaction, airway inflammation and mucin production. Importantly, CLN significantly (p < 0.001) decreased IgE/IgG1 production, airway eosinophilia, mucin production and hypersensitivity induced by allergenic extracts from ragweed pollen grains and house dust mites. Conclusion: CLN itself is non-allergenic; however, it is effective in preventing allergic responses to known indoor and outdoor allergens. These data support the safe application of CLN and its potential use in the prevention of allergic inflammation in humans.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Colostrinin Decreases Hypersensitivity and Allergic Responses to Common Allergens

Boldogh¹,

Aguilera-Aguirre²,

Bácsi³

et al. 2008

Int Arch Allergy Immunol

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“…Most importantly, CLN induces complex signaling pathways and mediates cell differentiation in a manner comparable to hormones and neurotrophins [19]. It has also been shown to delay the onset of proliferative senescence in diploid murine and human fibroblast cells by protecting their mitochondria from age-associated changes [20]. CLN impacts on signaling pathways and modulates gene expression in cellular redox regulation, cell proliferation and differentiation [19][20][21].…”

Section: Introductionmentioning

confidence: 99%

“…It has also been shown to delay the onset of proliferative senescence in diploid murine and human fibroblast cells by protecting their mitochondria from age-associated changes [20]. CLN impacts on signaling pathways and modulates gene expression in cellular redox regulation, cell proliferation and differentiation [19][20][21]. These complex effects could explain the inhibition of amyloid β (Aβ) aggregation, the protection of cells from beta amyloid-induced apoptosis [22], and the improvement of cognitive function in Alzheimer's disease (AD) patients after CLN-treatment [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Effects of Colostrinin™ on gene expression-transcriptomal network analysis

Szaniszlo

Germán

Hajas

et al. 2009

International Immunopharmacology

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“…In the light of evidence demonstrating oxidative stress as an early event and a key factor in the pathogenesis of AD (Chauhan & Chauhan, 2006;Zhu et al, 2004), CLN's inhibition of reactive oxygen species and nitric oxide production can result in beneficial effects in AD therapy (Bacsi, Woodberry, Kruzel, & Boldogh, 2007;Boldogh et al, 2003;Mikulska & Lisowski, 2003;Zab"ocka, Janusz, Maca"a, & Lisowski, 2005). CLN may be a promising pharmacological agent, which suppresses microglial activation by affecting the differentiation/maturation process of cells of monocyte/macrophage lineage (Kubis, Marcinkowska, Janusz, & Lisowski, 2005) and affects not only adaptive, but also innate, immunity by regulation of secretion of inflammation mediators (Zab"ocka, Janusz, Maca"a, & Lisowski, 2007).…”

Section: Introductionmentioning

confidence: 99%