Influence of protein expression system on elicitation of IgE antibody responses: Experience with lactoferrin

Almond, Rachael; Flanagan, Brian; Kimber, Ian; Dearman, Rebecca J.

doi:10.1016/j.tox.2012.06.018

Cited by 7 publications

(6 citation statements)

References 39 publications

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“…However, native human lactoferrin had antigenicity and generated specific IgG against human lactoferrin in mice, in which iron binding capacity or its glycosylation may contribute to its antigenicity (Almond et al. , ) Lactoferrin from cow milk has been correlated with the severity of atopic dermatitis (Röckmann et al. ).…”

Section: Discussionmentioning

confidence: 99%

“…Lactoferrin is generally considered to ameliorate the severity of inflammation and allergies (Hill and Newburg 2015;Giansanti et al 2016), and it has been reported that the single intranasal administration improved allergic rhinitis in mice (Wang et al 2013). However, native human lactoferrin had antigenicity and generated specific IgG against human lactoferrin in mice, in which iron binding capacity or its glycosylation may contribute to its antigenicity (Almond et al 2012(Almond et al , 2013 Lactoferrin from cow milk has been correlated with the severity of atopic dermatitis (R€ ockmann et al 2014). Therefore, the induction of allergic airway inflammation by human lactoferrin was anticipated.…”

Section: Discussionmentioning

confidence: 99%

“…However, native human lactoferrin had antigenicity in mice and generates specific IgG, in which iron binding capacity or its glycosylation may contribute to its antigenicity (Almond et al. , ). When lactoferrin from human or other animal origins is administered into blood or mucosal tissue, it may become an allergen.…”

Section: Introductionmentioning

confidence: 99%

“…The amelioration of inflammation has been attributed to decreases in the generation of O 2 - (Britigan et al 1994) and the down-regulated expression of TNFa (Baveye et al 1999), IL-1b (Legrand et al 2004), and IL-6 and IL-8 (Zimecki et al 1998). However, native human lactoferrin had antigenicity in mice and generates specific IgG, in which iron binding capacity or its glycosylation may contribute to its antigenicity (Almond et al 2012(Almond et al , 2013. When lactoferrin from human or other animal origins is administered into blood or mucosal tissue, it may become an allergen.…”

Section: Introductionmentioning

confidence: 99%

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Human lactoferrin induces asthmatic symptoms in NC/Nga mice

et al. 2017

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Lactoferrin in commercial supplements is known to exert anti‐viral and anti‐allergic effects. However, this is the first study to evaluate the induction of allergic airway inflammation in NC/Nga mice. Human lactoferrin was administered intraperitoneally with aluminum oxide for sensitization. Five days later, lactoferrin was inoculated intranasally for 5 days, and then on the 12th day, the single inoculation of lactoferrin intranasally was performed as a challenge. On the 13th day, airway hypersensitivity was assessed (AHR), a bronchoalveolar fluid (BALF) cell analysis was conducted, serum IgE and serum lactoferrin‐specific IgG and IgE levels as well as the mRNA expression levels of cytokines and chemokines in the lung were measured, and a histopathological analysis of the lung was performed. Human lactoferrin increased AHR, the number of eosinophils in BALF, serum lactoferrin‐specific IgG levels, and the mRNA levels of IL‐13, eotaxin 1, and eotaxin 2. Moreover, the accumulation of inflammatory cells around the bronchus and the immunohistochemical localization of arginase I and human lactoferrin were detected. Collectively, these results indicate that human lactoferrin induced allergic airway inflammation in mice. Therefore, the commercial use of human lactoferrin in supplements warrants more intensive study.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Human lactoferrin induces asthmatic symptoms in NC/Nga mice

et al. 2017

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“…These included 2 studies of apples engineered to have weaker Mal d 1 expression, which showed decreased apple sensitization and decreased symptoms after ingestion as measured on a visual analog scale compared with conventional apples. 96,110 In addition, 2 studies of GM peanut, 95,96 2 of rice, 69,72 and single studies of GM egg and tomato showed weaker IgE binding to the GM product compared with the conventional product. 108,110 In reference to the second query ("Is the use of GMO products, compared with conventional counterparts, associated with the development of allergic disease or a risk of development of allergic disease?…”

Section: Studies Demonstrating No Harm or Potential Benefitmentioning

confidence: 99%

The allergenicity of genetically modified foods from genetically engineered crops

Dunn

Vicini

Glenn

et al. 2017

Annals of Allergy, Asthma & Immunology

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INSTRUCTIONSCredit can now be obtained, free for a limited time, by reading the review article and completing all activity components. Please note the instructions listed below:Review the target audience, learning objectives and all disclosures.Complete the pre-test.Read the article and reflect on all content as to how it may be applicable to your practice.Complete the post-test/evaluation and claim credit earned. At this time, physicians will have earned up to 1.0 AMA PRA Category 1 Credit TM . Minimum passing score on the post-test is 70%. Overall Purpose Participants will be able to demonstrate increased knowledge of the clinical treatment of allergy/asthma/immunology and how new information can be applied to their own practices. Learning ObjectivesAt the conclusion of this activity, participants should be able to:Recognize the testing and safety features that genetically modified products are subject to in determining their allergenicity Identify the basis and rationale for genetic modification Review the evidence regarding genetically modified products and any association with food allergy Release position to control or influence the content of an activity must disclose all relevant financial relationships with any commercial interest that have occurred within the past 12 months. All identified conflicts of interest must be resolved and the educational content thoroughly vetted for fair balance, scientific objectivity, and appropriateness of patient care recommendations. It is required that disclosure be provided to the learners prior to the start of the activity. Individuals with no relevant financial relationships must also inform the learners that no relevant financial relationships exist. Learners must also be informed when off-label, experimental/ investigational uses of drugs or devices are discussed in an educational activity or included in related materials. Disclosure in no way implies that the information presented is biased or of lesser quality. It is incumbent upon course participants to be aware of these factors in interpreting the program contents and evaluating recommendations. Moreover, expressed views do not necessarily reflect the opinions of ACAAI. All identified conflicts of interest have been resolved.

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Evaluation of Antibody Properties and Clinically Relevant Immunogenicity, Anaphylaxis, and Hypersensitivity Reactions in Two Phase III Trials of Tralokinumab in Severe, Uncontrolled Asthma

Carlsson

Braddock

Li³

et al. 2019

Drug Saf

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Introduction Tralokinumab is a monoclonal antibody (mAb) that neutralizes interleukin (IL)-13, a cytokine involved in the pathogenesis of asthma. Objective The objectives of this study were to characterize the potential immunogenic properties of tralokinumab and report data for anti-drug antibodies (ADAs) and hypersensitivity reactions from two phase III clinical trials. Methods The oligosaccharide structure of tralokinumab, Fab-arm exchange, and ADAs were characterized by standard techniques. Hypersensitivity adverse events (AEs) were evaluated in two pivotal clinical trials of tralokinumab in severe, uncontrolled asthma: STRATOS 1 and 2 (NCT02161757 and NCT02194699). Results No galactose-α-1,3-galactose (α-Gal) epitopes were found in the Fab region of tralokinumab and only 4.5% of glycoforms contained α-Gal in the Fc region. Under non-reducing conditions, Fab-arm exchange did not take place with another immunoglobulin (Ig) G 4 mAb (mavrilimumab). However, following glutathione reduction, a hybrid antibody with monovalent bioactivity was detected. ADA incidences (titers) were as follows: STRATOS 1—every 2 weeks (Q2 W) 0.8% (26.0), every 4 weeks (Q4 W) 0.5% (26.0), placebo 0.8% (52.0); STRATOS 2—Q2 W 1.2% (39.0), placebo 0.8% (13.0). Participant-reported hypersensitivity AE rates were as follows: STRATOS 1—Q2 W 25.9%, Q4 W 25.0%, placebo 25.5%; STRATOS 2—Q2 W 13.2%, placebo 9.0%. External evaluation for anaphylaxis by Sampson criteria found no tralokinumab-related severe hypersensitivity or anaphylaxis reactions. Conclusion Preclinical assessments suggested a low likelihood of immunogenicity for tralokinumab. In STRATOS 1 and 2, ADA incidence was low, no differences were found between tralokinumab-treated and placebo groups in reporting of hypersensitivity reactions, and there were no Sampson criteria-evaluated anaphylaxis events with tralokinumab treatment. Together, the results suggest that tralokinumab treatment would not increase the risk for severe hypersensitivity or anaphylactic reactions. Electronic supplementary material The online version of this article (10.1007/s40264-018-00788-w) contains supplementary material, which is available to authorized users.

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Influence of protein expression system on elicitation of IgE antibody responses: Experience with lactoferrin

Cited by 7 publications

References 39 publications

Human lactoferrin induces asthmatic symptoms in NC/Nga mice

Human lactoferrin induces asthmatic symptoms in NC/Nga mice

The allergenicity of genetically modified foods from genetically engineered crops

Evaluation of Antibody Properties and Clinically Relevant Immunogenicity, Anaphylaxis, and Hypersensitivity Reactions in Two Phase III Trials of Tralokinumab in Severe, Uncontrolled Asthma

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