The Predictive Value of Eosinophil Cationic Protein and Lactate Dehydrogenase in Asthma: A Comparative Study of Serum Versus Sputum

Obaidi, Amina Hamed Ahmad Al; Samarai, Abdul Ghani Mohamed Al; Al-Janabi, Jasim; Yahia, Abdulkareem

doi:10.1097/wox.0b013e3181b2fe64

Cited by 11 publications

(9 citation statements)

References 21 publications

(30 reference statements)

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“…Moreover, we also detected significant differential expression between the two responder groups in LDHC ( Fig 4B ). The level of lactate dehydrogenase level in sputum has been established as a diagnostic marker for asthma [ 28 , 29 ], and our data suggest that it might also be a useful marker for steroid treatment response. Among all verified sites, no CpG sites were found to be strongly associated with poorly controlled asthma (ACT score), or base line asthma symptom scores.…”

Section: Discussionmentioning

confidence: 60%

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Nasal DNA methylation differentiates corticosteroid treatment response in pediatric asthma: A pilot study

et al. 2017

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BackgroundTreatment response to systemic corticosteroid in asthmatic children is heterogeneous and may be mediated by epigenetic mechanism(s). We aim to identify DNA methylation (DNAm) changes responsive to steroid, and DNAm biomarkers that distinguish treatment response.Materials and methodsWe followed 33 children (ages 5–18) presenting to the Emergency Department (ED) for asthma exacerbation. Based on whether they met discharge criteria in ≤24 hours, participants were grouped into good and poor responders to steroid treatment. Nasal samples were collected upon presentation to the ED (T0) and 18–24 hours later (T1). Genome-wide DNAm was measured for both time points in 20 subjects, and compared between T0 and T1 in good and poor responders respectively. DNAm at T1 was also compared between two responder groups. DNAm of selected CpGs was verified in the complete cohort, and expression of associated genes was examined. Interactions between DNAm, common single nucleotide polymorphism (SNP) located at the CpG sites and treatment responses were assessed.ResultsThree CpGs located in the OTX2 promoter showed responder-specific DNAm changes from T0 to T1, in which DNAm decreased in good but not in poor responders. Good and poor responders showed differential DNAm at T1 in 127 CpGs without and 182 CpGs with common SNP co-localization. Negative correlations between DNAm and gene expression were observed at CpGs located within the LDHC promoter, suggesting an impact of DNAm on gene regulation. Interactions between SNPs, DNAm and treatment response were detected.ConclusionAcute systemic steroid treatment modifies nasal DNAm in good responders. Nasal DNAm, dependent or independent of SNPs, can differentiate response to treatment in acute asthmatic children.

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Section: Discussionmentioning

confidence: 60%

“…LDHC encodes lactate dehydrogenase and is highly expressed in asthmatics. Its level in sputum has been established as a diagnostic marker for asthma [ 28 , 29 ]. DNHD1 encodes Dynein Heavy Chain Domain 1, which is a protein complex that is involved in microtubule movement and expressed in the lung.…”

Section: Resultsmentioning

confidence: 99%

Nasal DNA methylation differentiates corticosteroid treatment response in pediatric asthma: A pilot study

et al. 2017

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“…The ToxinPred server also identi ed L4 as being toxic. While performing in silico analysis to assess antigenicity and toxicity of epitopes located on the huPrP 3D structure, we also noticed that some antigenic epitopes were predicted to be allergenic by AllergenFP [52] and AllerTop [51] L10 (76)(77)(78)(79)(80)(81)(82)(83)(84)(85)(86) with AllerTop server. Of interest, L4 was mapped to the neurotoxic antibodies POM1 and ICSM18 and L2 was mapped to ICSM35 and POM3 while L9 and L10 were both mapped to POM2.…”

Section: Discussionmentioning

confidence: 94%

“…Among the identi ed allergenic-related proteins, VIM was found to be involved in the progression of allergic diseases via in ammasome [74,75] and VIM-P38MAPK complex facilitates mast cell activation via FcϵRI/CCR1 activation [76]. LDHA was identi ed as a potential marker in allergic alveolitis, airway in ammation, allergic encephalomyelitis, asthma disease [77][78][79][80]. PRDX1 was found as a negative regulator of in ammation [81], Th2-type airway in ammation, and allergen-related hyperresponsiveness [82].…”

Section: Gene Ontology (Go) Analysis Of Allergy Related Proteins Assomentioning

confidence: 99%

Treatment of Microglia with Anti-PrP Antibodies Induces Neuronal Allergenicity

Adhikari

Sakiz

Habiba

et al. 2020

Preprint

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Background: Previous reports identified proteins associated with ‘apoptosis’ following cross-linking PrPC with motif-specific anti-PrP antibodies in vivo and in vitro. The molecular mechanisms underlying this IgG-mediated neurotoxicity and the role of the activated proteins in the apoptotic pathways leading to neuronal death has not been properly defined. Previous reports implicated a number of proteins, including apolipoprotein E, cytoplasmic phospholipase A2, prostaglandin and calpain with anti-PrP antibody-mediated ‘apoptosis’, however, these proteins are also known to play an important role in allergy. In this study, we investigated whether cross-linking PrPC with anti-PrP antibodies stimulates a neuronal allergenic response.Methods: Initially, we predicted the allergenicity of the epitope sequences associated with ‘neurotoxic’ anti-PrP antibodies using allergenicity prediction servers. We then investigated whether anti-PrP antibody treatment of neuronal (N2a) and microglia (N11) cell lines leads to a neuronal allergenic response.Results: We found that both tail- and globular-epitopes were allergenic. Specifically, binding regions that contain epitopes for ‘neurotoxic’ antibodies such as ICSM18 (146-159), ICSM35 (91-110), POM 1 (138-147), POM 2 (57-88) and POM 3 (95-100) lead to activation of allergenic related proteins. Following direct application of anti-PrPC antibodies on N2a cells, mass spectrometry analysis identified 4 neuronal allergenic-related proteins when compared with untreated cells. Furthermore, mass spectrometry analysis identified 8 neuronal allergenic-related proteins following cross-linking N11 cells with anti-PrPC antibodies prior to co-culture with N2a cells, when compared with untreated cells. Of importance, we showed that the allergenic effects triggered by the anti-PrP antibodies were more potent when antibody-treated microglia were co-cultured with the neuroblastoma cell line. Furthermore, in both direct and co-culture with antibody-treated microglia, we demonstrate that the allergenic proteome was part of the PrPC-interactome. Conclusions: This study showed for the first time that anti-PrP antibody binding to PrPC triggers a neuronal allergenic response (we termed ‘IgG-Mediated Neuronal Allergenic Toxicity’) and highlights the important role of microglia in triggering IgG-mediated neuronal allergenic toxicity. Moreover, this study provides an important impetus for including allergenic assessment of therapeutic antibodies for neurodegenerative to derive safe and targeted biotherapeutics.

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“…[2][3][4] Even in asymptomatic periods asthmatic lungs show evidence of inflammation compared to controls and there is much interest in how chronic or repeated episodes of inflammation which associated by induction of different mediators that may cause remodeling of the airways and supporting vasculature leading to disease progression. [4][5][6] Asthma is a complex chronic inflammatory and immunologically mediated disease of the airways that involves the activation of many inflammatory and structural cells all of which release inflammatory mediators that result in the typical pathophysiological changes of asthma. [7,8] The airway inflammation underlying asthma is regulated by a network of mutually interacting cytokines.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Interleukin- 5 in Mild and Moderate Asthmatic Patients Following Corticosteroid Therapy

Salih¹,

Alnuaemi²

2018

IJMS

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Background: Asthma is a very common chronic disease in Iraqi community. Involving the respiratory system in which the airways occasionally constrict, become inflamed, and are lined with excessive amounts of mucus often in response to one or more triggers. Aim: this study was conducted to determine the role of interleukin 5 as asthmatic biomarker in Iraqi community in order to target the trait. Patients and Methods: Serum level of interleukin-5 [SIL-5] which is one of the inflammatory markers in asthma was estimated in 90 persons including those with asthma on steroid therapy (35 patients) and those without steroid (35 patients) therapy and the healthy control group (20 persons). Results: The mean level of SIL-5 was high in moderate asthmatic patients without steroid in their treatment protocol (16.56 pg/ml), while it was less in mild asthmatic patients without steroid therapy. SIL-5 mean values were lower in mild and moderate asthmatic patients who receive steroid therapy (3.94 pg/ml, 4.10 pg/ml respectively). While it was least in the control healthy group (3.32 pg/ml). Conclusion: serum IL-5 is predictive biomarkers for asthma severity and treatment response monitoring in Iraqi subjects with asthma

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The Predictive Value of Eosinophil Cationic Protein and Lactate Dehydrogenase in Asthma: A Comparative Study of Serum Versus Sputum

Cited by 11 publications

References 21 publications

Nasal DNA methylation differentiates corticosteroid treatment response in pediatric asthma: A pilot study

Nasal DNA methylation differentiates corticosteroid treatment response in pediatric asthma: A pilot study

Treatment of Microglia with Anti-PrP Antibodies Induces Neuronal Allergenicity

Evaluation of Interleukin- 5 in Mild and Moderate Asthmatic Patients Following Corticosteroid Therapy

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