Interleukin-17A expression in patients presenting with nasal polyposis

Brazilian Journal of Otorhinolaryngology

Print version ISSN 1808-8694

Braz. j. otorhinolaryngol. vol.79 no.5 São Paulo Sept./Oct. 2013

http://dx.doi.org/10.5935/1808-8694.20130110 

ORIGINAL ARTICLES

Melissa Ameloti Gomes Avelino1, Isabela Jubé Wastowski2, Ricardo Gimenes Ferri3, Thaís Gomes Abrahão Elias4, Ana Paula Lindoso Lima4, Larissa Mesquita Nunes5, Shirley Shizue Nagata Pignatari6

¹PhD; Adjunct Professor - Federal University of Goiás.

²2 PhD; Professor - State University of Goiás

³MSc; Professor - Pontifical Catholic University of Goiás.

⁴Medical Student - Pontifical Catholic University of Goiás.

⁵Medical Student - Pontifical Catholic University of Goiás.

⁶MD; PhD; Professor - Federal University of São Paulo.

ABSTRACT

Sinonasal polyposis (SNP) is a chronic inflammatory pathology of the nasal/paranasal cavities which affects from 1%-4% of the population. Although polyps seem to be a manifestation of chronic inflammation of nasal/paranasal sinus mucosa in both allergic and non-allergic subjects, the pathogenesis of nasal polyposis remains unknown. Interleukin-17A (IL-17A) is a key inflammatory cytokine in many disorders. Little attention has been paid to the role of IL-17A in chronic inflammatory disorders.

OBJECTIVE:

To investigate the expression of IL-17A in the SNP and verify if this expression is a marker of good or bad prognosis.

METHOD:

Prospective study with 25 patients presenting with SNP were subjected to the immunohistochemistry technique. After a skin prick test, all patients were divided into atopic and nonatopic groups, and asthmatic or non-asthmatic.

RESULTS:

The IL-17A expression was observed in both atopic and nonatopic patients. The numbers of IL-17A positive cells were greater in nasal polyps of atopic patients than nonatopic (p = 0.0128).

CONCLUSION:

These results indicate that IL-17A may play an important role in the pathology of SNP. Considering the inflammatory properties of IL-17A, this study suggests that it could increase susceptibility to atopy and asthma.

Keywords: allergy and immunology; interleukin-17; nasal polyps

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Measles virus-derived peptide/food antigen adducts facilitate the establishment of antigen specific oral tolerance

J Physiol Pharmacol. 2013 Feb;64(1):95-102.

He C, Song CH, Cheng L, Chen T, Liu C, Liu Z, Yang PC.

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Abstract

Allergy is a skewed T helper (Th)2 polarization response in the body; its treatment is not satisfactory currently. Oral tolerance dysfunction plays a critical role in the pathogenesis of allergy. The present study aims to restore the breached intestinal tolerance with an artificial adduct of a measles virus C protein-derived small peptide (MVCP) and a model antigen, ovalbumin (MOA), and to observe the effect of MOA on inhibition of intestinal allergy in a mouse model. The MOA was formed by the MVCP and ovalbumin. The effect of MOA on regulation of the properties of dendritic cells (DC) and CD4(+) T cells was observed with a cell culture model and a mouse model of the gut Th2 pattern inflammation. After treatment with MOA, mouse intestinal DCs showed high levels of aldehyde dehydrogenase (ALDH) activity and expressed transforming growth factor (TGF)-beta; the frequency of Treg in the intestine was also significantly increased. The treatment with MOA efficiently suppressed the antigen-specific Th2 pattern inflammation in the intestine. Administration with the MOA can induce the development of antigen-specific oral tolerance and inhibit the antigen-specific allergic reaction in the intestine. The adduct of MOA has the therapeutic potential for the allergen related immune inflammation.

PMID:

 

23568976

 

[PubMed - indexed for MEDLINE] 

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A case of losartan induced angioedema

CASE REPORT
Year : 2010  |  Volume : 64  |  Issue : 2  |  Page : 81-84

A case of losartan induced angioedema

Chitra Nair
Heavy Water Plant Kota, PO Anushakti, Via Kota, Rajasthan, India

Date of Web Publication

28-Mar-2012

Correspondence Address:
Chitra Nair
M 18 RH 4, Sector 6, Vashi, Navi Mumbai
India

DOI: 10.4103/0019-5359.94404

¤ Abstract

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) target the renin-angiotensin system and are used in the management of hypertension. Both classes of drugs have similar side effects. ARBs are considered to be much better tolerated than ACE inhibitors with lesser incidence of side effects. Angioedema is a very rare side effect associated with ACE inhibitors (ACEI) and even rarer so with ARBs. The cause for angioedema in ACE inhibitors is said to be the rise in bradykinin levels. It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown. We present here a rare case of late onset angioedema associated with losartan (an ARB) in a female patient. She had been started on an ARB as a first line treatment for uncomplicated mild to moderate hypertension. She had no prior exposure to ACE inhibitors and did not have any other significant medical history. Though rare angioedema is a serious recognized side effect of ARB therapy and the patients started on them should be warned to look for the early signs so as to take corrective action.

Keywords: Losartan, angiotensin receptor blocker, angioedema

How to cite this article: Nair C. A case of losartan induced angioedema. Indian J Med Sci 2010;64:81-4

How to cite this URL: Nair C. A case of losartan induced angioedema. Indian J Med Sci [serial online] 2010 [cited 2014 Feb 10];64:81-4. Available from: http://www.indianjmedsci.org/text.asp?2010/64/2/81/94404

Asthma: Gln27Glu and Arg16Gly polymorphisms of the beta2-adrenergic receptor gene as risk factors

Research

Ana Carolina de Paiva, Fernando Augusto Marson, José Dirceu Ribeiro and Carmen Sílvia Bertuzzo

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Allergy, Asthma & Clinical Immunology 2014, 10:8  doi:10.1186/1710-1492-10-8

Published: 5 February 2014

Abstract (provisional)

Background

Asthma is caused by both environmental and genetic factors. The ADRB2 gene, which encodes the beta 2-adrenergic receptor, is one of the most extensively studied genes with respect to asthma prevalence and severity. The Arg16Gly (+46A > G) and Gln27Glu (+79C > G) polymorphisms in the ADRB2 gene cause changes in the amino acids flanking the receptor ligand site, altering the response to bronchodilators and the risk of asthma through complex pathways. The ADRB2 polymorphisms affect beta-adrenergic bronchodilator action and are a tool to identify at-risk populations.

Objective

To determine the frequency of these two polymorphisms in allergic asthma patients and healthy subjects and to correlate these data with the occurrence and severity of asthma.

Methods

Eighty-eight allergic asthma patients and 141 healthy subjects were included in this study. The ADRB2 polymorphisms were analyzed using the amplification-refractory mutation system - polymerase chain reaction (ARMS-PCR) technique. The statistical analysis was performed with the SPSS 21.0 software using the Fisher's Exact and chi2 tests.

Results

The ADRB2 polymorphisms were associated with asthma occurrence. The Arg16Arg, Gln27Gln and Gln27Glu genotypes were risk factors; the odds ratios were 6.782 (CI = 3.07 to 16.03), 2.120 (CI = 1.22 to 3.71) and 8.096 (CI = 3.90 to 17.77), respectively. For the Gly16Gly and Glu27Glu genotypes, the odds ratios were 0.312 (CI = 0.17 to 0.56) and 0.084 (CI = 0.04 to 0.17), respectively. The haplotype analysis showed that there were associations between the following groups: Arg16Arg-Gln27Gln (OR = 5.108, CI = 1.82 to 16.37), Gly16Gly-Glu27Glu (OR = 2.816, CI = 1.25 to 6.54), Arg16Gly-Gln27Glu (OR = 0.048, CI = 0.01 to 0.14) and Gly16Gly-Gln27Glu (OR = 0.1036, CI = 0.02 to 0.39). The polymorphism Gln27Glu was associated with asthma severity, as the Gln27Gln genotype was a risk factor for severe asthma (OR = 2.798, CI = 1.099 to 6.674) and the Gln27Glu genotype was a protective factor for mild (OR = 3.063, CI = 1.037 to 9.041) and severe (OR = 0.182, CI = 0.048 to 0.691) asthma.

Conclusions

The Arg16Gly and Gln27Glu polymorphisms in the ADRB2 gene are associated with asthma presence and severity.

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Evaluation of a Multiplex ELISA for Autoantibody Profiling in Patients with Autoimmune Connective Tissue Diseases

Autoimmune Diseases
Volume 2014 (2014), Article ID 896787, 6 pages
http://dx.doi.org/10.1155/2014/896787

Research Article

Alejandro Caro Pérez,¹ Sarita Kumble,² Krishnanand D. Kumble,² M. Consuelo Alonso Cañizal,¹ Luis M. Jiménez Jiménez,³ Lorena Alonso Díez,¹ and Pilar Durán Parejo³

¹Gennova Research, Gennova Scientific S.L. Seville, Spain
²Pictor Limited, Auckland, New Zealand
³Department of Metabolopathy, Hospital Virgen del Rocio, Seville, Spain

Received 4 October 2013; Accepted 30 October 2013; Published 16 January 2014

Academic Editor: Ricard Cervera

Copyright © 2014 Alejandro Caro Pérez et al. This is an open access article distributed under theCreative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The performance of immunoassays for the detection of autoantibodies is of critical importance in the diagnosis and assessment of patients with autoimmune connective tissue diseases (ACTD). Our objective was to compare the features of two multiplexed assays—INNO-LIA ANA and Gennova-PictArray ENA ELISA—for measurement of multiple autoantibodies and their utility as a clinical tool in ACTD diagnosis. The antigens included SS-A/Ro (60 and 52), SSB/La, Sm, Sm/RNP, CENP-B, Jo-1, and Scl-70. Stored sera from 85 ACTD patients and 80 controls consisting of patients with vasculitis, rheumatoid arthritis and infectious diseases, as well as healthy subjects were analyzed jointly with clinical and laboratory data. Agreement between the two methods varied between 58 and 99% (Cohen’s kappa: 0.21–0.71) mostly for SSA and SSB. The frequency of specific autoantibodies measured using the two methods was more variable for SSA, SSB, and RNP/Sm. There were a higher number of ambiguous results when using INNO-LIA. The optimized cut-off values of the Gennova-PictArray resulted in over 99% specificities in samples obtained from the control group. Sensitivity patterns were more accurate in Gennova-PictArray than in INNO-LIA, as suggested in previously reported studies. A third method could be applied to determine which of the two methods is more accurate.

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Short report

New efficacy of LTRAs (montelukast sodium): it possibly prevents food-induced abdominal symptoms during oral immunotherapy

Masaya Takahashi, Shoichiro Taniuchi^*, Kazuhiko Soejima, Kyoko Sudo, Yasuko Hatano andKazunari Kaneko

• *Corresponding author: Shoichiro Taniuchi taniuchi@takii.kmu.ac.jp

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Allergy, Asthma & Clinical Immunology 2014, 10:3  doi:10.1186/1710-1492-10-3

Published: 17 January 2014

Abstract

Background

The aim of the study was to elucidate whether leukotriene receptor antagonists (LTRAs) can prevent severe allergic reactions, which occur during oral immunotherapy (OIT) in children with food allergies.

Findings

Five children with food allergies [3 allergic to hen’s egg (HE), 1 to wheat, and one to cow’s milk (CM); aged between 7 and 12 years; median, 8.5 years] who were started on LTRAs during OIT were retrospectively selected from among 63 children undergoing OIT. In the rush phase, after the administration of the initial dose which was set in open food challenge test, the subsequent doses were increased by approximately 1.2 times of the previous dose and were administered every 2 hours, 4 times a day. The target doses of hen’s egg, wheat (udon noodle), and cow’s milk in the rush phase were 50 g, 200 g, and 200 ml, respectively. The ingestion of the target dose was continued at home every day for at least a year in the maintained phase.

Four participants experienced intractable abdominal pain during the rush phase; therefore, the loading dose was not increased in these children. However, the administration of LTRAs prevented their symptoms, resulting in the completion of the rush phase. One participant also experienced intractable abdominal pain during the maintenance phase. After receiving LTRAs, the target dose was able to tolerated.

Conclusion

The findings from this retrospective study suggest that the administration of LTRAs is useful for the prevention of adverse allergic reactions such as abdominal pain during OIT.

Keywords: 

Abdominal pain; Food allergy; LTRA (montelukast sodium); Rush oral immunotherapy

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• Int J Mol Sci
• v.15(1); Jan 2014
• PMC3907844

Int J Mol Sci. 2014 January; 15(1): 878–894.

Published online 2014 January 9. doi:  10.3390/ijms15010878

PMCID: PMC3907844

Effect of Nanoparticles Exposure on Fractional Exhaled Nitric Oxide (FENO) in Workers Exposed to Nanomaterials

Wei-Te Wu,1,† Hui-Yi Liao,1,† Yu-Teh Chung,1 Wan-Fen Li,2 Tsui-Chun Tsou,1 Lih-Ann Li,1 Ming-Hsiu Lin,3 Jiune-Jye Ho,3 Trong-Neng Wu,1,4 and Saou-Hsing Liou1,5,6,*

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Abstract

Fractional exhaled nitric oxide (FENO) measurement is a useful diagnostic test of airway inflammation. However, there have been few studies of FENO in workers exposed to nanomaterials. The purpose of this study was to examine the effect of nanoparticle (NP) exposure on FENO and to assess whether the FENO is increased in workers exposed to nanomaterials (NM). In this study, both exposed workers and non-exposed controls were recruited from NM handling plants in Taiwan. A total of 437 subjects (exposed group = 241, non-exposed group = 196) completed the FENO and spirometric measurements from 2009–2011. The authors used a control-banding (CB) matrix to categorize the risk level of each participant. In a multivariate linear regression analysis, this study found a significant association between risk level 2 of NP exposure and FENO. Furthermore, asthma, allergic rhinitis, peak expiratory flow rate (PEFR), and NF-κB were also significantly associated with FENO. When the multivariate logistic regression model was adjusted for confounders, nano-TiO2 in all of the NM exposed categories had a significantly increased risk in FENO > 35 ppb. This study found associations between the risk level of NP exposure and FENO (particularly noteworthy for Nano-TiO2). Monitoring FENO in the lung could open up a window into the role nitric oxide (NO) may play in pathogenesis.

Keywords: nanoparticles, nanomaterials, workers’s respiratory health, airway inflammation, Fractional exhaled nitric oxide, occupational epidemiology

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Abstract

Fractional exhaled nitric oxide (FENO) measurement is a useful diagnostic test of airway inflammation. However, there have been few studies of FENO in workers exposed to nanomaterials. The purpose of this study was to examine the effect of nanoparticle (NP) exposure on FENO and to assess whether the FENO is increased in workers exposed to nanomaterials (NM). In this study, both exposed workers and non-exposed controls were recruited from NM handling plants in Taiwan. A total of 437 subjects (exposed group = 241, non-exposed group = 196) completed the FENO and spirometric measurements from 2009–2011. The authors used a control-banding (CB) matrix to categorize the risk level of each participant. In a multivariate linear regression analysis, this study found a significant association between risk level 2 of NP exposure and FENO. Furthermore, asthma, allergic rhinitis, peak expiratory flow rate (PEFR), and NF-κB were also significantly associated with FENO. When the multivariate logistic regression model was adjusted for confounders, nano-TiO2 in all of the NM exposed categories had a significantly increased risk in FENO > 35 ppb. This study found associations between the risk level of NP exposure and FENO (particularly noteworthy for Nano-TiO2). Monitoring FENO in the lung could open up a window into the role nitric oxide (NO) may play in pathogenesis.

Keywords: 

Research

dsRNA-induced changes in gene expression profiles of primary nasal and bronchial epithelial cells from patients with asthma, rhinitis and controls

Ariane H Wagener, Aeilko H Zwinderman, Silvia Luiten, Wytske J Fokkens, Elisabeth H Bel,Peter J Sterk and Cornelis M van Drunen

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Respiratory Research 2014, 15:9  doi:10.1186/1465-9921-15-9

Published: 29 January 2014

Abstract (provisional)

Background

Rhinovirus infections are the most common cause of asthma exacerbations. The complex responses by airway epithelium to rhinovirus can be captured by gene expression profiling. We hypothesized that: a) upper and lower airway epithelium exhibit differential responses to double-stranded RNA (dsRNA), and b) that this is modulated by the presence of asthma and allergic rhinitis.

Objectives

Identification of dsRNA-induced gene expression profiles of primary nasal and bronchial epithelial cells from the same individuals and examining the impact of allergic rhinitis with and without concomitant allergic asthma on expression profiles.

Methods

This study had a cross-sectional design including 18 subjects: 6 patients with allergic asthma with concomitant rhinitis, 6 patients with allergic rhinitis, and 6 healthy controls. Comparing 6 subjects per group, the estimated false discovery rate was approximately 5%. RNA was extracted from isolated and cultured primary epithelial cells from nasal biopsies and bronchial brushings stimulated with dsRNA (poly(I:C)), and analyzed by microarray (Affymetrix U133+ PM Genechip Array). Data were analysed using R and the Bioconductor Limma package. Overrepresentation of gene ontology groups were captured by GeneSpring GX12.

Results

In total, 17 subjects completed the study successfully (6 allergic asthma with rhinitis, 5 allergic rhinitis, 6 healthy controls). dsRNA-stimulated upper and lower airway epithelium from asthma patients demonstrated significantly fewer induced genes, exhibiting reduced down-regulation of mitochondrial genes. The majority of genes related to viral responses appeared to be similarly induced in upper and lower airways in all groups. However, the induction of several interferon-related genes (IRF3, IFNAR1, IFNB1, IFNGR1, IL28B) was impaired in patients with asthma.

Conclusions

dsRNA differentially changes transcriptional profiles of primary nasal and bronchial epithelial cells from patients with allergic rhinitis with or without asthma and controls. Our data suggest that respiratory viruses affect mitochondrial genes, and we identified disease-specific genes that provide potential targets for drug development.

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