Interleukin-6 –174 G/C promoter gene polymorphism in nasal polyposis and asthma

Kosugi, E.M.; Camargo-Kosugi, C.M. de; Hirai, E.R.; Mendes-Neto, J.A.; Gregorio, L.C.; Guerreiro-da-Silva, I.D.C.; Weckx, L.L.M

doi:10.4193/rhin12.166

Cited by 16 publications

(11 citation statements)

References 28 publications

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“…In another study on the pathophysiology of nasal polyposis and asthma, the IL-6-174G/C SNP GG genotype was found more frequently in all nasal polyps and asthma groups (11).…”

Section: Discussionmentioning

confidence: 90%

Evaluation of autoinflammatory disease genes in nasal polyposis*

Köseoğlu¹,

Özcan²,

İkincioğulları³

et al. 2015

Turk J Med Sci

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Background/aim: To investigate cold-induced autoinflammatory syndrome 1 (CIAS1) gene polymorphisms that cause autoinflammatory diseases in patients with nasal polyposis (NP). Materials and methods:The study included 30 patients diagnosed with NP and 30 healthy age-matched individuals as a control group. CIAS1 polymorphisms were assessed by DNA sequence analysis. Patients with nasal polyps and the control group were compared in terms of gene polymorphisms. Each of the 8 polymorphisms of the CIAS1 gene was analyzed separately in the patient group. Results:The most frequently observed polymorphisms in the patient group were c.732G > A in 83%, c.663C > T in 23%, and c.1308C > A in 23% of the patients. c.732G > A polymorphism was evaluated separately. Guanine was transformed to adenine at the 732nd nucleotide position of the CIAS1 gene in the cDNA of chromosome 1. Conclusion:The CIAS1 gene c.732G > A polymorphism was thought to be responsible for an increase in disease susceptibility. The frequency of the "A" allele is higher in the patient group compared to the control group. Autoinflammatory diseases seem like a candidate to be one of these factors. This is the first report to define the role of autoinflammatory diseases among these factors.

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“…In another study on the pathophysiology of nasal polyposis and asthma, the IL-6-174G/C SNP GG genotype was found more frequently in all nasal polyps and asthma groups (11).…”

Section: Discussionmentioning

confidence: 90%

Evaluation of autoinflammatory disease genes in nasal polyposis*

Köseoğlu¹,

Özcan²,

İkincioğulları³

et al. 2015

Turk J Med Sci

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“…Although, no significant difference was observed in the distribution of homozygous and heterozygous genotypes of IL-6 (-174-G/C) polymorphism but GG acted as a prevalent genotype with a protective effect against allergy. Studies have explicitly described the prevalence of homozygous genotypes among the allergic population [29, 31].…”

Section: Discussionmentioning

confidence: 99%

“…Between high and low producing genotypes, former showed marked increase in SOCS3 mRNA level therefore it can be implied that IL-6 (-174-G/C) polymorphism has many aspects to be explored yet. Furthermore, the previous studies have indicated high producing genotype (GG) being linked to severity of the allergy [29, 31]. Despite being the low producing genotype, atopic cases with CC genotype had elevated IL-6 serum levels.…”

Section: Discussionmentioning

confidence: 99%

Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 (-174-G/C) polymorphism in atopic conditions

et al. 2019

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Hypersensitivity of the immune system is caused by elevated immunoglobulin E (IgE) levels in the serum, in response to a discrete allergen leading to allergic reactions. IgE-mediated inflammation is regulated by the cascade of defense related signaling molecules including interleukin-6 (IL-6) that plays pivotal role in the survival and maturation of mast cells during an allergic reaction. IL-6 mediated defense responses are tightly regulated by Suppressor of Cytokine Signaling 3 (SOCS3), an inhibitory molecules of Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) signaling, in a negative feedback mechanism. The given study focuses on the assessment of crosstalk between SOCS3 and IL-6 to unravel the molecular significance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. The expression study of SOCS3 through real-time PCR analysis revealed, a 5.9 mean fold increase in SOCS3 expression in atopic cases in comparison to control cases. Moreover, IL-6 has, also, been found significantly enhanced in the serum level of atopic cases (26.4 pg/ml) as compared to control cases (3.686 pg/ml). Female population was found to be at a higher risk to develop atopic condition than male population as females exhibited higher expression of both SOCS3 and IL-6 than males. Furthermore, the polymorphic study of IL-6 promoter region (IL-6 174-G/C) in atopic population has reasserted the importance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. Expression of SOCS3 and IL-6 serum levels were found to be highly correlated. Therefore establishing the role of IL-6 (-174-G/C) polymorphism on the expression of SOCS3 and IL-6 in atopic cases. Notably, the study established SOCS3 and IL-6 as potential targets for the diagnosis/prognosis of allergy and for the development of reliable therapeutic strategies to control atopic conditions in the near future.

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“…Also in this journal, a very relevant and interesting study of Bohman and colleagues clearly points to heredity as an important factor for development of nasal polyps (17) . Although a number of studies showed a higher prevalence of nasal polyps in diseases that clearly have a genetic cause like cystic fibrosis or Peutz-Jeghers syndrome in general polyps only gene polymorphism have been proven (18)(19)(20)(21) . Now it has been shown that nasal polyps have a 5 times higher prevalence in family members of polyp patients.…”

Section: How I Changed My Practice In the Last Five Years And What Ismentioning

confidence: 99%

How I changed my practice in the last five years and what is likely to change in the next five years

Fokkens¹

2015

Rhin

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Interleukin-6 –174 G/C promoter gene polymorphism in nasal polyposis and asthma

Cited by 16 publications

References 28 publications

Evaluation of autoinflammatory disease genes in nasal polyposis*

Evaluation of autoinflammatory disease genes in nasal polyposis*

Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 (-174-G/C) polymorphism in atopic conditions

How I changed my practice in the last five years and what is likely to change in the next five years

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