PMID- 38388670
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240225
IS  - 1710-1484 (Print)
IS  - 1710-1492 (Electronic)
IS  - 1710-1484 (Linking)
VI  - 20
IP  - 1
DP  - 2024 Feb 22
TI  - Association between interleukin-6-174G/C gene polymorphism and asthma severity: 
      exploring the role of total serum IgE, blood eosinophils, and FeNO as markers of 
      type 2 inflammation.
PG  - 15
LID - 10.1186/s13223-024-00880-0 [doi]
LID - 15
AB  - BACKGROUND: While a connection has been established between serum interleukin-6 
      (IL-6) levels and the IL-6 gene (- 174G/C) polymorphism in allergic diseases such 
      as asthma, its specific association with severe asthma remains unexplored. This 
      study examined the relationship between the IL-6 (- 174G/C) gene polymorphism and 
      mild and severe asthma, focusing on its influence on type 2 inflammation. 
      METHODS: Our study comprised 98 patients with mild asthma and 116 with severe 
      asthma. Additionally, we recruited 121 healthy participants to serve as controls 
      for comparative analyses. The IL-6 gene (- 174G/C) polymorphism was assessed 
      utilizing the polymerase chain reaction-restriction fragment length polymorphism 
      (PCR-RFLP) method. RESULTS: In our study, the risk of mild asthma exhibited a 
      significant fourfold increase in individuals with the GG genotype pattern 
      compared to healthy controls, yielding an odds ratio (OR) of 4.4 (p < 0.001). 
      Conversely, we found no significant correlation between the IL-6 - 174G/C gene 
      polymorphism and severe asthma when compared to the healthy control group. 
      However, a noteworthy pattern emerged when we compared subgroups of mild and 
      severe asthma. The risk of severe asthma increased fivefold in individuals with 
      the GC polymorphism pattern, with an OR of 4.99 (p < 0.001), while the likelihood 
      of mild asthma showed a similar fourfold increase with the GG polymorphism 
      pattern, OR = 4.4 (p < 0.001). Consequently, we observed a significantly higher 
      frequency of the C allele in patients with severe asthma, whereas the G allele 
      was more prevalent in individuals with mild asthma (p = 0.05). Additionally, the 
      correlation between markers of type 2 inflammation and the dominant model of the 
      IL-6 gene -174G/C polymorphism (CC + CG vs GG) revealed a significant increase in 
      total serum immunoglobulin E (IgE), Blood Eosinophil Counts (BEC), and Fractional 
      Exhaled Nitric Oxide (FeNO) levels in asthmatic patients with the CC + CG gene 
      pattern compared to those with GG, with p-values of 0.04, 0.03, and 0.04, 
      respectively. Furthermore, after adjusting for other risk factors, the likelihood 
      of developing severe asthma increased from fourfold to eightfold, with an OR of 
      8.12 (p = 0.01) with (CC + CG) gene pattern. Other predictors for severe asthma 
      included older age and childhood-onset disease (OR = 1.13 and 19.19, p < 0.001). 
      Allergic rhinitis (AR) and nasal polyps (NP) also demonstrated a substantial 
      association with an increased risk of severe asthma, with odds ratios of 5 and 
      32.29 (p = 0.01 and < 0.001), respectively. Additionally, elevated Body Mass 
      Index (BMI), BEC, and FeNO were linked to severe asthma, with ORs of 1.11, 1.00, 
      and 1.04, respectively (p = 0.04, 0.05, and 0.001). CONCLUSION: This study 
      illuminated the intricate relationship between the IL-6 gene polymorphism, type 2 
      inflammation markers, and diverse risk factors in shaping asthma severity. As a 
      significant association between the GG polymorphism of the IL-6 gene (- 174G/C) 
      and mild asthma was found, while possessing at least one C allele, whether in a 
      homozygous (CC) or heterozygous (CG) combination, independently predicts the 
      likelihood of severe asthma.
CI  - (c) 2024. The Author(s).
FAU - Al-Ahmad, Mona
AU  - Al-Ahmad M
AUID- ORCID: 0000-0003-2950-5363
AD  - Department of Microbiology, College of Medicine, Kuwait University, Safat, P.O. 
      Box 24923, 13110, Kuwait City, Kuwait. mona.alahmad@ku.edu.kw.
AD  - Department of Allergy, Al-Rashed Allergy Center, Ministry of Health, Kuwait City, 
      Kuwait. mona.alahmad@ku.edu.kw.
FAU - Ali, Asmaa
AU  - Ali A
AUID- ORCID: 0000-0002-7421-5085
AD  - Department of Laboratory Medicine, School of Medicine, Jiangsu University, 
      Zhenjiang, China.
AD  - Department of Allergy, Al-Rashed Allergy Center, Ministry of Health, Kuwait City, 
      Kuwait.
AD  - Department of Pulmonary Medicine, Abbassia Chest Hospital, Ministry of Health, 
      Cairo, Egypt.
FAU - Maher, Ahmed
AU  - Maher A
AD  - Department of Allergy, Al-Rashed Allergy Center, Ministry of Health, Kuwait City, 
      Kuwait.
FAU - Haider, Mohammad Z
AU  - Haider MZ
AUID- ORCID: 0000-0002-8187-0061
AD  - Department of Pediatrics, College of Medicine, Kuwait University, Kuwait City, 
      Kuwait.
LA  - eng
GR  - Project Number (M102/22)/Kuwait University Research Sector/
PT  - Journal Article
DEP - 20240222
PL  - England
TA  - Allergy Asthma Clin Immunol
JT  - Allergy, asthma, and clinical immunology : official journal of the Canadian 
      Society of Allergy and Clinical Immunology
JID - 101244313
PMC - PMC10885618
OTO - NOTNLM
OT  - IL-6-174G/C gene polymorphism
OT  - Mild and severe asthma
OT  - Type 2 inflammations
COIS- All authors declare no competing interests. Each author has revised and approved 
      the final version of the manuscript independently.
EDAT- 2024/02/23 00:42
MHDA- 2024/02/23 00:43
PMCR- 2024/02/22
CRDT- 2024/02/22 23:47
PHST- 2023/10/06 00:00 [received]
PHST- 2024/02/12 00:00 [accepted]
PHST- 2024/02/23 00:43 [medline]
PHST- 2024/02/23 00:42 [pubmed]
PHST- 2024/02/22 23:47 [entrez]
PHST- 2024/02/22 00:00 [pmc-release]
AID - 10.1186/s13223-024-00880-0 [pii]
AID - 880 [pii]
AID - 10.1186/s13223-024-00880-0 [doi]
PST - epublish
SO  - Allergy Asthma Clin Immunol. 2024 Feb 22;20(1):15. doi: 
      10.1186/s13223-024-00880-0.