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Asthma and TNF variants in Chinese and Malays

Tan EC, Lee BW, Tay AW, Chew FT, Tay AH

Allergy, 1999 Apr;54(4):402-3.
PMID: 10371104
Matched MeSH terms: Asthma/genetics*
Fulltext A Systematic Review of the Prevalence of Atopic Diseases in Children on the Arabian Peninsula

Al-Herz W

Med Princ Pract, 2018;27(5):436-442.
PMID: 30149382 DOI: 10.1159/000493267

OBJECTIVES: To study the available data on the prevalence of atopic diseases and food allergy in children living on the Arabian Peninsula.
METHODS: A PubMed search for relevant published articles was conducted using the following search terms singly or in combination: "atopy," "atopic disease," "atopic disorder," "International Study of Asthma and Allergies in Childhood," "ISAAC," "asthma," "allergic rhinitis," "eczema," and "food allergy" in combination with the names of countries of the Arabian Peninsula (Kuwait, United Arab Emirates, Bahrain, Qatar, Oman, Kingdom of Saudi Arabia, and Yemen). The search captured studies published up to December 2017.
RESULTS: A total of 8 publications reporting prevalence rates of any type of atopic disease in children in 7 countries of the Arabian Peninsula were retrieved. The prevalence of all atopic disorders was comparable between countries of the Arabian Peninsula. The overall prevalence of asthma ranged from 8 to 23%, while the reported prevalence of eczema ranged from 7.5 to 22.5%. There was great variation in the prevalence rates of rhinoconjunctivitis, which ranged from 6.3 to 30.5%. The prevalence of food allergy (8.1%) was reported for 1 country only, the United Arab Emirates.
CONCLUSIONS: The reported overall rates of atopic disease in countries of the Arabian Peninsula are comparable to those reported in other industrialized countries. This is probably related to the good economic status in the region, which is reflected in the living standards and lifestyle. Further, genetic factors, such as factors related to gene polymorphism, and the high rate of consanguinity in the region may contribute to the higher prevalence of atopic diseases.

Matched MeSH terms: Asthma/genetics
Unwinding circular RNA's role in inflammatory pulmonary diseases

Bhat AA, Gupta G, Goyal A, Thapa R, Almalki WH, Kazmi I, et al.

Naunyn Schmiedebergs Arch Pharmacol, 2024 May;397(5):2567-2588.
PMID: 37917370 DOI: 10.1007/s00210-023-02809-7

Circular RNAs (circRNAs) have emerged as pivotal regulators of gene expression and cellular processes in various physiological and pathological conditions. In recent years, there has been a growing interest in investigating the role of circRNAs in inflammatory lung diseases, owing to their potential to modulate inflammation-associated pathways and contribute to disease pathogenesis. Inflammatory lung diseases, like asthma, chronic obstructive pulmonary disease (COPD), and COVID-19, pose significant global health challenges. The dysregulation of inflammatory responses demonstrates a pivotal function in advancing these diseases. CircRNAs have been identified as important players in regulating inflammation by functioning as miRNA sponges, engaging with RNA-binding proteins, and participating in intricate ceRNA networks. These interactions enable circRNAs to regulate the manifestation of key inflammatory genes and signaling pathways. Furthermore, emerging evidence suggests that specific circRNAs are differentially expressed in response to inflammatory stimuli and exhibit distinct patterns in various lung diseases. Their involvement in immune cell activation, cytokine production, and tissue remodeling processes underscores their possible capabilities as therapeutic targets and diagnostic biomarkers. Harnessing the knowledge of circRNA-mediated regulation in inflammatory lung diseases could lead to the development of innovative strategies for disease management and intervention. This review summarizes the current understanding of the role of circRNAs in inflammatory lung diseases, focusing on their regulatory mechanisms and functional implications.

Matched MeSH terms: Asthma/genetics
Fulltext Risk factors for wheeze in the last 12 months in preschool children

Quah BS, Mazidah AR, Simpson H

Asian Pac J Allergy Immunol, 2000 Jun;18(2):73-9.
PMID: 10928618

Most children with asthma develop their symptoms before the age of 5 years and many preschool wheezers continue to wheeze in the early school years. It is thus important to investigate the factors that predispose young children to wheeze. The objective of this study was to investigate the relevant environmental and family influences on recent wheeze (wheeze within the last 12 months) in preschool children. A cross-sectional study was conducted in five primary health clinics in the district of Kota Bharu from April to October 1998. Nurses from these clinics distributed Bahasa Malaysia questionnaires containing questions on asthma symptoms, environmental risk factors, family's social status and family history of atopy and wheeze to preschool children aged 1-5 years during their home visits. The respondents were parent(s) or carer(s) of the children. A total of 2,524 (87.7%) complete questionnaires were available for analysis of risk factors. One hundred and fifty six (6.2%) children had current wheeze. Significant risk factors associated with current wheeze were a family history of asthma (O.R. = 6.36, 95% C.I. = 4.45-9.09), neonatal hospital admission (O.R. = 2.38, 95% C.I. = 1.51 - 3.75), and a maternal (O.R. = 2.12, 95% C.I. = 1.31-3.41) or paternal (O.R. = 1.52, 95% C.I. = 0.95-2.43) history of allergic rhinitis. Among environmental factors examined, namely, household pets, carpeting in bedroom, use of fumigation mats, mosquito coils and aerosol insect repellents, maternal and paternal smoking, and air conditioning, none were associated with an increased risk of wheeze. In conclusion, the strongest association with current wheeze was a family history of asthma. Also significant were neonatal hospital admission and a history of allergic rhinitis in either the mother or father. None of the environmental factors studied were related to current wheeze in preschool children.
Study site: Klinik Kesihatan, Kelantan, Malaysia

Matched MeSH terms: Asthma/genetics*
Relationship between various cytokines implicated in asthma

Ayakannu R, Abdullah NA, Radhakrishnan AK, Lechimi Raj V, Liam CK

Hum Immunol, 2019 Sep;80(9):755-763.
PMID: 31054782 DOI: 10.1016/j.humimm.2019.04.018

Asthma is a complex disorder involving immunologic, environmental, genetic and other factors. Today, asthma is the most common disease encountered in clinical medicine in both children and adults worldwide. Asthma is characterized by increased responsiveness of the tracheobronchial tree resulting in chronic swelling and inflammation of the airways recognized to be controlled by the T-helper 2 (Th2) lymphocytes, which secrete cytokines to increase the production of IgE by B cells. There are many cytokines implicated in the development of the chronic inflammatory processes that are often observed in asthma. Ultimately, these cytokines cause the release of mediators such as histamine and leukotrienes (LT), which in turn promote airway remodeling, bronchial hyperresponsiveness and bronchoconstriction. The CD4+ T-lymphocytes from the airways of asthmatics express a panel of cytokines that represent the Th2 cells. The knowledge derived from numerous experimental and clinical studies have allowed physicians and scientists to understand the normal functions of these cytokines and their roles in the pathogenesis of asthma. The main focus of this review is to accentuate the relationship between various cytokines implicated in human asthma. However, some key findings from animal models will be highlighted to support the discoveries from clinical studies.

Matched MeSH terms: Asthma/genetics*
Fulltext Single nucleotide polymorphism in the promoter of the human interleukin-13 gene is associated with asthma in Malaysian adults

Radhakrishnan AK, Raj VL, Tan LK, Liam CK

Biomed Res Int, 2013;2013:981012.
PMID: 23865080 DOI: 10.1155/2013/981012

Asthma susceptibility genes are mapped to a region on human chromosome 5q31-q33, which contains a cluster of proinflammatory cytokine genes such as interleukin-13 (IL-13), which is associated with asthma. This study investigated the allele frequencies of two single nucleotide polymorphisms (SNPs) (-1111C>T and 4257C>A) in the IL-13 gene between asthmatics and healthy volunteers as well as the relationship between these SNPs and IL-13 production. DNA extracted from buffy coat of asthmatic and control subjects was genotyped using the PCR-RFLP method. Amount of IL-13 produced by mitogen-stimulated peripheral blood leucocytes PBLs (PBLs) was determined by ELISA. The frequencies of the -1111C and 4257G wild-type alleles were 0.52 and 0.55 in asthmatics and were 0.67 and 0.56 in controls. A significant (P < 0.05) association was found between genotype and allele frequencies of SNP at position -1111C>T between asthmatic and control groups (OR, 1.810; 95% CI = 1.184 to 2.767; P < 0.05). The mitogen-stimulated PBLs from asthmatics produced higher amounts of IL-13 production (P < 0.001). The 4257GA heterozygous and 4257AA homozygous mutant alleles were associated with higher IL-13 production in asthmatics (P < 0.05). Our results show that the -1111T mutant allele are associated with asthma and the 4257A mutant alleles are associated with elevated IL-13 production.

Matched MeSH terms: Asthma/genetics*
An orally active geranyl acetophenone attenuates airway remodeling in a murine model of chronic asthma

Lee YZ, Shaari K, Cheema MS, Tham CL, Sulaiman MR, Israf DA

Eur J Pharmacol, 2017 Feb 15;797:53-64.
PMID: 28089919 DOI: 10.1016/j.ejphar.2017.01.011

2,4,6-Trihydroxy-3-geranyl acetophenone (tHGA) is a synthetic compound that is naturally found in Melicope ptelefolia. We had previously demonstrated that parenteral administration of tHGA reduces pulmonary inflammation in OVA-sensitized mice. In this study, we evaluated the effect of orally administered tHGA upon airway remodeling in a murine model of chronic asthma. Female BALB/C mice were sensitized intraperitoneally with ovalbumin (OVA) on day 0, 7 and 14, followed by aerosolized 1% OVA 3 times per week for 6 weeks. Control groups were sensitized with saline. OVA sensitized animals were either treated orally with vehicle (saline with 1% DMSO and Tween 80), tHGA (80, 40, 20mg/kg) or zileuton (30mg/kg) 1h prior to each aerosolized OVA sensitization. On day 61, mice underwent methacholine challenge to determine airway hyperresponsiveness prior to collection of bronchoalveolar lavage (BAL) fluid and lung samples. BAL fluid inflammatory cell counts and cytokine concentrations were evaluated while histological analysis and extracellular matrix protein concentrations were determined on collected lung samples. Oral tHGA treatment attenuated airway hyperresponsiveness and inhibited airway remodeling in a dose-dependent fashion. tHGA's effect on airway remodeling could be attributed to the reduction of inflammatory cell infiltration and decreased expression of cytokines associated with airway remodeling. Oral administration of tHGA attenuates airway hyperresponsiveness and remodeling in OVA-induced BALB/c mice. tHGA is an interesting compound that should be evaluated further for its possible role as an alternative non-steroidal pharmacological approach in the management of asthma.

Matched MeSH terms: Asthma/genetics