Cytokine gene polymorphisms and serum cytokine levels in patients with idiopathic pulmonary fibrosis

Alhamad, Esam H.; Cal, Joseph G; Shakoor, Zahid; Almogren, Ahmad; Al-Boukai, Ahmad A.

doi:10.1186/1471-2350-14-66

Cited by 30 publications

(21 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The haplotype frequencies are shown in Table 3; three haplotypes were identified. The genotype and haplotype frequencies of IL10 polymorphisms in the control group were consistent with previously published studies from different regions in Saudi Arabian [1,11] and European populations [20]. Polymorphisms at -819 and -592 positions were found in complete linkage disequilibrium (LD) as it has been reported previously in different populations [12,15].…”

Section: Distribution Of Il10 Polymorphisms In a Saudi Populationsupporting

confidence: 89%

IL10 Promoter Polymorphisms are Associated with Rheumatic Heart Disease in Saudi Arabian Patients

et al. 2015

View full text Add to dashboard Cite

Rheumatic heart disease (RHD) is an inflammatory disease that develops following streptococcal infections. IL10 helps to balance immune responses to pathogens. IL10 polymorphisms have been associated with RHD, although results remain inconclusive. Our aim was to investigate the association between IL10 polymorphisms and RHD in Saudi Arabian patients. IL10 promoter polymorphisms (-1082A/G, -829C/T, and -592C/A) were genotyped in 118 RHD patients and 200 matched controls using the TaqMan allelic discrimination assay. There was a significant difference in IL10-1082 genotype frequency between patients and controls (p = 0.01). -1082G allele carriage (GG+GA vs AA) and the (-1082, -819, -592) GCC haplotype carriage were associated with an increased risk of RHD (p = 0.004, OR 2.1, 95% CIs 1.7-3.4 and p = 0.004, OR 2, 95% CIs 1.3-3.4, respectively). The ACC haplotype was associated with a decrease in RHD risk (p = 0.015, OR 0.6, 95% CIs 0.4-0.9). IL10 promoter polymorphisms may play an important role in the development of RHD and provide an opportunity for therapeutic stratification.

show abstract

Section: Distribution Of Il10 Polymorphisms In a Saudi Populationsupporting

confidence: 89%

IL10 Promoter Polymorphisms are Associated with Rheumatic Heart Disease in Saudi Arabian Patients

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Nonetheless, its exact mechanism is yet unknown. Many studies have been done on changes causing lung damage at the cellular level (12)(13)(14). It is reported that the damage caused by reactive oxygen and nitrogen species, whose release is increased by activated infl ammatory cells, causing initiation of lipid peroxidation, hydroxylation, and nitrifi ying amino acids, has an important role in the pathogeny of lung fi brosis (15).…”

Section: Discussionmentioning

confidence: 99%

Attenuation of bleomycin induced lung fibrosis by erdosteine and inhibition of the inducible nitric oxide synthase

Kayhan¹,

Tütüncü²,

Güzel³

et al. 2015

BLL

View full text Add to dashboard Cite

Background and objectives: Despite advances in treatment modalities, the discovery of optimal medical therapies still remains a necessity in the management of pulmonary fi brosis. Material and methods:The experiments were performed in 35 adult Sprague Dawley rats, randomly allotted into one of fi ve groups (n=7). The control group was treated with 1 ml/kg, 0.9 % saline; the BLM group was given a single dose of BLM (2.5 U/kg); the BLM+ER group was treated with ER (10 mg/kg/day po) for 14 days after BLM administration; the BLM+SMT group was treated with i.p injections of SMT (20 mg/kg/ day) for 14 days after BLM administration; the BLM+ER+SMT group was treated with ER and SMT for 14 days after BLM administration. At the end of day 14, the results of histopathological, biochemical, and immunohistochemical investigations were analyzed. Results: Serum TNF-α, nitrate/nitrite, and TBARS levels signifi cantly increased in BLM group compared to control group (p < 0.001, p < 0.001 and p < 0.05 respectively). Lung tissue content of IL-6 was found to be lower in BLM+ER, BLM+SMT and BLM+ER+SMT groups compared to BLM group by immunhistochemical examinations (p < 0.01, p < 0.01 and p < 0.001, respectively). Similarly, the TNF-α reactions (p < 0.01 for each group) and NF-kB expressions were shown to be signifi cantly different among the study groups (p < 0.05, p < 0.05 and p < 0.001, respectively). Conclusion: Based on our study, ER and SMT attenuate BLM-induced pulmonary fi brosis; the combination of two agents has a greater protective effi cacy against fi brosis than one alone, reducing the infl ammatory markers (Tab. 2, Fig. 2, Ref. 31). Text in PDF www.elis.sk.

show abstract

“…Moreover, genetic delivery of IL-10 significantly attenuates the TGF- β production in the lung of mice with bleomycin-induced pulmonary fibrosis [ 48 ]. In humans greater percentage of peripheral CD4 + T lymphocytes produced IL-10 and higher serum levels of IL-10 were found in patients with IPF than normal subjects [ 49 ]. Moreover, the extent of IL-10 production correlated with forced vital capacity of the patients [ 120 ].…”

Section: Role Of Il-10 Family Members In Fibrotic Diseasesmentioning

confidence: 99%

Fibrosis Related Inflammatory Mediators: Role of the IL‐10 Cytokine Family

Sziksz

Pap

Lippai

et al. 2015

Mediators of Inflammation

216

193

View full text Add to dashboard Cite

Importance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney diseases, inflammatory bowel disease, and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem. According to some estimates about 45% of all deaths are attributed to FDs in the developed world. Independently of their etiology the common hallmark of FDs is chronic inflammation. Infiltrating immune cells, endothelial, epithelial, and other resident cells of the injured organ release an orchestra of inflammatory mediators, which stimulate the proliferation and excessive extracellular matrix (ECM) production of myofibroblasts, the effector cells of organ fibrosis. Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function. Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis. Therefore, there is an urgent need for the more comprehensive understanding of the pathomechanism of fibrosis and development of novel diagnostic and therapeutic strategies. In the present review we provide an overview of the common key mediators of organ fibrosis highlighting the role of interleukin-10 (IL-10) cytokine family members (IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26), which recently came into focus as tissue remodeling-related inflammatory cytokines.

show abstract

Cytokine gene polymorphisms and serum cytokine levels in patients with idiopathic pulmonary fibrosis

Cited by 30 publications

References 44 publications

IL10 Promoter Polymorphisms are Associated with Rheumatic Heart Disease in Saudi Arabian Patients

IL10 Promoter Polymorphisms are Associated with Rheumatic Heart Disease in Saudi Arabian Patients

Attenuation of bleomycin induced lung fibrosis by erdosteine and inhibition of the inducible nitric oxide synthase

Fibrosis Related Inflammatory Mediators: Role of the IL‐10 Cytokine Family

Contact Info

Product

Resources

About