Correlation of serum TNF alpha level with severity of chronic obstructive pulmonary disease

Mathanraj, S; Kumar, V. Hanuman; Yuvarajan, S; Reddy, Vikram

doi:10.18203/2320-6012.ijrms20173020

Cited by 4 publications

(3 citation statements)

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“… 63–65 Mathanraj et al (2017) reported elevated levels of serum TNFA levels associated with increased severity of COPD. 66 Production of TNFA from peripheral blood monocytes is also increased in COPD patients and has been implicated in skeletal muscle apoptosis found in some COPD patients. 67 Interactions of TNFA and TNFR1 leads to clustering of TRADD (TNF (Tumor Necrosis Factor) R1 (Receptor Type 1)-Associated Death Domain) results in activation of caspases leading to “Caspase Cascade” and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…62 Apoptosis of interstitial cells, alveolar epithelial cells, inflammatory cells, and endothelial cells in lung tissue samples is associated with COPD. [63][64][65] Mathanraj et al (2017) reported elevated levels of serum TNFA levels associated with increased severity of COPD. 66 Production of TNFA from peripheral blood monocytes is also increased in COPD patients and has been implicated in skeletal muscle apoptosis found in https://doi.org/10.2147/COPD.S337635…”

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confidence: 99%

“…[63][64][65] Mathanraj et al (2017) reported elevated levels of serum TNFA levels associated with increased severity of COPD. 66 Production of TNFA from peripheral blood monocytes is also increased in COPD patients and has been implicated in skeletal muscle apoptosis found in https://doi.org/10.2147/COPD.S337635…”

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confidence: 99%

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Effect of Smoking and Its Cessation on the Transcript Profile of Peripheral Monocytes in COPD Patients

Trivedi

Bade

Madan

et al. 2022

COPD

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Rationale: Smoking is the primary cause of chronic obstructive pulmonary disease (COPD); however, only 10-20% of smokers develop the disease suggesting possible genomic association in the causation of the disease. In the present study, we aimed to explore the whole genome transcriptomics of blood monocytes from COPD smokers (COPD-S), COPD Exsmokers (COPD-ExS), Control smokers (CS), and Control Never-smokers (CNS) to understand the differential effects of smoking, COPD and that of smoking cessation. Methods: Exploratory analyses in form of principal component analysis (PCA) and hierarchical component analysis (uHCA) were performed to evaluate the similarity in gene expression patterns, while differential expression analyses of different supervised groups of smokers and never smokers were performed to study the differential effect of smoking, COPD and smoking cessation. Differentially expressed genes among groups were subjected to post-hoc enrichment analysis. Candidate genes were subjected to external validation by quantitative RT-PCR experiments. Results: CNS made a cluster completely segregated from the other three subgroups (CS, COPDS and COPD-ExS). About 550, 8 and 5 genes showed differential expression, respectively, between CNS and CS, between CS and COPD-S, and between COPD-S and COPD-ExS. Apoptosis, immune response, cell adhesion, and inflammation were the top process networks identified in enrichment analysis. Two candidate genes (CASP9 and TNFRSF1A) found to be integral to several pathways in enrichment analysis were validated in an external validation experiment. Conclusion: Control never smokers had formed a cluster distinctively separated from all smokers (COPDS, COPD-ExS, and CS), while amongst all smokers, control smokers had aggregated in a separate cluster. Smoking cessation appeared beneficial if started at an early stage as many genes altered due to smoking started reverting towards the baseline, whereas only a few COPD-related genes showed reversal after smoking cessation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Effect of Smoking and Its Cessation on the Transcript Profile of Peripheral Monocytes in COPD Patients

Trivedi

Bade

Madan

et al. 2022

COPD

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Association of Elevated Serum GM-CSF, IFN-γ, IL-4, and TNF-αConcentration with Tobacco Smoke Induced Chronic Obstructive Pulmonary Disease in a South Indian Population

Mitra

Vishweswaraiah

Thimraj

et al. 2018

International Journal of Inflammation

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Background Chronic obstructive pulmonary disease (COPD) is a devastating condition with limited pharmacotherapeutic options and exceptionally high public-health burden globally as well as in India. Tobacco smoking is the primary cause for COPD among men in India. Systemic inflammation involving altered regulation of cytokines controlling the host defense mechanism is a hallmark of COPD pathogenesis. However, biomarker discovery studies are limited among Indian COPD patients. Methods We assessed the serum concentrations [median (25th-75th percentile) pg/ml] of interleukin (IL)-2,4,6,8,10, granulocyte macrophage colony stimulating factor (GM-CSF), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) using a multiplexed immunoassay. Our study cohort consisted of 30 tobacco smokers with COPD (TS COPD) and 20 tobacco smokers without COPD (TS CONTROL) from South India. The study population was matched for age, sex (male), and tobacco consumption (pack-years). COPD was diagnosed according to the global initiative for chronic obstructive lung disease (GOLD) criteria of persistent airflow obstruction determined by the ratio of postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) of <0.7. A validated structured questionnaire-based survey [Burden of Obstructive Lung Disease (BOLD) study] and spirometry were performed during house to house visit of the field study. Statistical analysis included nonparametric (two-tailed) Mann–Whitney U and Spearman rank test, as appropriate (significance: p<0.05). Results Serum GM-CSF [69.64 (46.67, 97.48); 36.78 (30.07, 53.88), p=0.014], IFN-γ [51.06 (17.00, 84.86); 11.70 (3.18, 32.81), p=0.017], IL-4 [9.09 (1.8, 19.9); 1.8 (1.8, 4.46); p=0.024], and TNF-α [20.68 (5.5, 29.26); 3.5 (3.5, 4.5); p<0.001] concentrations (pg/ml) were increased in TS COPD subjects compared to TS CONTROL. A weak correlation between lung function parameters and cytokine concentrations was detected. Conclusion Our pilot study reveals GM-CSF, IFN-γ, IL-4, and TNF-α as plausible COPD susceptibility biomarkers within the investigated South Indian population that needs to be validated in a larger cohort.

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Inflammatory Biomarkers Interleukin 1 Beta (IL-1β) and Tumour Necrosis Factor Alpha (TNF-α) Are Differentially Elevated in Tobacco Smoke Associated COPD and Biomass Smoke Associated COPD

Shetty

Krishnarao

Kumar³

et al. 2021

Toxics

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Chronic obstructive pulmonary disease (COPD), the leading cause of mortality and morbidity worldwide, is characterized by abnormal activation of inflammatory cells. The increased pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), further amplify the inflammation. We evaluated the dose response relationship of IL-1β and TNF-α levels and severity of airflow limitation, and differential responses in IL-1β and TNF-α between biomass COPD (BMS-COPD) and tobacco smoke COPD (TS-COPD) using a case control design in 160 subjects. Patients with COPD had higher serum levels of both IL-1β and TNF-α compared to healthy controls. A large difference in TNF-α was observed between TS-COPD and BMS-COPD, where TS-COPD patients had much higher levels. Serum IL-1β levels were higher in BMS-COPD. Levels of IL-1β correlated better with severity of airflow limitation than TNF-α levels. Both TNF-α and IL-1β levels had a negative linear relationship with Forced Expiratory Volume in 1st second (FEV1) and six-minute walk distance. The correlations were stronger with FEV1 than six-minute walk distance. The correlations of TNF-α and IL-1β with St George Respiratory Questionnaire (SGRQ) scores and body mass index (BMI) were not significant. In conclusion, the levels of pro-inflammatory cytokines TNF-α and IL-1β are differently elevated in TS-COPD and BMS-COPD, respectively.

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Correlation of serum TNF alpha level with severity of chronic obstructive pulmonary disease

Cited by 4 publications

References 20 publications

Effect of Smoking and Its Cessation on the Transcript Profile of Peripheral Monocytes in COPD Patients

Effect of Smoking and Its Cessation on the Transcript Profile of Peripheral Monocytes in COPD Patients

Association of Elevated Serum GM-CSF, IFN-γ, IL-4, and TNF-αConcentration with Tobacco Smoke Induced Chronic Obstructive Pulmonary Disease in a South Indian Population

Inflammatory Biomarkers Interleukin 1 Beta (IL-1β) and Tumour Necrosis Factor Alpha (TNF-α) Are Differentially Elevated in Tobacco Smoke Associated COPD and Biomass Smoke Associated COPD

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