Cytokine profile in the sputum of subjects with post-tuberculosis airflow obstruction and in those with tobacco related chronic obstructive pulmonary disease

Guiedem, Elise; Pefura-Yone, E.W.; Ikomey, George Mondinde; Nkenfou, Céline Nguefeu; Mesembe, Martha; Yivala, Mbanyamsig Mispa; Chendi, Bih Hycenta; Jacobs, Graeme Brendon; Chegou, Novel N.; Okomo, Marie Claire

doi:10.1186/s12865-020-00381-w

Cited by 9 publications

(7 citation statements)

References 33 publications

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“…Elevated levels of IL-17 and IL-23 indicate that autoimmunity is responsible for the aforementioned changes in Buerger's disease. IL-17 along with IL-1 (52) and IL-22 showed a similar behavior, but most of the values were measured in the context of diseases such as COPD in TOA patients, nally they had TNF-α next to them, which guarantees their behavior as the correlation with this cytokine in TOA (53)(54)(55).…”

Section: Discussionmentioning

confidence: 78%

A scope systematic review to clarify immune response to tobacco in Buerger

Ahmadi,

Khaghanzadeh,

Mirlohi

et al. 2024

Preprint

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Background Progressive Thromboangiitis Obliterans (TAO) is a progressive and segmental inflammatory disorder known as Buerger's disease that affects the medium and small arteries of the upper limbs. The major risk factor for Buerger's disease is cigarettes and tobacco products, which can activate several inflammatory and pre-inflammatory parameters. Methods For this systematic review, based on the accepted criteria of Prisma, we searched from 2017 to 2022 in PubMed, Web of Science, science direct and followed the results of Google Scholar cytokines. We reviewed the literature on these smoking-related immune parameters in Buerger's disease as a potential treatment for this disease. Results In TOA patients, IL-17, RORγt, HMGB1 and RAGE mRNA expression are positively correlated with symptom severity. TLR family is associated with changes in the TOA population as a significant difference in TLR4 in the resting and acute phases. TLR9 may also be responsible for the secretion of IL-8 TNF involves in inflammation, muscle weakness, and pain in TOA. significant difference of IL-33 levels between TOA patients, healthy smokers and non-smokers of this cytokine. Conclusion Our results suggest that Buerger's disease can be considered an autoimmune disease caused by smoking. Buerger increase pro-inflammation markers in TOA and reduce angiogenetic factors. We recommend that pro-inflammatory cytokines should be considered in treatment and diagnosis programs and further research should focus on them.

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Section: Discussionmentioning

confidence: 78%

A scope systematic review to clarify immune response to tobacco in Buerger

Ahmadi,

Khaghanzadeh,

Mirlohi

et al. 2024

Preprint

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“…Some of the 3-plex cytokines (IL-1β and TNF-α) were positively correlated with neutrophil percentages in Cohort B, so similar neutrophil counts between COPD patients and controls in cohort B reduces the possibility to elucidate between group differences for these cytokines. Previous studies have shown conflicting results for IL-1β and TNF-α, with increased levels in COPD patients and no difference versus controls being reported [ 33 , 34 ]. Nevertheless, despite the differences in clinical and immunoassay characteristics between cohorts, there were significant differences between COPD patients and controls for IL-6 and IL-8 in both cohorts, consistent with previous studies [ 15 , 33 , 34 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown conflicting results for IL-1β and TNF-α, with increased levels in COPD patients and no difference versus controls being reported [ 33 , 34 ]. Nevertheless, despite the differences in clinical and immunoassay characteristics between cohorts, there were significant differences between COPD patients and controls for IL-6 and IL-8 in both cohorts, consistent with previous studies [ 15 , 33 , 34 , 35 ]. We also showed statistically significant increases in IL-1β, IL-6 and TNF-α during an exacerbation, as previously reported [ 36 , 37 ]…”

Section: Discussionmentioning

confidence: 99%

Validation of Sputum Biomarker Immunoassays and Cytokine Expression Profiles in COPD

et al. 2022

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Immunoassays are commonly used to assess airway inflammation in sputum samples from chronic obstructive pulmonary disease (COPD) patients. However, assay performance and validation in this complex matrix is inconsistently reported. The aim of this study was to assess the suitability of various immunoassays for use with sputum samples, followed by use of validated immunoassays to evaluate biomarker levels in COPD patients. Assays were assessed for recombinant reference standard suitability, optimal sample dilution, standard recovery in the biological matrix and reproducibility. Validated assays were used to assess sputum supernatants in Cohort A (n = 30 COPD, n = 10 smokers, n = 10 healthy) and Cohort B (n = 81 COPD, n = 15 smokers, n = 26 healthy). Paired baseline and exacerbation samples from 14 COPD patients were assessed in cohort A, and associations with sputum cell counts and bacterial colonisation investigated in cohort B. 25/32 assays passed validation; the primary reason for validation failure was recombinant reference standard suitability and sample dilution effects. Interleukin (IL-)6 and IL-8 were significantly increased in COPD patients compared to healthy subjects and smokers for both cohorts. Tumour necrosis factor (TNF)α and IL-1β were higher in COPD compared to smokers using one immunoassay but not another, partly explained by different absolute recovery rates. IL-1β, IL-2, IL-4, IL-8, IL-17A, Granulocyte colony stimulating factor (G-CSF), Interferon (IFN-)γ, Interferon gamma induced protein (IP-)10, Macrophage inflammatory protein (MIP)-1α, MIP-1β and TNF-α levels correlated with sputum neutrophil percentage in COPD patients. IL-1β, IL-4, IL-8, G-CSF and IFN-γ levels were associated with Haemophilus influenzae colonisation in COPD patients. Current smokers had lower levels of IL-1β, IL-4, IL-8, G-CSF, IFN-γ, IP-10, Monocyte chemoattractant protein (MCP)-1, MIP-1α, MIP-1β and TNF-α. Validated immunoassays applied to sputum supernatants demonstrated differences between COPD patients and controls, the effects of current smoking and associations between Haemophilus influenzae colonisation and higher levels of selected cytokines. Immunoassay validation enabled inflammatory mediators associated with different COPD characteristics to be determined.

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“…[ 11 12 ] But some study showed opposite result i.e., COPD patients had more severe airflow obstruction than Post-TB OAD. [ 16 ]…”

Section: Discussionmentioning

confidence: 99%

“…[ 5 ] Though both COPD and Post-TB OAD patients have obstructive airways pathology but progression of diseases and outcome were different, this could be due to different causal pathway as cytokines inflammatory markers associated with two diseases were different. [ 16 ]…”

Section: Discussionmentioning

confidence: 99%

Treatment outcome among Post TB obstructive airways diseases and COPD

Swain

Pothal

Behera

et al. 2021

Journal of Family Medicine and Primary Care

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Context: Post Tubercular Obstructive Airways Diseases (Post-TB OAD) is a sequela of Pulmonary TB but diseases progression may not same like Chronic Obstructive Pulmonary Diseases (COPD). Aim: To compare the frequency and severity of exacerbations, change of FEV1, frequency of hospitalization and mortality among COPD and post TB OAD patients. Setting and Design: Hospital-based prospective cohort study. Methods and Material: COPD cohort was diagnosed based on symptoms, history of exposure to risk factors and post bronchodilator FEV1/FVC ratio <70%. Post TB OAD cohort was diagnosed like COPD along with past history of Pulmonary TB. Both cohorts were followed up every 3-monthly intervals for up to 12 months. Statistical Analysis: Comparison of categorical variable was done by Chi-square test and continuous variable by unpaired t test. Longitudinal data of FEV1% were analyzed by repeated measure ANOVA test. Results: Totally, 68 patients with Post TB OAD and 66 COPD patients were taken into this study. The frequency of exacerbation (3.52 ± 1.84 verses 2.70 ± 1.37), number of severe exacerbation (56 verses 24) and frequency of hospitalization (1.37 ± 0.81 verses 0.97 ± 0.94) more seen in post-TB OAD cohort in compared to COPD cohort which is statistically significant. Mortality more seen in post-TB OAD group (14 verses 6). Rate of decline FEV1 per year more seen in Post-TB OAD (0.27 ± 0.28 lit verses 0.17 ± 0.26 liter) as compared to COPD. There was overall decreasing trend of FEV1% over period of 12 month but without any difference among two cohort. Conclusion: There was more in frequency of exacerbations, number of severe exacerbations, frequency of hospitalization and number of mortalities among post TB OAD compared to COPD.

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Cytokine profile in the sputum of subjects with post-tuberculosis airflow obstruction and in those with tobacco related chronic obstructive pulmonary disease

Cited by 9 publications

References 33 publications

A scope systematic review to clarify immune response to tobacco in Buerger

A scope systematic review to clarify immune response to tobacco in Buerger

Validation of Sputum Biomarker Immunoassays and Cytokine Expression Profiles in COPD

Treatment outcome among Post TB obstructive airways diseases and COPD

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