ObjectiveThe inflammatory profile of chronic obstructive pulmonary disease (COPD) related to tobacco is known in certain studies while that of the post tuberculosis form is not yet known. This study aimed to evaluate the levels of neutrophils, macrophages and lymphocytes cells in sputum of COPD patients with history of smoking or anterior tuberculosis. Enumeration of cells in samples was analyzed using standard microscopy.ResultsWe enrolled 92 participants, 46 (50%) were COPD subjects comprising 22 (47.83%) smokers and 24 (52.17%) with anterior tuberculosis while 46 (50%) healthy persons constituted the control group. The levels of neutrophils, lymphocytes and monocytes were statistically higher in COPD patients compared to the control group with p-values of 0.0001 respectively. Neutrophils levels were higher in COPD patients with history of tobacco than in COPD patients with anterior tuberculosis with a mean rate of 4.72 × 106/ml and 2.48 × 106/ml respectively (p = 0.04). The monocytes and lymphocytes levels were not statistically different between the two sub-groups of COPD patients with p-value of 0.052 and 0.91 respectively. Neutrophils are the only inflammatory cells that were significantly higher in COPD patients with history of smoking as compared to COPD patients with anterior tuberculosis.

Background Previous studies have shown that tuberculosis (TB) is a risk factor for chronic airflow limitation. Chronic obstructive pulmonary disease (COPD) is recognized as the result of chronic inflammation, usually related to noxious particles. Post-TB airflow obstruction and tobacco-related COPD have the same functional pathway characterized by persistent airflow limitation. We sought to compare the profile of 29 cytokines in the sputum of subjects with post-TB airflow obstruction and those with COPD related to tobacco. Results The forced expiratory volume in the first second (FEV1) and forced expiratory volume/forced vital capacity (FEV/FVC) ratio were lower in the COPD patients with the history of smoking compared to the post-TB airflow obstruction subgroup. The stages of the disease were more advanced in COPD / tobacco patients. Among the cytokines, IL-1α, IL-1β, MIP-1β, sCD40L and VEGF levels were higher in COPD patients, compared to the controls with p values ​​of 0.003, 0.0001, 0.03, 0.0001 and 0.02 respectively. When the two COPD subgroups were compared, IL-1α, IL-6, TNF-α and IL-8 levels were higher in the COPD patients with the history of tobacco compared to the COPD patients with the history of TB with p-values ​​of 0.031, 0.05, 0.021 and 0.016, respectively. Conclusion COPD related to tobacco is more severe than post-TB airflow obstruction. The pathogenesis of post-TB airflow obstruction appears to involve the cytokines IL-1RA, IL-1α, IL-1β, IL-17, GRO and sCD40L, while COPD related to tobacco involves more cytokines.

Diagnosis of tuberculosis still faces a lot of challenges and is one of the priorities in the field of tuberculosis management. Deciphering the complex tuberculosis pathogenicity network could provide biomarkers for diagnosis. We discussed the distribution of HLA-B17, -DQB and -DRB together with QuantiFERON test results in tuberculosis infection. A case control study was done during which a total of 337 subjects were enrolled comprising 227 active tuberculosis (ATB), 46 latent tuberculosis infection (LTBI) and 64 healthy controls (HC). Sequence-specific primer polymerase chain reaction and immune epitope database were used to genotype samples and determine the epitope binding ability of the over-represented alleles respectively. QuantiFERON test was done according to manufacturer's instructions. The peptides HLA-B*5801 and HLA-DRB1*12 and the peptides HLA-B*5802 and HLA-DQB1*03 were found to be associated with latent tuberculosis while the haplotypes DRB1*10-DQB1*02 and DRB1*13-DQB1*06 were found to be associated with active tuberculosis (All p-values≤0.05). The association of HLA-B*5801 and HLA-B*5802 with latent tuberculosis was linked to their ability to bind or not mycobacterial antigens. DRB1*10-DQB1*02 haplotype was found to be over-represented in LTBI compared to ATB (p-value = 0.0015) while DRB1*13-DQB1*06 was found to be under-represented in LTBI compared to ATB (p-value = 0.0335). The DRB1*10-DQB1*02 haplotype was only found in the LTBI when compared with the ATB group. The present study suggests the following algorithm to discriminate LTBI from ATB: QuantiFERON+ and DRB1*10-DQB1*02 haplotype + may indicate LTBI; QuantiFERON+ and DRB1*10-DQB1*02 haplotype - may indicate ATB.

Background: Previous studies have shown that tuberculosis (TB) is a risk factor for chronic airflow limitation. Chronic obstructive pulmonary disease (COPD) is recognized as the result of chronic inflammation, usually related to noxious particles. Post-TB airflow obstruction and tobacco-related COPD have the same functional pathway characterized by persistent airflow limitation. We sought to compare the profile of 29 cytokines in the sputum of subjects with post-TB airflow obstruction and those with COPD related to tobacco.Results: The forced expiratory volume in the first second (FEV1) and forced expiratory volume/forced vital capacity (FEV/FVC) ratio were lower in the COPD patients with the history of smoking compared to the post-TB airflow obstruction subgroup. The stages of the disease were more advanced in COPD / tobacco patients. Among the cytokines, IL-1α, IL-1β, MIP-1β, sCD40L and VEGF levels were higher in COPD patients, compared to the controls with p values ​​of 0.003, 0.0001, 0.03, 0.0001 and 0.02 respectively. When the two COPD subgroups were compared, IL-1α, IL-6, TNF-α and IL-8 levels were higher in the COPD patients with the history of tobacco compared to the COPD patients with the history of TB with p-values ​​of 0.031, 0.05, 0.021 and 0.016, respectively. Conclusion: COPD related to tobacco is more severe than post-TB airflow obstruction. The pathogenesis of post-TB airflow obstruction appears to involve the cytokines IL-1RA, IL-1α, IL-1β, IL-17, GRO and sCD40L, while COPD related to tobacco involves more cytokines.

Background: Previous studies have shown that tuberculosis (TB) is a risk factor for chronic airflow limitation. Chronic obstructive pulmonary disease (COPD) is recognized as the result of chronic inflammation, usually related to noxious particles. Post-TB airflow obstruction and tobacco-related COPD have the same functional pathway characterized by persistent airflow limitation. We sought to compare the profile of 29 cytokines in the sputum of subjects with post-TB airflow obstruction and those with COPD related to tobacco.Results: The forced expiratory volume in the first second (FEV1) and forced expiratory volume/forced vital capacity (FEV/FVC) ratio were lower in the COPD patients with the history of smoking compared to the post-TB airflow obstruction subgroup. The stages of the disease were more advanced in COPD / tobacco patients. Among the cytokines, IL-1α, IL-1β, MIP-1β, sCD40L and VEGF levels were higher in COPD patients, compared to the controls with p values ​​of 0.003, 0.0001, 0.03, 0.0001 and 0.02 respectively. When the two COPD subgroups were compared, IL-1α, IL-6, TNF-α and IL-8 levels were higher in the COPD patients with the history of tobacco compared to the COPD patients with the history of TB with p-values ​​of 0.031, 0.05, 0.021 and 0.016, respectively.Conclusion: COPD related to tobacco is more severe than post-TB airflow obstruction. The pathogenesis of post-TB airflow obstruction appears to involve the cytokines IL-1RA, IL-1α, IL-1β, IL-17, GRO and sCD40L, while COPD related to tobacco involves more cytokines.

Background: Previous studies have shown that tuberculosis (TB) is a risk factor for chronic airflow limitation. Chronic obstructive pulmonary disease (COPD) is recognized as the result of chronic inflammation, usually related to noxious particles. Post-TB airflow obstruction (post-TB/AFO) and tobacco-related COPD (COPD/tobacco) have the same functional pathway characterized by persistent airflow limitation. We sought to compare the profile of 29 cytokines in the sputum of subjects with post-TB/AFO and those with COPD/tobacco. Results: The forced expiratory volume in the first second (FEV 1 ) and FEV1/forced vital capacity (FEV 1 /FVC) ratio were lower in the COPD/tobacco subgroup compared to the COPD/post-TB subgroup. The stages of the disease were more advanced in COPD / tobacco patients. Among the cytokines, IL-1α, IL-1β, MIP-1β, sCD40L and VEGF levels were higher in COPD patients, compared to the controls with p values ​​of 0.003, 0.0001, 0.03, 0.0001 and 0.02 respectively. When the two COPD subgroups were compared, IL-1α, IL-6, TNF-α and IL-8 levels were higher in the COPD/tobacco subgroup compared to the COPD/post-TB subgroup with p-values ​​of 0.031, 0.05, 0.021 and 0.016 respectively. Conclusion: COPD/tobacco is more severe than post-TB/AFO. The pathogenesis of post-TB/AFO appears to involve the cytokines IL-1RA, IL-1α, IL-1β, IL-17, GRO and sCD40L, while COPD/tobacco involves more cytokines.

Tuberculosis (TB) is an infectious disease which could cause depressive phenomena like those observed in Human Immunodeficiency Virus (HIV). Our study aimed at evaluating the changes of T-cells and certain blood parameters during intensive phase of TB treatment. In this prospective cohort, 140 consenting tuberculosis patients were enrolled. 5ml of blood was collected at baseline (M0), after one month (M1) and after two months (M2). Enumeration of CD4 cells, CD8 cells, and hematological parameters were done following standard protocols.The 118 participants comprised 63 (53.4%) TB/HIV negative patients (group 1) and 55 (46.6%) TB/HIV positive patients (group 2). At M0, blood levels of CD4, hemoglobin, total lymphocytes and platelets in group 2 were significantly lower than those of group 1 with p values of 0.001, 0.002, 0.018 and 0.032 respectively. CD8 level was significantly low in group 1 as compared to group 2 (p value: 0.38). Monocytes were low in both groups with no significant difference (p value: 0.097). At M2, there was a significant increase in the levels of CD4, CD8, monocytes, and hemoglobin as compared to M0. There was no significant change on level of total lymphocytes and platelets. In group 2: At M2, there was a significant increase in the levels of CD4, monocytes, hemoglobin, and platelets, and no statistically significant change on levels of CD8 cells and total lymphocytes. TB infection may result in lymphopenia, monopenia, and anemia, while co-infection with HIV may add thrombopenia to the mentioned disorders.

Background: Chronic viral hepatitis B (HBV) is characterised by progressive hepatocyte destruction and T-cell depletion. The mechanisms of the CD95-CD95 ligand (CD95L) signalling pathway during this chronic disease and the cirrhotic process remains unclear.Objective: We evaluated the involvement of the CD95-CD95L receptor-ligand system in T-cell depletion and hepatic cytolysis in patients with chronic HBV.Methods: This was a cross-sectional study conducted from September to December 2018 at the Yaoundé General Hospital, Cameroon. Four mL of whole blood was collected and analysed. The CD95 and CD95L levels, as well as the CD4+ T-cell and CD8+ T-cell counts, were performed by enzyme-linked immunosorbent assay and flow cytometry.Results: Of the 130 HBV-positive patients, 36 (27.7%) were cirrhotic and 94 (72.3%) were non-cirrhotic. The cirrhotic patients had significantly elevated CD95 (p 0.001) and CD95L (p = 0.001) plasma levels, compared with non-cirrhotic patients. The CD4/CD8 ratios were lower in cirrhotic patients, compared to non-cirrhotic patients (p 0.001). There were statistically significant correlations between CD95 level and CD4+ T-cell counts, between CD95 level and CD8+ T-cell counts, between CD95 level and the CD4/CD8 ratio, between CD95 level and fibrosis score, and between CD95L level and fibrosis score.Conclusion: CD95 and CD95L could be involved in T-cell depletion and hepatic cytolysis during the pathogenesis of chronic HBV and could potentially be used as biomarkers for immunological and hepatic monitoring in patients with chronic HBV.