thromboplastin and Tuberculosis--Pulmonary

<b>Background and Objective:</b> Immune complexes and pro-inflammatory cytokines deduced from communicable diseases have been manifested to induce pro coagulopathy and tissue factor (TF) assertion in macrophages and the endothelial cells that remain at critical risk in tuberculosis (TB) patients. The current study was carried out among Sudanese patients with Pulmonary tuberculosis aimed to determine the long-term impacts of Tb infection on the coagulation cascade. <b>Materials and Methods:</b> A cross-sectional study was conducted among 30 patients who are already diagnosed with tuberculosis compared with the control group. Pulmonary Tuberculosis diagnosis of cases was emphasized in accordance with clinical examination, chest X-ray and positive Ziehl-Neelsen (ZN) smear. The questionnaire was used for the collection of demographic and baseline data. About 2.5 mL of venous blood was collected in trisodium citrate containers and 2.5 mL of blood was collected in EDTA container. SPSS version 21 statistical software was used for statistical analysis. <b>Results:</b> PLT count showed a significant difference (p = 0.03) with a mean (329.20×10³ and 287.60×10³ μL¹) among patients and control, respectively. APPT shows a significant difference (p = 0.00), Mean of PLT decreased as the disease progressed (336.20±36.02, 345.43±16.02, 511.04±42.02) showed a significant correlation between PLT count of test and duration of disease (p = 0.00). Additionally, a significant correlation between PLT count, MPV and APTT and the status of the patient's drug resistance was revealed (p<u><</u>0.02, 0.01 and 0.02). <b>Conclusion:</b> There is a significant alteration in coagulation parameters (PT, APTT and platelets count) among Sudanese pulmonary tuberculosis patients, which may indicate a feature of a hypercoagulable state.

Topics: Cross-Sectional Studies; Endothelial Cells; Humans; Inflammation Mediators; Sputum; Thromboplastin; Tuberculosis; Tuberculosis, Pulmonary

Tissue factor (TF) is a transmembrane glycoprotein that plays an essential role in hemostasis by activating coagulation. TF is also expressed by monocytes/macrophages as part of the innate immune response to infections. In the current study, we determined the role of TF expressed by myeloid cells during Mycobacterium tuberculosis (M. tb) infection by using mice lacking the TF gene in myeloid cells (TF(Δ) ) and human monocyte derived macrophages (MDMs). We found that during M. tb infection, a deficiency of TF in myeloid cells was associated with reduced inducible nitric oxide synthase (iNOS) expression, enhanced arginase 1 (Arg1) expression, enhanced IL-10 production and reduced apoptosis in infected macrophages, which augmented M. tb growth. Our results demonstrate that a deficiency of TF in myeloid cells promotes M2-like phenotype in M .tb infected macrophages. A deficiency in TF expression by myeloid cells was also associated with reduced fibrin deposition and increased matrix metalloproteases (MMP)-2 and MMP-9 mediated inflammation in M. tb infected lungs. Our studies demonstrate that TF expressed by myeloid cells has newly recognized abilities to polarize macrophages and to regulate M. tb growth.

Topics: Animals; Bacteremia; Blood Coagulation; Cell Differentiation; Female; Fibrin; Host-Pathogen Interactions; Humans; Immunity, Innate; Lung; Macrophages; Mice, Inbred C57BL; Mice, Knockout; Mycobacterium tuberculosis; Pneumonia; Thromboplastin; Tuberculoma; Tuberculosis, Pulmonary

Mycobacterium tuberculosis, the causative agent of tuberculosis, drives the formation of granulomas, structures in which both immune cells and the bacterial pathogen cohabit. The most abundant cells in granulomas are macrophages, which contribute as both cells with bactericidal activity and as targets for M. tuberculosis infection and proliferation during the entire course of infection. The mechanisms and factors involved in the regulation and control of macrophage microenvironment-specific polarization and plasticity are not well understood, as some granulomas are able to control bacteria growth and others fail to do so, permitting bacterial spread. In this issue of the European Journal of Immunology, Venkatasubramanian et al. [Eur. J. Immunol. 2016. 46: 464-479] show that mice lacking the tissue factor gene in myeloid cells have augmented M. tuberculosis growth and increased inflammation in the lungs. This suggests that tissue factor, an initiator of coagulation, is important for the generation of fibrin, which supports granuloma formation. This article demonstrates for the first time the involvement of tissue factor in inducing effective immunity against M. tuberculosis, and sheds new lights on the complex interplay between host inflammatory response, the coagulation system, and the control of M. tuberculosis infection.

Topics: Animals; Bacteremia; Blood Coagulation; Cell Differentiation; Fibrin; Host-Pathogen Interactions; Humans; Immunity, Innate; Lung; Macrophages; Mice; Mice, Knockout; Mycobacterium tuberculosis; Pneumonia; Thromboplastin; Tuberculoma; Tuberculosis, Pulmonary

Topics: Adult; Blood Coagulation; Chronic Disease; Factor XIII; Female; Fibrinogen; Fibrinolysis; Hemoptysis; Humans; Male; Middle Aged; Plasminogen; Thromboplastin; Tuberculosis, Pulmonary

Topics: Blood Coagulation Disorders; Blood Coagulation Tests; Fibrinogen; Humans; Thromboplastin; Tuberculosis, Pulmonary

Topics: Humans; Pleurisy; Thromboplastin; Tuberculosis; Tuberculosis, Pulmonary

Topics: Aminosalicylic Acid; Anti-Bacterial Agents; Blood; Hemostatics; Prothrombin; Thromboplastin; Tuberculosis; Tuberculosis, Pulmonary