Suppression of Mycobacterium Tuberculosis Induced Reactive Oxygen Species andTumor Necrosis Factor-Alpha Activity in Human Monocytes of Systemic LupusErythematosus Patients by Reduced Glutathione

Azfar, Shah Farhan; Islam, Najmul

doi:10.5001/omj.2012.03

Cited by 7 publications

(5 citation statements)

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“…This produces ∙O 2 which dismutate into hydrogen peroxide (H 2 O 2 ) and thus generate ∙OH radicals which are toxic to MTB [ 20 ]. Following inhalation of MTB, alveolar macrophages engulf the bacilli and initiate their killing using a number of mechanisms including the generation of ROI and RNI [ 21 , 22 ].…”

Section: Role Of Reactive Oxygen Specious (Ros) In Pathogenesis Of Tbmentioning

confidence: 99%

“…Thus, NADPH oxidase has an important role in host defense against MTB and any patients with a loss of function mutation in genes encoding components of this enzyme complex could be deficient in killing bacilli. Indeed, mutations in the CYBB gene encoding the gp91 (phox) subunit of the phagocyte NADPH oxidase is associated with MTB [ 21 ]. In addition, a hemizygous splice mutation in intron 5 of CYBB was linked to the concomitant occurrence of chronic granulomatous disease (CGD) with MTB [ 24 ].…”

Section: Role Of Reactive Oxygen Specious (Ros) In Pathogenesis Of Tbmentioning

confidence: 99%

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Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis

et al. 2014

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Tuberculosis (TB) is considered a major worldwide health problem with 10 million new cases diagnosed each year. Our understanding of TB immunology has become greater and more refined since the identification of Mycobacterium tuberculosis (MTB) as an etiologic agent and the recognition of new signaling pathways modulating infection. Understanding the mechanisms through which the cells of the immune system recognize MTB can be an important step in designing novel therapeutic approaches, as well as improving the limited success of current vaccination strategies. A great challenge in chronic disease is to understand the complexities, mechanisms, and consequences of host interactions with pathogens. Innate immune responses along with the involvement of distinct inflammatory mediators and cells play an important role in the host defense against the MTB. Several classes of pattern recognition receptors (PRRs) are involved in the recognition of MTB including Toll-Like Receptors (TLRs), C-type lectin receptors (CLRs) and Nod-like receptors (NLRs) linked to inflammasome activation. Among the TLR family, TLR1, TLR2, TLR4, and TLR9 and their down-stream signaling proteins play critical roles in the initiation of the immune response in the pathogenesis of TB. The inflammasome pathway is associated with the coordinated release of cytokines such as IL-1β and IL-18 which also play a role in the pathogenesis of TB. Understanding the cross-talk between these signaling pathways will impact on the design of novel therapeutic strategies and in the development of vaccines and immunotherapy regimes. Abnormalities in PRR signaling pathways regulated by TB will affect disease pathogenesis and need to be elucidated. In this review we provide an update on PRR signaling during M. tuberculosis infection and indicate how greater knowledge of these pathways may lead to new therapeutic opportunities.

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Section: Role Of Reactive Oxygen Specious (Ros) In Pathogenesis Of Tbmentioning

confidence: 99%

Section: Role Of Reactive Oxygen Specious (Ros) In Pathogenesis Of Tbmentioning

confidence: 99%

Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis

et al. 2014

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“…When the body is activated during infection or tissue damage, it can transmit signals via ligands and receptors back to cells, causing subsequent inflammatory cascade reactions [ 39 ]. TNF- α can not only induce a massive release of a variety of inflammatory factors and stimulate the development of inflammation [ 40 ] but also directly consume the antioxidant substance glutathione in the body [ 41 ] and stimulate neutrophils and endothelial cells to release oxygen free radicals and other free radicals [ 42 ]. MAPK14 (p38) and MAPK8 (JNK) can receive and prolong the path and duration of TNF signal transduction and jointly affect the level of systemic inflammation response, the area of tissue damage, and the degree of organ function impairment by activating NF- κ B [ 43 ].…”

Section: Resultsmentioning

confidence: 99%

Utilising Network Pharmacology to Explore Underlying Mechanism of Astragalus membranaceus in Improving Sepsis-Induced Inflammatory Response by Regulating the Balance of IκBα and NF-κB in Rats

Haiyang

Ling

Cai

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. The purpose of the present study was to explore the mechanism of Astragalus membranaceus in the treatment of sepsis. Methods. We searched the active components and targets of Astragalus membranaceus using the TCMSP and BATMAN databases. Then, the GeneCards, MalaCards, and OMIM databases were used to screen out relevant targets of sepsis. The common targets of the former two gene sets were uploaded to the STRING database to create an interaction network. DAVID was used to perform KEGG enrichment analysis of the core targets. Based on the results of KEGG and previous studies, key pathways for the development of sepsis were identified and experimentally validated. Result. We obtained 3,370 sepsis-related targets in databases and 59 active components in Astragalus membranaceus through data mining, corresponding to 1,130 targets. The intersection of the two types of targets led to a total of 318 common targets and 84 core targets were obtained after screening again. The KEGG and previous studies showed that these 84 core targets were involved in sepsis by regulating TNF, MAPK, and PI3K pathways. TNF, MAPK8, NF-κB, and IκBα are crucial in sepsis. Experimental validation demonstrated that some markers in sepsis model rats were improved after the intervention with Astragalus granules and their chemical components. Among them, IL-1β, IL-6, and TNF-α in rat serum were reduced. The mRNA and protein expression of TNF-α, IL-6, MMP9, MAPK8, and NF-κB were reduced in rat blood. However, the mRNA and protein expression of IκBα and PI3K were increased in rat blood. Conclusion. The AST could affect the TNF, PI3K, and MAPK pathway cascade responses centred on IκBα and NF-κB, attenuate the expression of IL-6 and MMP9, and interfere with the inflammatory response during sepsis.

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“…In addition, Iliaz et al ( 37 ) indicated that neutrophil/lymphocyte ratio could be used as a reference in the differential diagnosis of tuberculosis. Furthermore, previous investigations have suggested that suppression of M. tuberculosis growth can upregulate TNF-α, which increases the levels of human monocytes in patients with pulmonary tuberculosis ( 38 , 39 ). These reports suggest that inhibition of inflammatory cells may be a potential target for the treatment of pulmonary tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

Inflammation responses in patients with pulmonary tuberculosis in an intensive care unit

et al. 2018

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Pulmonary tuberculosis caused by Mycobacterium tuberculosis remains a global problem. Inflammatory responses are the primary characteristics of patients with pulmonary tuberculosis in intensive care units (ICU). The aim of the present study was to investigate the clinical importance of inflammatory cells and factors for patients with pulmonary tuberculosis in ICU. A total of 124 patients with pulmonary tuberculosis in ICU were recruited for the present study. The inflammatory responses in patients with pulmonary tuberculosis in ICU were examined by changes in inflammatory cells and factors in the serum. The results indicated that serum levels of lymphocytes, plasma cells, granulocytes and monocytes were increased in patients with pulmonary tuberculosis in ICU compared with healthy controls. The serum levels of inflammatory factors interleukin (IL)-1, IL-6, IL-10, IL-12, and IL-4 were upregulated in patients with pulmonary tuberculosis in ICU. Lower plasma concentrations of IL-2, IL-15 and interferon-γ were detected in patients with pulmonary tuberculosis compared with healthy controls. It was demonstrated that high mobility group box-1 protein expression levels were higher in the serum of patients with pulmonary tuberculosis compared with healthy controls. Notably, an imbalance of T-helper cell (Th)1/Th2 cytokines was observed in patients with pulmonary tuberculosis. Pulmonary tuberculosis caused by M. tuberculosis also upregulated expression of matrix metalloproteinase (MMP)-1 and MMP-9 in hPMCs. In conclusion, these outcomes demonstrated that inflammatory responses and inflammatory factors are associated with the progression of pulmonary tuberculosis, suggesting that inhibition of inflammatory responses and inflammatory factors may be beneficial for the treatment of patients with pulmonary tuberculosis in ICU.

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Suppression of Mycobacterium Tuberculosis Induced Reactive Oxygen Species andTumor Necrosis Factor-Alpha Activity in Human Monocytes of Systemic LupusErythematosus Patients by Reduced Glutathione

Abstract: Data shows that SLE patients are more susceptible to developing Mycobacterium tuberculosis, as ROS and TNF-α in SLE patients could activate the replication of mycobacterial Ag85B (30 kDa) after bacilli infection.

Cited by 7 publications

References 0 publications

Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis

Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis

Utilising Network Pharmacology to Explore Underlying Mechanism of Astragalus membranaceus in Improving Sepsis-Induced Inflammatory Response by Regulating the Balance of IκBα and NF-κB in Rats

Inflammation responses in patients with pulmonary tuberculosis in an intensive care unit

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