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macrophage tuberculosis

Ashutosh Tripathi, Vishal Srivastava, Bhupendra N Singh
Tuberculosis continues to be one of the deadliest infectious disease worldwide. MicroRNAs (miRNAs) are small non-coding entities that play critical role as post-transcriptional regulators and are transcriptionally deregulated upon mycobacterial infection. In this study, we found significant upregulation of hsa-let-7b-5p in Mycobacterium tuberculosis (MTB) infected THP-1 human macrophages. Concomitantly, we detected the reduced level of Fas protein, one of the targets of hsa-let-7b-5p, in MTB infected THP-1 macrophages...
February 19, 2018: FEMS Microbiology Letters
Stephen V Gordon, Tanya Parish
MΦ, Macrophage; DC, Dendritic cell; CORD, Cord factor; MDR, Multidrug resistance.Mycobacterium tuberculosis is an expert and deadly pathogen, causing the disease tuberculosis (TB) in humans. It has several notable features: the ability to enter non-replicating states for long periods and cause latent infection; metabolic remodelling during chronic infection; a thick, waxy cell wall; slow growth rate in culture; and intrinsic drug resistance and antibiotic tolerance. As a pathogen, M. tuberculosis has a complex relationship with its host, is able to replicate inside macrophages, and expresses diverse immunomodulatory molecules...
February 21, 2018: Microbiology
Caiqin Zhang, Li Yang, Ningning Zhao, Yong Zhao, Changhong Shi
Tuberculosis (TB) is a major bacterial infectious disease worldwide that is predominantly caused by Mycobacterium tuberculosis (Mtb). The comorbidity of multiple drug-resistant TB strains with HIV and diabetes is widespread. In the presence of these diseases, host immunity is weakened, allowing the recovery of dormant bacilli and leading to recurrent TB infection. As an important component of the host innate and adaptive immune responses, macrophage autophagy plays a significant role in protecting the host against TB...
February 20, 2018: DNA and Cell Biology
Nisha Singh, Pallavi Kansal, Zeeshan Ahmad, Naveen Baid, Hariom Kushwaha, Neeraj Khatri, Ashwani Kumar
IFNG (interferon gamma)-induced autophagy plays an important role in the elimination of intracellular pathogens, such as Mycobacterium tuberculosis (Mtb). However, the signaling cascade that leads to the increase in autophagy flux in response to IFNG is poorly defined. Here, we demonstrate that HMOX1 (heme oxygenase 1)-generated carbon monoxide (CO) is required for the induction of autophagy and killing of Mtb residing in macrophages in response to immunomodulation by IFNG. Interestingly, IFNG exposure of macrophages induces an increase in intracellular calcium levels that is dependent on HMOX1 generated CO...
February 19, 2018: Autophagy
Rui Yang, Enzhuo Yang, Ling Shen, Robert L Modlin, Hongbo Shen, Zheng W Chen
The ability of Mycobacterium tuberculosis to block host antimicrobial responses in infected cells provides a key mechanism for disease pathogenesis. The immune system has evolved to overcome this blockade to restrict the infection, but it is not clear whether two key innate cytokines (IL-12/IL-18) involved in host defense can enhance antimycobacterial mechanisms. In this study, we demonstrated that the combination of IL-12 and IL-18 triggered an antimicrobial response against mycobacteria in infected macrophages (THP-1 and human primary monocyte-derived macrophages) and pulmonary epithelial A549 cells...
February 16, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
Dongfang Wang, Xiuling Gu, Xiaoman Liu, Songtao Wei, Bin Wang, Min Fang
Tuberculosis remains a threat to public health. The major problem for curing this disease is latent infection, of which the underlying mechanisms are still not fully understood. Previous studies indicate that NK cells do not play a role in inhibiting the growth of Mycobacterium tuberculosis in the lung, and recent studies have revealed that NK cells regulate the adaptive immunity during mycobacterial infection. By using a mouse model of direct lung infection with M.bovis BCG, we found that the presence of NK cells postponed the priming and activation of T cells after BCG infection...
February 15, 2018: Cellular Microbiology
Yoon-Tae Chung, Virginia Pasquinelli, Javier O Jurado, Xisheng Wang, Na Yi, Peter F Barnes, Veronica E Garcia, Buka Samten
cAMP is critical in immune regulation, and Mycobacterium tuberculosis (Mtb) intoxicates macrophages through cAMP secretion. To examine the role of cAMP in the immune response to Mtb infection, we determined cAMP levels in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of T cell IFN-γ production. PBMC from tuberculosis patients contained significantly higher cAMP levels than latent tuberculosis infected subjects (LTBI), with an inverse correlation with Mtb-stimulated IFN-γ production...
February 8, 2018: Journal of Infectious Diseases
Shashirekha Mundhra, Ruslana Bryk, Natalie Hawryluk, Tuo Zhang, Xiuju Jiang, Carl F Nathan
Genetic deficiency of protein kinase R (PKR) in mice was reported to enhance macrophage activation in vitro in response to interferon-γ (IFNγ) and to reduce the burden of Mycobacterium tuberculosis (Mtb) in vivo (Wu et al. PloS One. 2012 7:e30512). Consistent with this, treatment of wild-type (WT) macrophages in vitro with a novel PKR inhibitor (Bryk et al., Bioorg. Med. Chem. Lett. 2011 21:4108-4114) also enhanced IFNγ-dependent macrophage activation (Wu et al. PloS One. 2012 7:e30512). Here we show that co-treatment with IFNγ and a new PKR inhibitor identified herein to be highly but not completely selective likewise induced macrophages to produce more reactive nitrogen intermediates (RNI) and tumor necrosis factor alpha (TNFα) and less interleukin 10 (IL-10) than seen with IFNγ alone...
February 13, 2018: European Journal of Immunology
Zhengjun Yi, Kunshan Gao, Ruifang Li, Yurong Fu
Cell wall deficient (CWD) forms of Mycobacterium tuberculosis (Mtb) confers a marked resistance to immune system of the host. However, there is limit data on the effect of intracellular CWD-Mtb infection on macrophages. In the study, effects of CWD-Mtb on cell viability, cytokine response and miRNA expression of macrophages were analyzed. Cell viability was reduced, levels of interleukin-1α (IL-1α), IL-1β, IL-6, IL-10 and interferon-γ (IFN-γ) were also significantly changed after infection of RAW264.7 cells with CWD-Mtb...
February 7, 2018: International Journal of Molecular Medicine
Wei Zhang, Chen Niu, Rui-Yang Fu, Zheng-Yu Peng
OBJECTIVE: To evaluate the expression of genes encoding SR proteinsand alternative splicing of IL4 and TLR4 in Mycobacterium tuberculosis (M. tb) H37Rv-infected macrophages. MATERIALS AND METHODS: THP-1 cells were induced to differentiate into macrophages with 200 nM PMA, and H37Rv strains were used for macrophage infection. After RNA extraction, qRT-PCR was performed to evaluate the expression of many SR proteins as well as the alternative splicing of IL4 and TLR4...
February 13, 2018: Bioengineered
Alexandre C C Vieira, Luíse L Chaves, Marina Pinheiro, Sofia A Costa Lima, Domingos Ferreira, Bruno Sarmento, Salette Reis
Tuberculosis (TB) is still a devastating disease and more people have died of TB than any other infectious diseases throughout the history. The current therapy consists of a multidrug combination in a long-term treatment, being associated with the appearance of several adverse effects. Thus, solid lipid nanoparticles (SLNs) were developed using mannose as a lectin receptor ligand conjugate for macrophage targeting and to increase the therapeutic index of rifampicin (RIF). The developed SLNs were studied in terms of diameter, polydispersity index, zeta potential, encapsulation efficiency (EE) and loading capacity (LC)...
February 12, 2018: Artificial Cells, Nanomedicine, and Biotechnology
Marcelo J Kuroda, Chie Sugimoto, Yanhui Cai, Kristen M Merino, Smriti Mehra, Mariluz Araínga, Chad J Roy, Cecily C Midkiff, Xavier Alvarez, Elizabeth S Didier, Deepak Kaushal
Background: Tuberculosis (TB) and human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) profoundly affect the immune system and synergistically accelerate disease progression. It is believed that CD4+ T-cell depletion by HIV is the major cause of immunodeficiency and reactivation of latent TB. Previous studies demonstrated that blood monocyte turnover concurrent with tissue macrophage death from virus infection better predicted AIDS onset than CD4+ T-cell depletion in macaques infected with simian immunodeficiency virus (SIV)...
February 8, 2018: Journal of Infectious Diseases
Nargis Khan, Maziar Divangahi
No abstract text is available yet for this article.
February 8, 2018: Journal of Infectious Diseases
Jorge Castro-Garza, Miriam Lorena Luévano-Martínez, Licet Villarreal-Treviño, Jaime Gosálvez, José Luis Fernández, Martha Imelda Dávila-Rodríguez, Catalina García-Vielma, Silvia González-Hernández, Elva Irene Cortés-Gutiérrez
BACKGROUND: Mycobacterium tuberculosis is an intracellular pathogen, which may either block cellular defensive mechanisms and survive inside the host cell or induce cell death. Several studies are still exploring the mechanisms involved in these processes. OBJECTIVES: To evaluate the genomic instability of M. tuberculosis-infected macrophages and compare it with that of uninfected macrophages. METHODS: We analysed the possible variations in the genomic instability of Mycobacterium-infected macrophages using the DNA breakage detection fluorescence in situ hybridisation (DBD-FISH) technique with a whole human genome DNA probe...
March 2018: Memórias do Instituto Oswaldo Cruz
Paola da Costa Souza, Patrícia Suemi Dondo, Gabriela Souza, Deborah Lopes, Marcel Moscardi, Vinicius de Miranda Martinho, Rodolfo Daniel de Mattos Lourenço, Tabatha Prieto, Marcelo Luiz Balancin, Aline Kawassaki Assato, Walcy Rosolia Teodoro, Silvia Rodrigues, Mariana Lima, Maria Vera Castellano, Ester Coletta, Edwin Roger Parra, Vera Luiza Capelozzi
This study analyzed the Type 1 and Type 2T helper (Th-1/Th-2) cytokines (including interleukins), immune cellular, matrix profile and pathogens in granulomas with unexplained etiology and compared to infectious and non-infectious etiology. Surgical lung biopsies from 108 patients were retrospectively reviewed. Histochemistry, immunohistochemistry, immunofluorescence, morphometry and polymerase chain reaction (PCR) were employed, respectively, to evaluate total collagen and elastin fibers, collagen I and III, immune cells, cytokines, metalloproteinase-9 (MMP-9), myofibroblasts and multiple usual and unusual pathogens...
February 2, 2018: Human Pathology
Xiaoqian Zhai, Tao Luo, Xuan Peng, Pengjiao Ma, Chuhan Wang, Chunxi Zhang, Jing Suo, Lang Bao
Genetic variations among genes of Mycobacterium tuberculosis may be associated with antigenic variation and immune evasion, which complicates the pathogenesis of M. tuberculosis. The hyper-virulent M. tuberculosis Beijing strains harbored several large sequence deletions, among which RD207 attributed to the deletion of CRISPR loci and several Cas genes. RD207 also gave rise to a truncated gene Rv2820c-Bj with 60% deletion in length at the 3'-end and a new 3'-end of five amino acid mutations. It has been reported that Rv2820c-Bj correlated with enhanced intracellular survival of M...
January 30, 2018: Infection, Genetics and Evolution
Qian Pan, Feng-Lan Zhao, Bang-Ce Ye
Enhanced intracellular survival (Eis) proteins were found to enhance the intracellular survival of mycobacteria in macrophages by acetylating aminoglycoside antibiotics to confer resistance to these antibiotics and by acetylating DUSP16/MPK-7 to suppress host innate immune defenses. Eis homologs composing of two GCN5 N-acetyltransferase regions and a sterol carrier protein fold are found widely in gram-positive bacteria. In this study, we found that Eis proteins have an unprecedented ability to acetylate many arylalkylamines, are a novel type of arylalkylamine N-acetyltransferase AANAT (EC 2...
February 5, 2018: Scientific Reports
Min Wan, Xiao Tang, Rokeya Sultana Rekha, S S V Jagadeeswara Rao Muvva, Susanna Brighenti, Birgitta Agerberth, Jesper Z Haeggström
Prostaglandin (PG)E2 is an arachidonic acid-derived lipid mediator that plays an important role in inflammation and immunity. In this study, we demonstrate that PGE2 suppresses basal and 1,25-dihydroxy vitamin D3 (VD3)-induced expression of hCAP18/LL-37 via E prostanoid (EP)2 and EP4 receptors. In humans, VD3 up-regulates vitamin D receptor (VDR) expression and promotes transcription of the cathelicidin hCAP18/LL-37 gene, whereas PGE2 counteracts this effect. We find that PGE2 induces the cAMP/PKA-signaling pathway and enhances the expression of the inhibitory transcription factor cAMP-responsive modulator/inducible cAMP early repressor, which prevents VDR expression and induction of hCAP18/LL-37 in human macrophages...
January 17, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Elena Ufimtseva, Natalya Eremeeva, Ekaterina Petrunina, Tatiana Umpeleva, Svetlana Karskanova, Sergey Bayborodin, Diana Vakhrusheva, Marionella Kravchenko, Sergey Skornyakov
Tuberculosis (TB), with the Mycobacterium tuberculosis (Mtb) as the causative agent, remains to be a serious world health problem. Traditional methods used for the study of Mtb in the lungs of TB patients do not provide information about the number and functional status of Mtb, especially if Mtb are located in alveolar macrophages. We have developed a technique to produce ex vivo cultures of cells from different parts of lung tissues surgically removed from patients with pulmonary TB and compared data on the number of cells with Mtb inferred by the proposed technique to the results of bacteriological and histological analyses used for examination of the resected lungs...
2018: PloS One
Ankita Saini, Sahil Mahajan, Nancy Ahuja, Ella Bhagyaraj, Rashi Kalra, Ashok Kumar Janmeja, Pawan Gupta
Mycobacterium tuberculosis instigates interactions with host factors to promote its survival within the host inimical conditions. Among such factors, nuclear receptors (NRs) seem to be promising candidates owing to their role in bacterial pathogenesis. However, only few members of NR superfamily have been implicated in M. tuberculosis infection and there is a dearth of comprehensive knowledge about expression or function of the entire superfamily. In this study, we performed detailed expression analysis and identified key NRs getting differentially regulated in murine macrophages and dendritic cells (DC) upon infection with H37Rv...
February 2, 2018: Scientific Reports
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