The pathogen recognition sensor, NOD2, is variably expressed in patients with pulmonary tuberculosis
NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-alpha synthesis is markedly reduced in M...
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Published in | BMC infectious diseases Vol. 7; no. 1; p. 96 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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BioMed Central Ltd
16.08.2007
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Abstract | NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-alpha synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB).
We analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro, we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells.
No significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro.
There are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. |
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AbstractList | Abstract Background NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-α synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB). Methods We analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro, we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells. Results No significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro. Conclusion There are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. BACKGROUND: NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-α synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB). METHODS: We analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro, we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells. RESULTS: No significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro. CONCLUSION: There are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. Abstract Background NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-α synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB). Methods We analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro , we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells. Results No significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro . Conclusion There are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-alpha synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB). We analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro, we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells. No significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro. There are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. BACKGROUNDNOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal mechanisms. TNF-alpha synthesis is markedly reduced in MTB-antigen stimulated-mononuclear cells expressing mutant NOD2 proteins. NOD2 agonists also induce resistance to apoptosis, and may thus facilitate the survival of MTB in infected macrophages. To further define a role for NOD2 in disease pathogenesis, we analysed NOD2 transcriptional responses in pulmonary leucocytes and mononuclear cells harvested from patients with pulmonary tuberculosis (PTB). METHODSWe analysed NOD2 mRNA expression by real-time polymerase chain-reaction in alveolar lavage cells obtained from 15 patients with pulmonary tuberculosis and their matched controls. We compared NOD2 transcriptional responses, in peripheral leucocytes, before and after anti-tuberculous treatment in 10 patients. In vitro, we measured NOD2 mRNA levels in MTB-antigen stimulated-mononuclear cells. RESULTSNo significant differences in NOD2 transcriptional responses were detected in patients and controls. In some patients, however, NOD2 expression was markedly increased and correlated with toll-like-receptor 2 and 4 expression. In whole blood, NOD2 mRNA levels increased significantly after completion of anti-tuberculosis treatment. NOD2 expression levels did not change significantly in mononuclear cells stimulated with mycobacterial antigens in vitro. CONCLUSIONThere are no characteristic NOD2 transcriptional responses in PTB. Nonetheless, the increased levels of NOD2 expression in some patients with severe tuberculosis, and the increases in expression levels within peripheral leucocytes following treatment merit further studies in selected patient and control populations. |
ArticleNumber | 96 |
Audience | Academic |
Author | Chang, Jung-Su Rook, Graham A W Johnson, Margaret A Lala, Sanjay Dheda, Keertan Keshav, Satish Huggett, Jim F Kim, Louise U Zumla, Alimuddin |
AuthorAffiliation | 3 Lung Infection and Immunity Unit, Department of Medicine, Division of Pulmonology, University of Cape Town, South Africa 1 Centre for Gastroenterology, Royal Free and University College Medical School & Royal Free Hospital NHS Trust, London, UK 4 Dept. of Thoracic and HIV Medicine, Royal Free Hospital NHS Trust, London, UK 2 Centre for Infectious Diseases and International Health, Royal Free Hospital NHS Trust, London, UK |
AuthorAffiliation_xml | – name: 4 Dept. of Thoracic and HIV Medicine, Royal Free Hospital NHS Trust, London, UK – name: 2 Centre for Infectious Diseases and International Health, Royal Free Hospital NHS Trust, London, UK – name: 3 Lung Infection and Immunity Unit, Department of Medicine, Division of Pulmonology, University of Cape Town, South Africa – name: 1 Centre for Gastroenterology, Royal Free and University College Medical School & Royal Free Hospital NHS Trust, London, UK |
Author_xml | – sequence: 1 givenname: Sanjay surname: Lala fullname: Lala, Sanjay email: s.lala@mweb.co.za organization: Centre for Gastroenterology, Royal Free and University College Medical School & Royal Free Hospital NHS Trust, London, UK. s.lala@mweb.co.za – sequence: 2 givenname: Keertan surname: Dheda fullname: Dheda, Keertan – sequence: 3 givenname: Jung-Su surname: Chang fullname: Chang, Jung-Su – sequence: 4 givenname: Jim F surname: Huggett fullname: Huggett, Jim F – sequence: 5 givenname: Louise U surname: Kim fullname: Kim, Louise U – sequence: 6 givenname: Margaret A surname: Johnson fullname: Johnson, Margaret A – sequence: 7 givenname: Graham A W surname: Rook fullname: Rook, Graham A W – sequence: 8 givenname: Satish surname: Keshav fullname: Keshav, Satish – sequence: 9 givenname: Alimuddin surname: Zumla fullname: Zumla, Alimuddin |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17705850$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1002_jcp_27271 crossref_primary_10_1155_2012_383829 crossref_primary_10_1128_microbiolspec_TBTB2_0016_2016 crossref_primary_10_1007_s13277_015_3781_8 crossref_primary_10_1016_j_cyto_2017_09_027 crossref_primary_10_1159_000341472 crossref_primary_10_1371_journal_ppat_1011389 crossref_primary_10_1111_j_1462_5822_2010_01544_x crossref_primary_10_1016_j_genrep_2021_101395 crossref_primary_10_1016_j_gene_2019_06_025 |
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Snippet | NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium... Abstract Background NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species,... BACKGROUNDNOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including... BACKGROUND: NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including... Abstract Background NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species,... |
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SubjectTerms | Adolescent Adult Binding proteins Bronchoalveolar Lavage Fluid - immunology Control Diagnosis Female Gene expression Genetic aspects Health aspects Humans Interleukin-4 - biosynthesis Interleukin-4 - genetics Interleukin-4 - immunology Leukocytes - immunology Leukocytes - metabolism Leukocytes - physiology Leukocytes, Mononuclear - immunology Male MAP Kinase Signaling System Middle Aged Mycobacterium tuberculosis - immunology Nod2 Signaling Adaptor Protein - biosynthesis Nod2 Signaling Adaptor Protein - genetics Nod2 Signaling Adaptor Protein - immunology Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis RNA, Messenger - genetics Toll-Like Receptor 2 - biosynthesis Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - biosynthesis Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - immunology Transcription, Genetic Tuberculosis Tuberculosis, Pulmonary - genetics Tuberculosis, Pulmonary - immunology Tuberculosis, Pulmonary - metabolism Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology |
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Title | The pathogen recognition sensor, NOD2, is variably expressed in patients with pulmonary tuberculosis |
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