Factors Associated With In Vitro Interferon-gamma Production in Tuberculosis
Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and cli...
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Published in | Journal of the Formosan Medical Association Vol. 110; no. 4; pp. 239 - 246 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
01.04.2011
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Abstract | Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which
Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear.
We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs).
General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively).
Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. |
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AbstractList | Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear. Methods: We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs). Results: General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively). Conclusion: Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear. We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs). General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively). Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear.BACKGROUND/PURPOSEMacrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear.We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs).METHODSWe evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs).General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively).RESULTSGeneral linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively).Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response.CONCLUSIONProduction of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. Background/Purpose Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear. Methods We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs). Results General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively). Conclusion Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is inhibited in tuberculosis (TB) patients. The production of IFN-γ is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear. We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN-γ, IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs). General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN-γ response. The production of IFN-γ was not affected by IL-10 and IL-18. There was a significant relationship between the IFN-γ response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively). Production of IFN-γ in PBMCs was associated with active pulmonary TB and IL-12 response. Background/Purpose: Macrophage activation assisted by interferon-gamma (IFN- gamma ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN- gamma (production is inhibited in tuberculosis (TB) patients. The production of IFN- gamma is influenced by many factors, such as interleukin (IL)-10, IL-12, IL-18, and clinical diseases; but the relative importance of each factor is unclear. Methods: We evaluated the effects of these factors in 46 healthy individuals, 81 patients with TB, and 88 patients with non-TB pneumonia. The responses of IFN- gamma , IL-10, IL-12 and IL-18 were determined from phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs). Results: General linear model analysis showed that disease status and IL-12 response were the independent factors associated with the IFN- gamma response. The production of IFN- gamma was not affected by IL-10 and IL-18. There was a significant relationship between the IFN- gamma response and the IL-12 response among patients with non-TB pneumonia, patients with TB, and healthy participants (Pearson's correlation coefficients of 0.466, 0.483, and 0.464, respectively). Conclusion: Production of IFN- gamma in PBMCs was associated with active pulmonary TB and IL-12 response. |
Author | Wu, Wen-Chen Chu, Chien-Ming Wu, Huang-Pin Liu, Yu-Chih Yu, Chung-Chieh Chuang, Duen-Yau |
Author_xml | – sequence: 1 givenname: Chung-Chieh surname: Yu fullname: Yu, Chung-Chieh organization: Division of Pulmonary Medicine, Chang Gung Memorial Hospital, Keelung, Chang Gung University College of Medicine, Taoyuan, Taiwan – sequence: 2 givenname: Yu-Chih surname: Liu fullname: Liu, Yu-Chih organization: Division of Pulmonary Medicine, Chang Gung Memorial Hospital, Keelung, Chang Gung University College of Medicine, Taoyuan, Taiwan – sequence: 3 givenname: Chien-Ming surname: Chu fullname: Chu, Chien-Ming organization: Division of Pulmonary Medicine, Chang Gung Memorial Hospital, Keelung, Chang Gung University College of Medicine, Taoyuan, Taiwan – sequence: 4 givenname: Duen-Yau surname: Chuang fullname: Chuang, Duen-Yau organization: Department of Chemistry, National Chung-Hsing University, Taichung, Taiwan – sequence: 5 givenname: Wen-Chen surname: Wu fullname: Wu, Wen-Chen organization: Department of Respiratory Therapy, Chang Gung Memorial Hospital, Keelung, Taiwan – sequence: 6 givenname: Huang-Pin surname: Wu fullname: Wu, Huang-Pin email: whanpyng@cgmh.org.tw organization: Division of Pulmonary Medicine, Chang Gung Memorial Hospital, Keelung, Chang Gung University College of Medicine, Taoyuan, Taiwan |
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Keywords | interleukin-18 interferon-gamma interleukin-10 tuberculosis interleukin-12 |
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Snippet | Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which
Mycobacterium tuberculosis is killed, but IFN-γ (production is... Background/Purpose Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ... Macrophage activation assisted by interferon-gamma (IFN-γ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but IFN-γ (production is... Background/Purpose: Macrophage activation assisted by interferon-gamma (IFN- gamma ) is a primary mechanism by which Mycobacterium tuberculosis is killed, but... |
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SubjectTerms | Adult Aged Female Humans interferon-gamma Interferon-gamma - biosynthesis interleukin-10 Interleukin-10 - biosynthesis interleukin-12 Interleukin-12 - biosynthesis interleukin-18 Interleukin-18 - biosynthesis Internal Medicine Linear Models Male Middle Aged Mycobacterium tuberculosis tuberculosis Tuberculosis - immunology |
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Title | Factors Associated With In Vitro Interferon-gamma Production in Tuberculosis |
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