Mycobacterium tuberculosis H37Ra and H37Rv differential growth and cytokine/chemokine induction in murine macrophages in vitro.

The role of tumor necrosis factor-alpha (TNF-alpha) in controlling growth of Mycobacterium tuberculosis in murine peritoneal macrophages infected in vitro was studied. TNF-alpha was shown to be required but not sufficient, and the amount of TNF-alpha produced by the infected cells did not correlate with the extent of growth control. In this system, TNF-alpha-dependent control of growth of the avirulent strain H37Ra was independent of inducible nitric oxide synthase (iNOS) and interferon-gamma (IFN-gamma), as shown by the infection of macrophages from selected gene-disrupted mice. TNF-alpha-mediated bacteriostasis of H37Ra in the infected macrophages was associated with increased expression of selected Th1-type cytokines and chemokines. In contrast, growth of the virulent strain H37Rv in macrophages involved upregulation by infected cells of Th2-type cytokines, including interleukin-5 (IL-5), IL-10, and IL-13. Taken together, these results suggest that the particular nature of macrophage activation and the cytokine and chemokine response to infection with different M. tuberculosis strains determine the ability of the cells to control the growth of the intracellular bacilli.

[1]  M. Reed,et al.  Differential Monocyte Activation Underlies Strain-Specific Mycobacterium tuberculosis Pathogenesis , 2004, Infection and Immunity.

[2]  John Chan,et al.  TNF Influences Chemokine Expression of Macrophages In Vitro and That of CD11b+ Cells In Vivo during Mycobacterium tuberculosis Infection1 , 2004, The Journal of Immunology.

[3]  Gang Liu,et al.  Apoptosis genes in human alveolar macrophages infected with virulent or attenuated Mycobacterium tuberculosis: a pivotal role for tumor necrosis factor. , 2003, American journal of respiratory cell and molecular biology.

[4]  R. Long,et al.  Anti-tumour necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management. , 2003, The Lancet. Infectious diseases.

[5]  Yu-Jin Jung,et al.  Evidence Inconsistent with a Negative Influence of T Helper 2 Cells on Protection Afforded by a Dominant T Helper 1 Response against Mycobacterium tuberculosis Lung Infection in Mice , 2002, Infection and Immunity.

[6]  Yu-Jin Jung,et al.  Virulent but not Avirulent Mycobacterium tuberculosis Can Evade the Growth Inhibitory Action of a T Helper 1–dependent, Nitric Oxide Synthase 2–independent Defense in Mice , 2002, The Journal of experimental medicine.

[7]  J. Keane,et al.  TNF-dependent BALB/c murine macrophage apoptosis following Mycobacterium tuberculosis infection inhibits bacillary growth in an IFN-gamma independent manner. , 2002, Tuberculosis.

[8]  S. Ehlers,et al.  IFN-γ and NO in mycobacterial disease: new jobs for old hands , 2002 .

[9]  Andrew G. D. Bean,et al.  TNF Regulates Chemokine Induction Essential for Cell Recruitment, Granuloma Formation, and Clearance of Mycobacterial Infection1 , 2002, The Journal of Immunology.

[10]  T. Ottenhoff,et al.  Innate Immunity to Mycobacterium tuberculosis , 2002, Clinical Microbiology Reviews.

[11]  R. Strieter,et al.  β-Chemokines Are Induced by Mycobacterium tuberculosis and Inhibit Its Growth , 2002, Infection and Immunity.

[12]  S. Chensue.  Molecular Machinations: Chemokine Signals in Host-Pathogen Interactions , 2001, Clinical Microbiology Reviews.

[13]  G. Kaplan,et al.  TNF-α Controls Intracellular Mycobacterial Growth by Both Inducible Nitric Oxide Synthase-Dependent and Inducible Nitric Oxide Synthase-Independent Pathways1 , 2001, The Journal of Immunology.

[14]  G. Kaplan,et al.  Virulence of a Mycobacterium tuberculosis clinical isolate in mice is determined by failure to induce Th1 type immunity and is associated with induction of IFN-α/β , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[15]  S. Chensue,et al.  Chemokine expression dynamics in mycobacterial (type-1) and schistosomal (type-2) antigen-elicited pulmonary granuloma formation. , 2001, The American journal of pathology.

[16]  G. Rook,et al.  M. tuberculosis: immunology and vaccination. , 2001, The European respiratory journal.

[17]  Hardy Kornfeld,et al.  Virulent Mycobacterium tuberculosis Strains Evade Apoptosis of Infected Alveolar Macrophages1 , 2000, The Journal of Immunology.

[18]  J. Sedgwick,et al.  Structural deficiencies in granuloma formation in TNF gene-targeted mice underlie the heightened susceptibility to aerosol Mycobacterium tuberculosis infection, which is not compensated for by lymphotoxin. , 1999, Journal of immunology.

[19]  Simon Paul,et al.  Mycobacterium tuberculosis Catalase and Peroxidase Activities and Resistance to Oxidative Killing in Human Monocytes In Vitro , 1999, Infection and Immunity.

[20]  J. Keane,et al.  Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha. , 1998, Journal of immunology.

[21]  P. Barnes,et al.  Chemokine Production by a Human Alveolar Epithelial Cell Line in Response to Mycobacterium tuberculosis , 1998, Infection and Immunity.

[22]  J. Mudgett,et al.  Identification of nitric oxide synthase as a protective locus against tuberculosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[23]  J. Keane,et al.  Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis , 1997, Infection and immunity.

[24]  A. Sampieri,et al.  Correlation between the kinetics of Th1, Th2 cells and pathology in a murine model of experimental pulmonary tuberculosis. , 1996, Immunology.

[25]  G. Kaplan,et al.  Comparable growth of virulent and avirulent Mycobacterium tuberculosis in human macrophages in vitro. , 1996, The Journal of infectious diseases.

[26]  I. Orme,et al.  Chemokine response in mice infected with Mycobacterium tuberculosis , 1995, Infection and immunity.

[27]  C. Lowenstein,et al.  Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice. , 1995, Immunity.

[28]  K. Tanaka,et al.  Effects of nitric oxide synthase inhibitors on murine infection with Mycobacterium tuberculosis , 1995, Infection and immunity.

[29]  A. Fortier,et al.  Isolation of Murine Macrophages , 1994, Current protocols in immunology.

[30]  A. Toniolo,et al.  Differential release of tumor necrosis factor-alpha from murine peritoneal macrophages stimulated with virulent and avirulent species of mycobacteria. , 1994, FEMS immunology and medical microbiology.

[31]  J. Flynn,et al.  An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection , 1993, The Journal of experimental medicine.

[32]  J. Abrams,et al.  Cytokine secretion by CD4 T lymphocytes acquired in response to Mycobacterium tuberculosis infection. , 1993, Journal of immunology.

[33]  A. Izzo,et al.  Mycobacterial virulence. Virulent strains of Mycobacteria tuberculosis have faster in vivo doubling times and are better equipped to resist growth-inhibiting functions of macrophages in the presence and absence of specific immunity , 1993, The Journal of experimental medicine.

[34]  R. Zinkernagel,et al.  Immune response in mice that lack the interferon-gamma receptor. , 1993, Science.

[35]  B. Bloom,et al.  Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages , 1992, The Journal of experimental medicine.

[36]  S. Kaufmann,et al.  Mycobacterial growth inhibition by interferon-gamma-activated bone marrow macrophages and differential susceptibility among strains of Mycobacterium tuberculosis. , 1987, Journal of immunology.

[37]  B. Champion,et al.  Activation of macrophages to inhibit proliferation of Mycobacterium tuberculosis: comparison of the effects of recombinant gamma-interferon on human monocytes and murine peritoneal macrophages. , 1986, Immunology.

[38]  D. Hoover,et al.  Macrophage activation to kill Leishmania tropica: defective intracellular killing of amastigotes by macrophages elicited with sterile inflammatory agents. , 1984, Journal of immunology.

[39]  D. Hoover,et al.  Intracellular replication of Leishmania tropica in mouse peritoneal macrophages: amastigote infection of resident cells and inflammatory exudate macrophages , 1982, Infection and immunity.

[40]  Youmans Gp,et al.  The enumeration of nonpathogenic viable tubercle bacilli from the organs of mice. , 1957 .

[41]  R. Dubos,et al.  VIRULENCE AND MORPHOLOGICAL CHARACTERISTICS OF MAMMALIAN TUBERCLE BACILLI , 1947, The Journal of experimental medicine.

[42]  R. Dubos,et al.  INFECTION OF MICE WITH MAMMALIAN TUBERCLE BACILLI GROWN IN TWEEN-ALBUMIN LIQUID MEDIUM , 1947, The Journal of experimental medicine.

[43]  E. Coligan.  Current protocols in immunology , 1991 .

[44]  M. Denis.  Interferon-gamma-treated murine macrophages inhibit growth of tubercle bacilli via the generation of reactive nitrogen intermediates. , 1991, Cellular immunology.

[45]  M Denis,et al.  Cytokine modulation of Mycobacterium tuberculosis growth in human macrophages. , 1990, International journal of immunopharmacology.

[46]  I. Orme,et al.  Materials and Methods Briefdefinitive Report Disseminated Tuberculosis in Interferon 7 Gene-disrupted Mice , 2022 .