Gamma Interferon

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Jack S. Remington - One of the best experts on this subject based on the ideXlab platform.

  • synergistic activity of azithromycin and Gamma Interferon in murine toxoplasmosis
    Antimicrobial Agents and Chemotherapy, 1991
    Co-Authors: Fausto G. Araujo, Jack S. Remington
    Abstract:

    A dose of 75 mg of azithromycin per kg of body weight per day combined with a dose of 2 micrograms of Gamma Interferon per day and administered for 10 days protected at least 40% of mice infected with a lethal inoculum of Toxoplasma gondii. Azithromycin administered alone protected less than 10% of the mice; Gamma Interferon had no protective effect.

  • Role of Gamma Interferon in Toxoplasma gondii infection.
    European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 1991
    Co-Authors: C. S. Subauste, Jack S. Remington
    Abstract:

    Toxoplasma gondii has emerged as an important pathogen in the ever increasing numbers of patients with disorders of the immune system. Better understanding of the mechanisms of resistance of the host against this protozoan is important for development of safe, effective alternative treatment regimens for toxoplasmosis. Gamma Interferon is the cytokine that plays a central role in protection againstToxoplasma gondii. The purpose of this review is to highlight the current knowledge of the role of Gamma Interferon inToxoplasma gondii infection.

Marcia B. Goldberg - One of the best experts on this subject based on the ideXlab platform.

  • An essential role for Gamma Interferon in innate resistance to Shigella flexneri infection.
    Infection and immunity, 1998
    Co-Authors: Sing Sing Way, Alain C. Borczuk, Rene Dominitz, Marcia B. Goldberg
    Abstract:

    Shigella spp. are the major cause of bacillary dysentery worldwide. To identify immune effectors associated with protection of the naive host during infection, the susceptibility to pulmonary Shigella infection of each of various mouse strains that have a targeted deletion in a specific aspect of the immune system was evaluated. Our results demonstrate that mice deficient in Gamma Interferon are 5 orders of magnitude more susceptible to Shigella than are wild-type mice, whereas mice deficient in B and T lymphocytes or in T lymphocytes alone exhibit no difference in susceptibility. Significantly lower numbers of shigellae were recovered from immunocompetent compared with Gamma-Interferon-deficient mice after infection. While immunocompetent mice were able to clear a sublethal Shigella inoculum by day 5 postinfection, progressively increasing numbers of shigellae were cultured from the lungs of Gamma Interferon-deficient mice over the same period. Histopathology of the lungs from immunocompetent mice infected with a sublethal Shigella inoculum showed mild inflammatory changes, whereas the lungs from Gamma Interferon-deficient mice demonstrated progressively worsening acute bronchiolitis with ulceration. Further, the time to death in Gamma Interferon-deficient mice correlates inversely with the size of the Shigella inoculum. To identify the cellular source of Gamma Interferon, we infected SCID mice, T-cell-receptor-deficient mice, beige mice (a mouse strain deficient in natural killer [NK] cell activity), and mice depleted of NK cells using anti-asialo-GM1. Each NK cell-deficient mouse strain exhibited a 10-fold-greater susceptibility to Shigella infection than immunocompetent mice. To test the protective effects of Gamma Interferon in vitro, survival of intracellular Shigella was examined in primary macrophages from wild-type mice, primary macrophages from Gamma Interferon-deficient mice, a macrophage cell line, and a fibroblast cell line. Following activation with Gamma Interferon, each cell type eradicated intracellular Shigella, while nonactivated macrophages fostered Shigella replication and nonactivated fibroblast cells fostered both Shigella replication and intercellular spread. Taken together, these data establish that NK cell-mediated Gamma Interferon is essential to resistance following primary Shigella infection. Shigellosis is an invasive disease of the human intestinal tract that is responsible for 200 million cases of bacillary dysentery and 650,000 fatalities annually (15). The disease process is thought to involve bacterial translocation across M cells within the gastrointestinal tract, phagocytosis by macrophages with subsequent lysis of the phagosomes, and induction of apoptosis in infected macrophages with release of proinflammatory mediators (12, 26, 30, 31). Inflammation further promotes Shigella invasion and intercellular spread between gut epithelial cells, which leads to necrosis (20, 21). These processes are thought to account for the diarrhea and dysentery that occur in the course of shigellosis. Immune mechanisms necessary for protection against shigellosis are poorly defined due to the lack of a convenient infection model. While both macrophage and epithelial cell lines can be infected with shigellae, the relative contributions of macrophage and epithelial-cell infection to pathogenesis are unclear. It is becoming increasingly evident that the host inflammatory response plays an important role in Shigella pathogenesis. Therefore, manipulable models which provide intact immune systems are necessary in order to elucidate the relationship between host cell infection, the inflammatory response following infection, and pathogenesis. Recently, a murine model of intranasal Shigella infection has been reported

Fausto G. Araujo - One of the best experts on this subject based on the ideXlab platform.

C. S. Subauste - One of the best experts on this subject based on the ideXlab platform.

  • Role of Gamma Interferon inToxoplasma gondii infection
    European Journal of Clinical Microbiology and Infectious Diseases, 1991
    Co-Authors: C. S. Subauste, J. S. Remington
    Abstract:

    Toxoplasma gondii has emerged as an important pathogen in the ever increasing numbers of patients with disorders of the immune system. Better understanding of the mechanisms of resistance of the host against this protozoan is important for development of safe, effective alternative treatment regimens for toxoplasmosis. Gamma Interferon is the cytokine that plays a central role in protection against Toxoplasma gondii . The purpose of this review is to highlight the current knowledge of the role of Gamma Interferon in Toxoplasma gondii infection.

  • Role of Gamma Interferon in Toxoplasma gondii infection.
    European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 1991
    Co-Authors: C. S. Subauste, Jack S. Remington
    Abstract:

    Toxoplasma gondii has emerged as an important pathogen in the ever increasing numbers of patients with disorders of the immune system. Better understanding of the mechanisms of resistance of the host against this protozoan is important for development of safe, effective alternative treatment regimens for toxoplasmosis. Gamma Interferon is the cytokine that plays a central role in protection againstToxoplasma gondii. The purpose of this review is to highlight the current knowledge of the role of Gamma Interferon inToxoplasma gondii infection.

J. S. Remington - One of the best experts on this subject based on the ideXlab platform.

  • Role of Gamma Interferon inToxoplasma gondii infection
    European Journal of Clinical Microbiology and Infectious Diseases, 1991
    Co-Authors: C. S. Subauste, J. S. Remington
    Abstract:

    Toxoplasma gondii has emerged as an important pathogen in the ever increasing numbers of patients with disorders of the immune system. Better understanding of the mechanisms of resistance of the host against this protozoan is important for development of safe, effective alternative treatment regimens for toxoplasmosis. Gamma Interferon is the cytokine that plays a central role in protection against Toxoplasma gondii . The purpose of this review is to highlight the current knowledge of the role of Gamma Interferon in Toxoplasma gondii infection.