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J Salinas - One of the best experts on this subject based on the ideXlab platform.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:A Th1 immune response involving gamma interferon (IFN-γ) production is required to eliminate Chlamydophila abortusinfections. In this study, the role of interleukin-12 (IL-12) in protecting against C. abortus infection was investigated using IL-12−/− and wild-type (WT) C57BL/6 mice to determine the role of this Th1-promoting cytokine. IL-12−/− mice were able to eliminate the C. abortus infection in a primary infection. However, there was a delay in the clearance of bacteria when IL-12−/− mice were infected with a sublethal dose of C. abortus, the delay being associated with a lower production of IFN-γ. The low level of IFN-γ was essential for survival of IL-12−/−infected mice. Both WT and IL-12−/− mice developed a Th1 immune response against C. abortus infection, since they both produced IFN-γ and Immunoglobulin G2a antibody isotype. In addition, when mice were given a secondary infectious challenge withC. abortus, a protective host response which resolved the secondary infection was developed by both WT and IL-12−/−mice. The lack of IL-12 resulted in few infiltrating CD4+ T cells in the liver relative to the number in WT mice, although the number of CD8+ T cells was slightly higher. The more intense Th1 response presented by WT mice may have a pathogenic effect, as the animals showed higher morbidity after the infection. In conclusion, these results suggest that although IL-12 expedites the clearance of C. abortus infection, this cytokine is not essential for the establishment of a protective host response against the infection.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: Laura Del Rio, A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:Chlamydophila abortus (Chlamydia psittaci serotype 1) is a gram-negative intracellular bacterium that replicates in cell phagosomes, thus preventing their fusion with lysosomes (12). This bacterium, which has been recorded worldwide, is the etiologic agent of enzootic abortion in small ruminants, infecting the placenta and causing abortion during the last trimester of gestation (35). In addition to the economic losses it causes, this pathogen also represents a potential zoonotic risk for pregnant women (7). Mouse models have been widely used to study the pathogenesis and immune response to chlamydial infections. Mice experimentally infected with the bacteria show a fever syndrome followed by abortion. This syndrome is similar to that presented in the natural infection of chlamydial abortion in humans and small ruminants. The host response is immediately activated in organs such as the liver and the spleen. Meanwhile, the bacteria replicate in the placenta, which is an immunocompromised organ (6). Although innate immune mechanisms, especially neutrophils, play an important role (3), chlamydial infection is ultimately controlled by a specific Th1 immune response characterized by the production of high levels of gamma interferon (IFN-γ) and the presence of T cells, particularly CD8+ T cells (5, 9, 11, 25, 26). However, the mechanisms involved in the development of this cellular immune response have been poorly studied in C. abortus infection. In murine experimental infections with other species of the family Chlamydiaceae, such as Chlamydia trachomatis and Chlamydophila pneumoniae, this response has been defined, at least in part, as being interleukin-12 (IL-12)-dependent (15, 21). We have recently reported that IL-12 is produced early during C. abortus infection (5), and it has been reported that treatment with exogenous IL-12 confers immediate and long-term protection in susceptible BALB/c mice intranasally infected with C. abortus (17). IL-12 is a heterodimeric cytokine, which is produced primarily by phagocytic cells and dendritic cells in response to infections caused by intracellular pathogens such as bacteria (19, 39), fungi (10, 23), protozoa (1, 14), and viruses (24, 28). It has been reported that IL-12 increases NK cell and T-lymphocyte cytotoxic activity, favors Th1 differentiation, and triggers the production of IFN-γ and other proinflammatory cytokines (22, 41). However, some recent findings point to a more complicated picture, the role of IL-12 in the immune response to certain intracellular pathogens seeming to be ambiguous. Indeed, this cytokine has both protective and pathogenic functions in infections with species such as Plasmodium (43, 44) and Leishmania (37). Furthermore, in the host response to some virus infections, a Th1 response was established in the absence of IL-12. This response was characterized by both T-cell IFN-γ release and Immunoglobulin G2a (IgG2a) production (29, 42). The aim of this study, therefore, was to further define the role of endogenous IL-12 in host resistance against C. abortus infection. For this purpose, we used wild-type (WT) C57BL/6 mice, a strain that is relatively resistant to chlamydial infection (8), and IL-12 p40-deficient mice (IL-12−/−) to assess the IL-12-mediated mechanisms that control the primary replication of the bacteria in the immune response to C. abortus infection.
Richard P Morrison - One of the best experts on this subject based on the ideXlab platform.
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chlamydia trachomatis genital tract infection of antibody deficient gene knockout mice
Infection and Immunity, 1997Co-Authors: K Feilzer, Harlan D Caldwell, Richard P MorrisonAbstract:The importance of antibody-mediated immunity in primary and secondary Chlamydia trachomatis genital tract infections was examined by using a definitive model of B-cell deficiency, the microMT/microMT gene knockout mouse. Vaginally infected B-cell-deficient microMT/microMT mice developed a self-limiting primary infection that was indistinguishable from infection of control C57BL/6 mice. Sera and vaginal secretions from infected mice were analyzed for anti-Chlamydia antibodies. C57BL/6 mice produced high-titered serum anti-Chlamydia Immunoglobulin G2a (IgG2a), IgG2b, and IgA antibodies, and vaginal washes contained predominately anti-Chlamydia IgA. Serum and vaginal washes from infected B-cell-deficient mice were negative for anti-Chlamydia antibody. T-cell proliferation and delayed-type hypersensitivity assays were used as measures of Chlamydia-specific cell-mediated immunity and were found to be comparable for C57BL/6 and B-cell-deficient mice. Seventy days following primary infection, mice were rechallenged to assess acquired immunity. B-cell-deficient mice which lack anti-Chlamydia antibodies were more susceptible to reinfection than immunocompetent C57BL/6 mice. However, acquired immune resistance was evident in both strains of mice and characterized by decreased shedding of chlamydiae and an infection of shorter duration. Thus, this study demonstrates that cell-mediated immune responses alone were capable of resolving chlamydial infection; however, in the absence of specific antibody, mice were more susceptible to reinfection. Therefore, these data suggest that both humoral and cell-mediated immune responses were important mediators of immune protection in this model, though cell-mediated immune responses appear to play a more dominant role.
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gene knockout mice establish a primary protective role for major histocompatibility complex class ii restricted responses in chlamydia trachomatis genital tract infection
Infection and Immunity, 1995Co-Authors: Richard P Morrison, K Feilzer, D B TumasAbstract:Mice with disrupted beta 2-microglobulin (beta 2m-/-), I-A (class II-/-), or CD4 (CD4-/-) genes were examined for their capacity to resolve Chlamydia trachomatis genital tract infection. C57BL/6 and beta 2m-/- mice resolved infection similarly and were culture negative by 4 to 5 weeks following infection. Conversely, major histocompatibility complex (MHC) class II-/- mice failed to resolve infection, and CD4-/- mice showed a significant delay (2 weeks). Secondary challenge of C57BL/6, beta 2m-/-, and CD4-/- mice established that acquired protective immunity, which was characterized by an infection of shortened duration and reduced shedding of infectious organisms, developed. Serological analysis of C57BL/6 and beta 2m-/- mice by enzyme-linked immunosorbent assays revealed no striking differences in the Immunoglobulin subclass specificity of the anti-Chlamydia response, although some differences were observed in the magnitude of the Immunoglobulin G2a (IgG2a) and IgG2b responses. Class II-/- mice produced lower-titered serum anti-Chlamydia antibodies of all isotypes. The serum antibody responses of CD4-/- mice were similar to those of C57BL/6 mice, except that the anti-Chlamydia IgA response was delayed by approximately 3 weeks. Analysis of vaginal washes for Chlamydia-reactive antibodies revealed the presence of IgG2a, IgG2b, and IgA in C57BL/6 and beta 2m-/- mice and primarily of IgA in CD4-/- mice. Vaginal washes from class II-/- mice were consistently antibody negative. Interestingly, the Chlamydia-specific IgA response in the vaginal washes of CD4-/- mice was delayed, but its appearance coincided with decreased shedding of infectious organisms and resolution of infection. Our results demonstrate that MHC class II-restricted T-cell responses are necessary for the development of protective immunity to Chlamydia genital tract infection and that local (vaginal) anti-Chlamydia IgA antibody coincides with the resolution of infection. A substantive role for MHC class I-restricted T-cell responses in protective immunity to Chlamydia genital tract infection was not confirmed.
A J Buendia - One of the best experts on this subject based on the ideXlab platform.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:A Th1 immune response involving gamma interferon (IFN-γ) production is required to eliminate Chlamydophila abortusinfections. In this study, the role of interleukin-12 (IL-12) in protecting against C. abortus infection was investigated using IL-12−/− and wild-type (WT) C57BL/6 mice to determine the role of this Th1-promoting cytokine. IL-12−/− mice were able to eliminate the C. abortus infection in a primary infection. However, there was a delay in the clearance of bacteria when IL-12−/− mice were infected with a sublethal dose of C. abortus, the delay being associated with a lower production of IFN-γ. The low level of IFN-γ was essential for survival of IL-12−/−infected mice. Both WT and IL-12−/− mice developed a Th1 immune response against C. abortus infection, since they both produced IFN-γ and Immunoglobulin G2a antibody isotype. In addition, when mice were given a secondary infectious challenge withC. abortus, a protective host response which resolved the secondary infection was developed by both WT and IL-12−/−mice. The lack of IL-12 resulted in few infiltrating CD4+ T cells in the liver relative to the number in WT mice, although the number of CD8+ T cells was slightly higher. The more intense Th1 response presented by WT mice may have a pathogenic effect, as the animals showed higher morbidity after the infection. In conclusion, these results suggest that although IL-12 expedites the clearance of C. abortus infection, this cytokine is not essential for the establishment of a protective host response against the infection.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: Laura Del Rio, A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:Chlamydophila abortus (Chlamydia psittaci serotype 1) is a gram-negative intracellular bacterium that replicates in cell phagosomes, thus preventing their fusion with lysosomes (12). This bacterium, which has been recorded worldwide, is the etiologic agent of enzootic abortion in small ruminants, infecting the placenta and causing abortion during the last trimester of gestation (35). In addition to the economic losses it causes, this pathogen also represents a potential zoonotic risk for pregnant women (7). Mouse models have been widely used to study the pathogenesis and immune response to chlamydial infections. Mice experimentally infected with the bacteria show a fever syndrome followed by abortion. This syndrome is similar to that presented in the natural infection of chlamydial abortion in humans and small ruminants. The host response is immediately activated in organs such as the liver and the spleen. Meanwhile, the bacteria replicate in the placenta, which is an immunocompromised organ (6). Although innate immune mechanisms, especially neutrophils, play an important role (3), chlamydial infection is ultimately controlled by a specific Th1 immune response characterized by the production of high levels of gamma interferon (IFN-γ) and the presence of T cells, particularly CD8+ T cells (5, 9, 11, 25, 26). However, the mechanisms involved in the development of this cellular immune response have been poorly studied in C. abortus infection. In murine experimental infections with other species of the family Chlamydiaceae, such as Chlamydia trachomatis and Chlamydophila pneumoniae, this response has been defined, at least in part, as being interleukin-12 (IL-12)-dependent (15, 21). We have recently reported that IL-12 is produced early during C. abortus infection (5), and it has been reported that treatment with exogenous IL-12 confers immediate and long-term protection in susceptible BALB/c mice intranasally infected with C. abortus (17). IL-12 is a heterodimeric cytokine, which is produced primarily by phagocytic cells and dendritic cells in response to infections caused by intracellular pathogens such as bacteria (19, 39), fungi (10, 23), protozoa (1, 14), and viruses (24, 28). It has been reported that IL-12 increases NK cell and T-lymphocyte cytotoxic activity, favors Th1 differentiation, and triggers the production of IFN-γ and other proinflammatory cytokines (22, 41). However, some recent findings point to a more complicated picture, the role of IL-12 in the immune response to certain intracellular pathogens seeming to be ambiguous. Indeed, this cytokine has both protective and pathogenic functions in infections with species such as Plasmodium (43, 44) and Leishmania (37). Furthermore, in the host response to some virus infections, a Th1 response was established in the absence of IL-12. This response was characterized by both T-cell IFN-γ release and Immunoglobulin G2a (IgG2a) production (29, 42). The aim of this study, therefore, was to further define the role of endogenous IL-12 in host resistance against C. abortus infection. For this purpose, we used wild-type (WT) C57BL/6 mice, a strain that is relatively resistant to chlamydial infection (8), and IL-12 p40-deficient mice (IL-12−/−) to assess the IL-12-mediated mechanisms that control the primary replication of the bacteria in the immune response to C. abortus infection.
J Sanchez - One of the best experts on this subject based on the ideXlab platform.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:A Th1 immune response involving gamma interferon (IFN-γ) production is required to eliminate Chlamydophila abortusinfections. In this study, the role of interleukin-12 (IL-12) in protecting against C. abortus infection was investigated using IL-12−/− and wild-type (WT) C57BL/6 mice to determine the role of this Th1-promoting cytokine. IL-12−/− mice were able to eliminate the C. abortus infection in a primary infection. However, there was a delay in the clearance of bacteria when IL-12−/− mice were infected with a sublethal dose of C. abortus, the delay being associated with a lower production of IFN-γ. The low level of IFN-γ was essential for survival of IL-12−/−infected mice. Both WT and IL-12−/− mice developed a Th1 immune response against C. abortus infection, since they both produced IFN-γ and Immunoglobulin G2a antibody isotype. In addition, when mice were given a secondary infectious challenge withC. abortus, a protective host response which resolved the secondary infection was developed by both WT and IL-12−/−mice. The lack of IL-12 resulted in few infiltrating CD4+ T cells in the liver relative to the number in WT mice, although the number of CD8+ T cells was slightly higher. The more intense Th1 response presented by WT mice may have a pathogenic effect, as the animals showed higher morbidity after the infection. In conclusion, these results suggest that although IL-12 expedites the clearance of C. abortus infection, this cytokine is not essential for the establishment of a protective host response against the infection.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: Laura Del Rio, A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:Chlamydophila abortus (Chlamydia psittaci serotype 1) is a gram-negative intracellular bacterium that replicates in cell phagosomes, thus preventing their fusion with lysosomes (12). This bacterium, which has been recorded worldwide, is the etiologic agent of enzootic abortion in small ruminants, infecting the placenta and causing abortion during the last trimester of gestation (35). In addition to the economic losses it causes, this pathogen also represents a potential zoonotic risk for pregnant women (7). Mouse models have been widely used to study the pathogenesis and immune response to chlamydial infections. Mice experimentally infected with the bacteria show a fever syndrome followed by abortion. This syndrome is similar to that presented in the natural infection of chlamydial abortion in humans and small ruminants. The host response is immediately activated in organs such as the liver and the spleen. Meanwhile, the bacteria replicate in the placenta, which is an immunocompromised organ (6). Although innate immune mechanisms, especially neutrophils, play an important role (3), chlamydial infection is ultimately controlled by a specific Th1 immune response characterized by the production of high levels of gamma interferon (IFN-γ) and the presence of T cells, particularly CD8+ T cells (5, 9, 11, 25, 26). However, the mechanisms involved in the development of this cellular immune response have been poorly studied in C. abortus infection. In murine experimental infections with other species of the family Chlamydiaceae, such as Chlamydia trachomatis and Chlamydophila pneumoniae, this response has been defined, at least in part, as being interleukin-12 (IL-12)-dependent (15, 21). We have recently reported that IL-12 is produced early during C. abortus infection (5), and it has been reported that treatment with exogenous IL-12 confers immediate and long-term protection in susceptible BALB/c mice intranasally infected with C. abortus (17). IL-12 is a heterodimeric cytokine, which is produced primarily by phagocytic cells and dendritic cells in response to infections caused by intracellular pathogens such as bacteria (19, 39), fungi (10, 23), protozoa (1, 14), and viruses (24, 28). It has been reported that IL-12 increases NK cell and T-lymphocyte cytotoxic activity, favors Th1 differentiation, and triggers the production of IFN-γ and other proinflammatory cytokines (22, 41). However, some recent findings point to a more complicated picture, the role of IL-12 in the immune response to certain intracellular pathogens seeming to be ambiguous. Indeed, this cytokine has both protective and pathogenic functions in infections with species such as Plasmodium (43, 44) and Leishmania (37). Furthermore, in the host response to some virus infections, a Th1 response was established in the absence of IL-12. This response was characterized by both T-cell IFN-γ release and Immunoglobulin G2a (IgG2a) production (29, 42). The aim of this study, therefore, was to further define the role of endogenous IL-12 in host resistance against C. abortus infection. For this purpose, we used wild-type (WT) C57BL/6 mice, a strain that is relatively resistant to chlamydial infection (8), and IL-12 p40-deficient mice (IL-12−/−) to assess the IL-12-mediated mechanisms that control the primary replication of the bacteria in the immune response to C. abortus infection.
M C Gallego - One of the best experts on this subject based on the ideXlab platform.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:A Th1 immune response involving gamma interferon (IFN-γ) production is required to eliminate Chlamydophila abortusinfections. In this study, the role of interleukin-12 (IL-12) in protecting against C. abortus infection was investigated using IL-12−/− and wild-type (WT) C57BL/6 mice to determine the role of this Th1-promoting cytokine. IL-12−/− mice were able to eliminate the C. abortus infection in a primary infection. However, there was a delay in the clearance of bacteria when IL-12−/− mice were infected with a sublethal dose of C. abortus, the delay being associated with a lower production of IFN-γ. The low level of IFN-γ was essential for survival of IL-12−/−infected mice. Both WT and IL-12−/− mice developed a Th1 immune response against C. abortus infection, since they both produced IFN-γ and Immunoglobulin G2a antibody isotype. In addition, when mice were given a secondary infectious challenge withC. abortus, a protective host response which resolved the secondary infection was developed by both WT and IL-12−/−mice. The lack of IL-12 resulted in few infiltrating CD4+ T cells in the liver relative to the number in WT mice, although the number of CD8+ T cells was slightly higher. The more intense Th1 response presented by WT mice may have a pathogenic effect, as the animals showed higher morbidity after the infection. In conclusion, these results suggest that although IL-12 expedites the clearance of C. abortus infection, this cytokine is not essential for the establishment of a protective host response against the infection.
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endogenous interleukin 12 is not required for resolution of chlamydophila abortus chlamydia psittaci serotype 1 infection in mice
Infection and Immunity, 2001Co-Authors: Laura Del Rio, A J Buendia, J Sanchez, M C Gallego, M R Caro, N Ortega, J Seva, F J Pallares, F Cuello, J SalinasAbstract:Chlamydophila abortus (Chlamydia psittaci serotype 1) is a gram-negative intracellular bacterium that replicates in cell phagosomes, thus preventing their fusion with lysosomes (12). This bacterium, which has been recorded worldwide, is the etiologic agent of enzootic abortion in small ruminants, infecting the placenta and causing abortion during the last trimester of gestation (35). In addition to the economic losses it causes, this pathogen also represents a potential zoonotic risk for pregnant women (7). Mouse models have been widely used to study the pathogenesis and immune response to chlamydial infections. Mice experimentally infected with the bacteria show a fever syndrome followed by abortion. This syndrome is similar to that presented in the natural infection of chlamydial abortion in humans and small ruminants. The host response is immediately activated in organs such as the liver and the spleen. Meanwhile, the bacteria replicate in the placenta, which is an immunocompromised organ (6). Although innate immune mechanisms, especially neutrophils, play an important role (3), chlamydial infection is ultimately controlled by a specific Th1 immune response characterized by the production of high levels of gamma interferon (IFN-γ) and the presence of T cells, particularly CD8+ T cells (5, 9, 11, 25, 26). However, the mechanisms involved in the development of this cellular immune response have been poorly studied in C. abortus infection. In murine experimental infections with other species of the family Chlamydiaceae, such as Chlamydia trachomatis and Chlamydophila pneumoniae, this response has been defined, at least in part, as being interleukin-12 (IL-12)-dependent (15, 21). We have recently reported that IL-12 is produced early during C. abortus infection (5), and it has been reported that treatment with exogenous IL-12 confers immediate and long-term protection in susceptible BALB/c mice intranasally infected with C. abortus (17). IL-12 is a heterodimeric cytokine, which is produced primarily by phagocytic cells and dendritic cells in response to infections caused by intracellular pathogens such as bacteria (19, 39), fungi (10, 23), protozoa (1, 14), and viruses (24, 28). It has been reported that IL-12 increases NK cell and T-lymphocyte cytotoxic activity, favors Th1 differentiation, and triggers the production of IFN-γ and other proinflammatory cytokines (22, 41). However, some recent findings point to a more complicated picture, the role of IL-12 in the immune response to certain intracellular pathogens seeming to be ambiguous. Indeed, this cytokine has both protective and pathogenic functions in infections with species such as Plasmodium (43, 44) and Leishmania (37). Furthermore, in the host response to some virus infections, a Th1 response was established in the absence of IL-12. This response was characterized by both T-cell IFN-γ release and Immunoglobulin G2a (IgG2a) production (29, 42). The aim of this study, therefore, was to further define the role of endogenous IL-12 in host resistance against C. abortus infection. For this purpose, we used wild-type (WT) C57BL/6 mice, a strain that is relatively resistant to chlamydial infection (8), and IL-12 p40-deficient mice (IL-12−/−) to assess the IL-12-mediated mechanisms that control the primary replication of the bacteria in the immune response to C. abortus infection.
