Immunology of Chlamydial Infections

Lamont, Hayes C.; Nichols, Roger

doi:10.1007/978-1-4684-1009-9_18

Cited by 5 publications

(4 citation statements)

References 215 publications

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“…Cell-mediated and humoral immune responses to chlamydiae have been recorded after infection in humans and in a variety of animal models (7), but the role of these responses in the control of acute, chronic, or asymptomatic chlamydial infections is poorly understood. Macrophages play a role in eliminating a wide variety of pathogenic microorganisms from the host and are essential for the maintenance of resistance to infection.…”

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Inhibition of Chlamydia trachomatis replication in HEp-2 cells by human monocyte-derived macrophages

Manor

Sarov

1988

Infect Immun

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Monocytes (M) and macrophages are important components of the immune response to foreign agents. Using an in vitro system, we studied the influence of human M and M-derived macrophages (MdM) on the replication of Chlamydia trachomatis (L2/434) in HEp-2 cells. M or MdM were added to infected cells at a ratio of 4:1, and the resultant chlamydial yield was evaluated in one-step growth experiments. Chlamydial DNA production was evaluated by dot hybridization. Both M and MdM reduced chlamydial yield and DNA production, but the reductions caused by MdM were more pronounced. Electron microscopy showed that while control HEp-2 cells at 48 h postinfection contained large inclusions in which most particles were elementary bodies, the infected HEp-2 cells exposed to MdM contained small vacuoles with abnormal reticulate bodies and very few typical elementary bodies. Separation of the MdM from the HEp-2 cells by a membrane reduced the inhibitory effect of the MdM relative to that of MdM in direct contact with the infected cells. Addition of tumor necrosis factor antibodies to C. trachomatis-infected HEp-2 cells exposed to MdM (either in direct contact or separated by a membrane from the infected cells) reduced the inhibition of chlamydial DNA production. These data suggest the possibility that MdM may modulate C. trachomatis replication in vivo.

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Inhibition of Chlamydia trachomatis replication in HEp-2 cells by human monocyte-derived macrophages

Manor

Sarov

1988

Infect Immun

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“…DISCUSSION Perturbation of the immune system by C. trachomatis has been well studied but incompletely characterized. Persistent infiltrates of lymphocytes and macrophages have been found in the conjunctiva and cornea during trachoma (25), and lymphoid hyperplasia is a significant component of LGV (39). Antibodies against chlamydiae and their surface components have been detected in tears, genital secretions, and serum of infected individuals (25,37).…”

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confidence: 99%

“…Persistent infiltrates of lymphocytes and macrophages have been found in the conjunctiva and cornea during trachoma (25), and lymphoid hyperplasia is a significant component of LGV (39). Antibodies against chlamydiae and their surface components have been detected in tears, genital secretions, and serum of infected individuals (25,37). During early infancy, a period normally associated with immune hyporesponsiveness, chlamydial pneumonia is associated with pronounced hyperglobulinemia (4,44) and excessive numbers of B lymphocytes and plasma cells in the peripheral blood (Levitt et al., in press).…”

Section: Nd Not Donementioning

confidence: 99%

“…The role of the immune system in protecting individuals against reinfection or in resolving ongoing infections by chlamydiae is unclear. Both humoral and cell-mediated immunity induced by chlamydiae have been proposed as major factors involved in limiting chlamydial infections in animals (24,25,43,47). However, caution should be exercised when extrapolating from these systems to humans; many of the strains of chlamydiae as well as the natural history of illness in animal models differ in human infections (23,31,37).…”

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Chlamydia trachomatis stimulates human peripheral blood B lymphocytes to proliferate and secrete polyclonal immunoglobulins in vitro

Bard¹,

Levitt²

1984

Infect Immun

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Infectious Chlamydia trachomatis (LGV strain), obligate intracellular bacteria, stimulated human peripheral blood lymphocytes to proliferate and secrete immunoglobulins in vitro. In contrast, mock-infected preparations were unable to induce similar responses in peripheral blood lymphocytes. Although levels of immunoglobulin secreted into the media of LGV-stimulated cultures were greater than 10 micrograms/ml, we estimated that less than 1% of these molecules were directed against the bacteria itself, suggesting polyclonal antibody production. Since stimulation with Formalin-killed bacteria resulted in comparable numbers of plaque-forming cells (PFC) as infectious particles, we concluded that the polyclonal immunoglobulin response was not dependent on the in vitro chlamydial infectious process. The polyclonal PFC response induced by LGV was highly sensitive to monocyte inhibition. Although LGV induced proliferation of predominantly B cells, the numbers of generated PFC was increased by the addition of autologous T cells. Neither lymphocyte proliferation nor PFC responses of normal human volunteers correlated significantly with the presence or titer of antichlamydial antibodies in their sera.

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Immune Mechanisms in Chlamydial Eye Infection: Cellular Immune Responses In Chronic and Acute Disease

Young

Taylor

1984

Journal of Infectious Diseases

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The current studies detail cell-mediated immune responses to Chlamydia trachomatis antigen in both acute and chronically infected monkeys. Peripheral blood mononuclear leukocytes (PBMLs) from three groups of animals (immunized before infection, not immunized before infection, and chronically infected) were tested for the capacity to proliferate in response to C. trachomatis antigen in vitro. Only those animals that had been systemically immunized before acute ocular infection responded significantly. Coculturing macrophages from nonresponding animals with T cells from D-histocompatible responding animals showed that the ability to present antigen was unaffected in nonresponding animals. These studies also demonstrated that removal of suppressor T cells from PBMLs before culture resulted in increased proliferation in the chronically infected group and suggested that the nonresponsiveness seen in chronic ocular disease may be mediated by suppressor T cells.

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Immunology of Chlamydial Infections

Cited by 5 publications

References 215 publications

Inhibition of Chlamydia trachomatis replication in HEp-2 cells by human monocyte-derived macrophages

Inhibition of Chlamydia trachomatis replication in HEp-2 cells by human monocyte-derived macrophages

Chlamydia trachomatis stimulates human peripheral blood B lymphocytes to proliferate and secrete polyclonal immunoglobulins in vitro

Immune Mechanisms in Chlamydial Eye Infection: Cellular Immune Responses In Chronic and Acute Disease

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