The ability of peripheral blood mononuclear cells of rabbits infected with Treponema pallidum to produce IL-2

Abstract

It was previously found that the cell-mediated immune response involved in protection against Treponema pallidum is distinctly suppressed during some periods in the course of syphilis infection in rabbits. This may be a result of the weak ability of cells to produce Interleukin-2 (IL-2) as well as of IL-2 absorption. The ability of peripheral blood mononuclear cells (PBMC) of syphilitic rabbits to produce IL-2 develops within the first two weeks after infection reaching a maximum in about the eleventh week. In infection of longer duration, this capability was distinctly lowered. This low level of activity (no higher than in PBMC of normal rabbits) was maintained for 31 weeks. The ability of PBMC to absorb IL-2, in parallel with its production, was found at the same time in the course of syphilis infection (7-11 weeks). In long-lasting syphilis (more than 12 weeks) both abilities seem to be inhibited. Sera of syphilitic rabbits were found to have a higher level of IL-2 inhibitor than those of normal rabbits. Only in syphilis lasting 9 to 11 weeks, when the production of IL-2 was the greatest, was the level of IL-2 inhibitor nearly the same as in normal rabbit sera. In syphilis lasting longer, the increased level of inhibitor was accompanied by a decreased ability of cells to produce IL-2. These findings suggest that IL-2 inhibitor may be bound to IL-2 or IL-2 receptor on T lymphocytes and in this way would lead to weakening of T cell function and resistance against Treponema pallidum infection.

Natural Pathogens of Laboratory Mice, Rats, and Rabbits and Their Effects on Research

“…Because most treponemes cannot be grown in vitro and because T. pallidum, the causative agent of human syphilis, is known to infect rabbits, the laboratory rabbit has been extensively used as a model of human syphilis (22,83,474,530,587). Consequently, a considerable body of information has been gathered on T. pallidum infections of rabbits, and cautious extrapolation to T. cuniculi is possible.…”

“…By using the rabbit-T. pallidum model, it has been demonstrated that the development of immunity is extremely complex and involves a composite of both stimulation and down-regulation (207). Mononuclear cells from rabbits chronically infected with T. pallidum may lose the ability to produce or bind IL-2 (530). Spleen cells of rabbits infected with T. pallidum produce antitreponemal lymphotoxins.…”

Endothelial dysfunction of syphilis: Pathogenesis

“…89 Previous studies have shown that there are high amounts of cytokines (IL-2, IL-6, IFNγ, TNF-α, IL-12, IL-17, IL-10, IL-23 and chemokines MCP-1, CXCL10, CX3CR1) existing in the lesions of primary and secondary syphilis or peripheral serum. [68][69][70][71][72][73]90 Under pathological conditions, certain pro-inflammatory mediators, especially TNF-α and IL-1β, may exacerbate ECD by upregulating the expression of adhesion molecules such as VCAM-1, ICAM-1, E-selectin and MCP-1, thereby promoting the adhesion and migration of leukocytes onto the endothelium. 91 In addition, IL-17, IFN-γ and CXCL13 are also abnormally highly expressed in peripheral blood and cerebrospinal fluid (CSF) of patients with neurosyphilis.…”

“…Cytokines include proteins from the tumour necrosis factor (TNF) family, interleukins, and chemokines 89 . Previous studies have shown that there are high amounts of cytokines (IL‐2, IL‐6, IFN‐γ, TNF‐α, IL‐12, IL‐17, IL‐10, IL‐23 and chemokines MCP‐1, CXCL10, CX3CR1) existing in the lesions of primary and secondary syphilis or peripheral serum 68–73,90 . Under pathological conditions, certain pro‐inflammatory mediators, especially TNF‐α and IL‐1β, may exacerbate ECD by upregulating the expression of adhesion molecules such as VCAM‐1, ICAM‐1, E‐selectin and MCP‐1, thereby promoting the adhesion and migration of leukocytes onto the endothelium 91 .…”