The pattern and level of cytokines secreted by Th1 and Th2 lymphocytes of syphilitic patients correlate to the progression of the disease

Abstract

The results of our previous work indicated that cell-mediated immune response, of importance in protection against Treponema pallidum, is distinctly inhibited at certain periods of syphilitic infection. Considering that cytokines, produced by Th1 lymphocytes, take part in this response and that their secretion may be regulated by cytokines of Th2 lymphocytes, we examined if, and in which stages of syphilis, such a regulation may exist. In this study we have examined the ability of cells to produce IL-2, IFN and TNF (Th1 or Th1 like cytokines) as well as IL-6 and IL-10 (Th2 or Th2 like cytokines). It was found that cells of syphilitic patients were able to produce IL-2, IFN, TNF, IL-10 and weakly IL-6 already in primary seronegative syphilis. At the same stage of syphilis, but seropositive, ability of Th1 lymphocytes to produce cytokines reached the highest values, whereas the cells producing IL-10 lost this ability. The cells producing IL-6 and MIF had the highest ability in secondary early syphilis. In this stage of syphilis again slightly increased the ability of cells to secrete IL-10, which reached the highest value in early latent syphilis. The growing ability to produce IL-6 and IL-10 was accompanied with a diminished production of IL-2, IFN and TNF nearly in all stages of syphilis. Only MIF, in contrast to other cytokines, was produced in late syphilis without distinct changes. The greatest suppression of Th1 lymphocytes to produce cytokines and cells to secretion of MIF was found in early latent syphilis when the level of IL-10 in cell culture supernates was the highest. High ability of Th2 lymphocytes to cytokines secretion in late syphilis and low ability of Th1 ones, which are very important for cell-mediated immune response, may be the reason for facilitating T. pallidum multiplication and development of latent stages of disease despite presence of immunologically competent cells.

Eosinophil‐rich syphilis: a report of four cases

“…4,7,13 Some studies suggest that eosinophil attractant cytokines play a role in these non-hypersensitivity phenomena. 12,14 Eosinophilic dermatosis of hematologic malignancy is a rare skin disease associated with chronic lymphocytic leukemia, which shows perivascular inflammation with increased eosinophils and mimics an insect bite. 13 Davis et al showed enhanced eosinophil survival in culture in the presence of tissue extracted from eosinophilic dermatosis of hematologic malignancy, indirectly revealing the presence of eosinophil attractant cytokines within lesions.…”

The Immunopathobiology of Syphilis: The Manifestations and Course of Syphilis Are Determined by the Level of Delayed-Type Hypersensitivity

“…However, if suppression of DTH is induced by AIDS or other induced immunosuppression (252), latency can be terminated more rapidly, and can be succeeded by a systemic infection that requires treatment with high doses of penicillin. In tertiary syphilis, studies of Th1 and Th2 cytokine production by lymphocytes demonstrated low Th1 cytokine production (cellular immunity) and high Th2 cytokine production (non-complement, fixing antibody response) (253). The authors propose that this cytokine imbalance is one of the reasons why T. pallidum multiplication and development of lesions occur in tertiary syphilis (253).…”

“…In tertiary syphilis, studies of Th1 and Th2 cytokine production by lymphocytes demonstrated low Th1 cytokine production (cellular immunity) and high Th2 cytokine production (non-complement, fixing antibody response) (253). The authors propose that this cytokine imbalance is one of the reasons why T. pallidum multiplication and development of lesions occur in tertiary syphilis (253). …”

Analysis of HIV-1 sequences before and after co-infecting syphilis

“…Thus, it is likely that the mutants harboring M184V were derived from latently infected reservoir cells which had been established while the patient had taken 3TC without NNRTI. Syphilis infection may have predisposed the reactivation of these proviruses [10,27].…”