Primary and Secondary Syphilis Lesions Contain mRNA for Thl Cytokines

Voorhis, Wesley C. Van; Barrett, Lynn K.; Koelle, David M.; Nasio, James M.; Plummer, Francis A.; Lukehart, Sheila A.

doi:10.1093/infdis/173.2.491

Cited by 118 publications

(83 citation statements)

References 12 publications

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“…have low IgA levels or no IgA secretion (9). In the present case, a Thl-dominant cytokine pattern was observed, as is usually seen in neurosyphilis (4)(5)(6) the longest latency of all neurosyphilis syndromes, occurring 25 to 30 years after primary infection (10). The peak of incidence of tabes dorsalis is in the fourth and fifth decades of life, but the present patient was only 28 years old on admission.…”

Section: Discussionsupporting

confidence: 58%

Rapidly Progressive Tabes Dorsalis Associated with Selective IgA Deficiency.

et al. 2001

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Tabes dorsalis is uncommonand progresses slowly from infection to clinical manifestation. Wereport a rare case of rapidly progressive tabes dorsalis associated with selective IgA deficiency (slgAD). A 28-year-old man was hospitalized with lightning back pain, nausea, and bladder bowel dysfunction. Serum and cerebrospinal fluid (CSF) revealed high titers of Treponema pallidum antibody, and the serum IgA level was less than 5 mg/dl. Thl-dominant cytokine expression was observed, as is usually seen in neurosyphilis. He was treated with Ceftriaxone and CSF pleocytosis disappeared. Wepostulate slgAD influenced the atypical rapid clinical course of tabes dorsalis in this patient. (Internal Medicine 40: 972-975, 2001)

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Section: Discussionsupporting

confidence: 58%

Rapidly Progressive Tabes Dorsalis Associated with Selective IgA Deficiency.

et al. 2001

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“…28 It is possible that reduced IL-10 production by C3H/HeJ mice explains their increased susceptibility to arthritis during B. burgdorferi infection. In syphilis there is also evidence that IL-10 is induced by the spirochete Treponema palidum in both humans 34 and experimental animals. 35 Although one may be tempted to assign the differences in disease severity between Bt1 and Bt2 infected mice to differences in the proinflammatory ability of Vsp1 and Vsp2, several lines of evidence indicate this is not the case: 1) Vsp1 and Vsp2, like all members of the Vsp/ OspC family of borrelia lipoproteins, have the same common lipid modification 7,11,36 ; 2) our measures of inflammation in the heart and the brain of mice infected with Bt1 and Bt2 show strong correlations with the pathogen load rather than with the Vsp that is expressed (H.G.…”

Section: Discussionmentioning

confidence: 99%

Role of Interleukin 10 during Persistent Infection with the Relapsing Fever Spirochete Borrelia turicatae

Gelderblom

Schmidt

Londoño

et al. 2007

The American Journal of Pathology

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Relapsing fever is an infection characterized by peaks of spirochetemia attributable to antibody selection against variable serotypes. In the absence of B cells, serotypes cannot be cleared, resulting in persistent infection. We previously identified differences in spirochetemia and disease severity during persistent infection of severe combined immunodeficiency mice with isogenic serotypes 1 (Bt1) or 2 (Bt2) of Borrelia turicatae. To investigate this further, we studied pathogen load, clinical disease, cytokine/chemokine production, and inflammation in mice deficient in B (Igh6 ؊/؊ ) or B and T (Rag1 ؊/؊ ) cells persistently infected with Bt1 or Bt2. The results showed that Igh6 ؊/؊ mice, despite lower spirochetemia, had a significantly aggravated disease course compared with Rag1 ؊/؊ mice. Measurement of cytokines revealed a significant positive correlation between pathogen load and interleukin (IL)-10 in blood, brain, and heart. Bt2-infected Rag1 ؊/؊ mice harbored the highest spirochetemia and, at the same time, displayed the highest IL-10 plasma levels. In the brain, Bt1, which was five times more neurotropic than Bt2, caused higher IL-10 production. Activated microglia were the main source of IL-10 in brain. IL-10 injected systemically reduced disease and spirochetemia. The results suggest IL-10 plays a protective role as a downregulator of inflammation and pathogen load during infection with relapsing fever spirochetes. (Am J

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“…Therefore, it is highly likely that the enrichment for CLA ϩ T cells and DCs in the blister fluids reflected the expression of receptors for these molecules (i.e., E-and P-selectin) by activated vascular endothelium. It also is plausible that the innate response to treponemal lipoproteins helps to set the stage for the Th1 bias observed in primary and secondary syphilis lesions (8,59). DC1 cells, the subpopulation that expressed maturation markers and both costimulatory molecules within blister fluid, promote Th1 differentiation (48,60) and would be expected to do so during infection when presenting processed treponemal Ags to naive T cells within draining lymph nodes.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular infiltrates composed of T lymphocytes, macrophages, and plasma cells are the sine qua non of syphilitic lesions (1)(2)(3)(4)(5)(6)(7). Immunocytochemical and RT-PCR analyses of early syphilitic skin lesions have revealed that these infiltrating cells, as well as keratinocytes and proximal vascular endothelium, are activated and that the T cells are elaborating cytokines consistent with a Th1 response (4,8). Because macrophages are both professional phagocytes and a rich source of proinflammatory mediators, their presence in large numbers is thought to be central to both lesion formation and resolution (2,4,6).…”

Section: The Cutaneous Response In Humans Tomentioning

confidence: 99%

The Cutaneous Response in Humans toTreponema pallidumLipoprotein Analogues Involves Cellular Elements of Both Innate and Adaptive Immunity

Sellati

Waldrop

Salazar

et al. 2001

The Journal of Immunology

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To extend prior studies implicating treponemal lipoproteins as major proinflammatory agonists of syphilitic infection, we examined the responses induced by intradermal injection of human subjects with synthetic lipoprotein analogues (lipopeptides) corresponding to the N termini of the 17- and 47-kDa lipoproteins of Treponema pallidum. Responses were assessed visually and by flow cytometric analysis of dermal leukocyte populations within fluids aspirated from suction blisters raised over the injection sites. Lipopeptides elicited dose-dependent increases in erythema/induration and cellular infiltrates. Compared with peripheral blood, blister fluids were highly enriched for monocytes/macrophages, cutaneous lymphocyte Ag-positive memory T cells, and dendritic cells. PB and blister fluids contained highly similar ratios of CD123−/CD11c+ (DC1) and CD123+/CD11c− (DC2) dendritic cells. Staining for maturation/differentiation markers (CD83, CD1a) and costimulatory molecules (CD80/CD86) revealed that blister fluid DC1, but not DC2, cells were more developmentally advanced than their peripheral blood counterparts. Of particular relevance to the ability of syphilitic lesions to facilitate the transmission of M-tropic strains of HIV-1 was a marked enhancement of CCR5 positivity among mononuclear cells in the blister fluids. Treponemal lipopeptides have the capacity to induce an inflammatory milieu reminiscent of that found in early syphilis lesions. In contrast with in vitro studies, which have focused upon the ability of these agonists to stimulate isolated innate immune effector cells, in this study we show that in a complex tissue environment these molecules have the capacity to recruit cellular elements representing the adaptive as well as the innate arm of the cellular immune response.

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Primary and Secondary Syphilis Lesions Contain mRNA for Thl Cytokines

Cited by 118 publications

References 12 publications

Rapidly Progressive Tabes Dorsalis Associated with Selective IgA Deficiency.

Rapidly Progressive Tabes Dorsalis Associated with Selective IgA Deficiency.

Role of Interleukin 10 during Persistent Infection with the Relapsing Fever Spirochete Borrelia turicatae

The Cutaneous Response in Humans toTreponema pallidumLipoprotein Analogues Involves Cellular Elements of Both Innate and Adaptive Immunity

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