Decreased expression of human heat shock protein 70 in the endometria and pathological lesions of women with adenomyosis and uterine myoma after GnRH agonist therapy

ObjectiveA prominent stress reaction in the pelvis of women with endometriosis and the role of human heat shock protein 70 (HSP70) in inflammation and the growth of endometriosis has been recently demonstrated. We report here expression of HSP70 in tissues derived from GnRH agonist (GnRHa)-untreated and -treated women with adenomyosis and uterine myoma.Study designThis is a case-controlled biological study. Biopsy specimens were collected from pathological lesions and eutopic endometria/autologous myometria of 30 women with adenomyosis, 35 women with uterine myoma and 15 control women during laparoscopy, laparotomy and hysteroscopy. Fourteen women with adenomyosis and 20 women with uterine myoma were treated with GnRHa for a variable period of 3?6 months before surgery. The immunoexpressions of HSP70 and CD68-positive M? in endometria, lesions/myometria were examined by immunohistochemistry. The immunoreactivity of HSP70 in tissues was analyzed by quantitative-histogram (Q-H) scores.ResultsComparing to control women, HSP70 immunoexpression was significantly higher in endometria/myometria and pathological lesions of women with adenomyosis and myoma. A significant positive correlation between Q-H scores of HSP70 and CD68-positive M? numbers was found in the endometria derived from women with adenomyosis (r = 0.388). Treatment with GnRHa significantly decreased Q-H scores of HSP70 in pathological lesions and endometria/myometria of women with adenomyosis and uterine myoma comparing to similar tissues derived from GnRHa-untreated women.ConclusionA variable amount of tissue stress reaction occurred in endometria and pathological lesions of women adenomyosis and uterine myoma that can be effectively suppressed after GnRHa treatment

Immune response to gut escherichia coli and susceptibility to adjuvant arthritis in the rats

We have investigated the humoral immune response to antigens of predominant gut aerobic bacterial strains (i.e. Escherichia coli) over the course of adjuvant arthritis and oil-induced arthritis in two inbred rat strains: Dark Agouti (DA) and Albino Oxford (AO). We report the presence of antibodies specific to proteins of Escherichia coli in molecular weight range between 20-30 kDa in sera of diseased DA rats, and the absence of these antibodies in the sera of AO rats. In DA rats, CFA and IFA provoked a stronger antibody response to Escherichia coli, especially of the IgG2b antibody class. Intramuscular administration of Escherichia coli preceding the adjuvant arthritis induction had no effect on the development and course of disease, as well as on the activation of T cells in the draining inguinal lymph nodes. Higher serum levels of natural and induced IgA antibodies, combined with a higher CD3(+)CD26(+) cell percentage were found in AO rats. The observed correlation between the serologic response to commensal flora and rats' genetic background as a defining factor for arthritis susceptibility may contribute to the process of creating a favorable (or less favorable) milieu for arthritis development

Common antigenicity between Japanese cedar (Cryptomeria japonica) pollen and Japanese cypress (Chamaecyparis obtusa) pollen, II. Determination of the cross‐reacting T‐cell epitope of Cry j 1 and Cha o 1 in mice

We have previously detected common antigenicity between Cry j 1 and Cha o 1 in B10.S mice. B10.S mice immunized with Cry j 1‐ or Cha o 1‐generated T cells and antibodies reactive to both allergens. In the present study, we investigated the cross‐reacting and Cry j 1‐specific T‐cell epitopes in B10.S mice. Lymph node cells from B10.S mice immunized with Cry j 1 recognized Cry j 1 p111–130, p211–230, and p310–330 as well as Cha o 1 p209–228. The existence of the cross‐reacting T‐cell epitope in Cry j 1 and Cha o 1 was confirmed by the response of newly established p211–230‐specific and Cha o 1 p209–228‐specific T‐cell lines. The minimum peptide sequence (p213–224) of the cross‐reacting T‐cell epitope was identical in Cry j 1 and Cha o 1. These findings clearly demonstrate that common antigenicity at the T‐cell level between Japanese cedar and cypress pollen allergens was caused by the existence of an identitical‐cell epitope in Cry j 1 and Cha o 1