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Biomedical subjects

M Biondo

Publications and source records attributed to M Biondo.

7 recordsLinked to original sources
PubMed2006

Prednisolone promotes remission and gastric mucosal regeneration in experimental autoimmune gastritis.

A cardinal feature of organ-specific autoimmunity is destructive pathology in the target organ. In human and experimental models of autoimmune gastritis, mononuclear cell infiltration and cellular destruction in the gastric mucosa are disease hallmarks. Strategies to cure autoimmune disease must not only establish immunological tolerance to autoantigen, but also rid the organ of pathogenic autoreactive cells. The present study has assessed the effect of prednisolone treatment in clearing the inflammatory infiltrate in experimental autoimmune gastritis and in preventing disease relapse in athymic compared with euthymic mice. Experimental autoimmune gastritis was induced by neonatal thymectomy or by transgenic expression of GM-CSF (PC-GMCSF mice). Groups of mice were treated with prednisolone (10 mg/kg per day) for 10 weeks or with prednisolone for 10 weeks followed by 10 weeks without prednisolone. Stomachs were examined for gross morphological changes, and by histology and immunohistochemistry for composition of inflammatory infiltrate and gastric mucosal integrity. Autoantibody to gastric H+/K+ ATPase was determined by ELISA. Prednisolone promoted remission of gastritis in both mouse models of experimental autoimmune gastritis, evident by reduction in stomach size, clearing of gastric inflammatory infiltrate, and regeneration of the gastric mucosa. Prednisolone withdrawal resulted in disease relapse in all PC-GMCSF mice, whereas approximately 40% of neonatal thymectomy mice retained normal stomach morphology and remained free of gastric pathology. It is concluded that prednisolone promotes remission and gastric mucosal regeneration in experimental autoimmune gastritis. Prolonged remission of autoimmune gastritis in some athymic mice suggests a role for the thymus in disease relapse.

Animals↗
PubMed2001

Local transgenic expression of granulocyte macrophage-colony stimulating factor initiates autoimmunity.

Mechanisms leading to breakdown of immunological tolerance and initiation of autoimmunity are poorly understood. Experimental autoimmune gastritis is a paradigm of organ-specific autoimmunity arising from a pathogenic autoimmune response to gastric H/K ATPase. The gastritis is accompanied by autoantibodies to the gastric H/K ATPase. The best characterized model of experimental autoimmune gastritis requires neonatal thymectomy. This procedure disrupts the immune repertoire, limiting its usefulness in understanding how autoimmunity arises in animals with intact immune systems. Here we tested whether local production of GM-CSF, a pro-inflammatory cytokine, is sufficient to break tolerance and initiate autoimmunity. We generated transgenic mice expressing GM-CSF in the stomach. These transgenic mice spontaneously developed gastritis with an incidence of about 80% after six backcrosses to gastritis-susceptible BALBc/CrSlc mice. The gastritis is accompanied by mucosal hypertrophy, enlargement of draining lymph nodes and autoantibodies to gastric H/K ATPase. An infiltrate of dendritic cells and macrophages preceded CD4 T cells into the gastric mucosa. T cells from draining lymph nodes specifically proliferated to the gastric H/K ATPase. CD4 but not CD8 T cells transferred gastritis to nude mouse recipients. CD4(+) CD25(+) T cells from the spleen retained anergic suppressive properties that were reversed by IL-2. We conclude that local expression of GM-CSF is sufficient to break tolerance and initiate autoimmunity mediated by CD4 T cells. This new mouse model should be useful for studies of organ-specific autoimmunity.

Adoptive Transfer↗
PubMed1995

[Effect of gonadotrophins, testosterone and growth hormone on spermatogenesis in two hypophysectomy patients].

Human chorionic gonadotrophin (hCG), human menopausal gonadotrophins (hMG) and somatotrope hormone (STH) were used for three months to induce spermatogenesis in a patient with azoospermia following hypophysectomy for Cushing's syndrome. Azoospermia reappeared when testosterone was substituted for hCG, despite continued treatment with FSH and STH. In a second patient who had undergone hypophysectomy for a craniopharyngioma presenting residual oligospermia, STH alone was uneffective in improving the sperm count. In both patients, the level of IGF-1 in seminal fluid was unchanged by STH despite increased serum IGF-1. The use of STH to induce spermatogenesis is discussed in light of its capacity to increase testosterone synthesis is response to hCG.

Adult↗
PubMed1987

[Treatment of male sterility by in vitro fertilization].

A pregnancy obtained through in vitro fertilization in a case of male sterility due to oligospermia with high FSH is reported. After a review of controlled studies dealing with classical andrological treatments (repair of varicocele, treatment of prostatitis and immunological sterility), the place of in vitro fertilization is evaluated in relation to intrauterine insemination using active sperm.

Adult↗