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Biomedical subjects

B Steiniger

Publications and source records attributed to B Steiniger.

At least 19 recordsLinked to original sources
PubMed1992

Class II MHC molecules and monocytes/macrophages in the respiratory system of conventional, germ-free and interferon-gamma-treated rats.

The localization of I-A-like class II major histocompatibility complex (MHC) molecules and cells of the monocyte/macrophage lineage was studied immunohistologically in the trachea and lungs of conventional, specified pathogen-free (SPF) and germ-free rats. In the three groups of animals I-A-like class II MHC molecules occurred in epithelia of the bronchus-associated lymphatic tissue (BALT), in B lymphocytes, in dendritic-shaped and elongated interstitial cells and in type II pneumocytes. Conventional and SPF rats were distinguished from germ-free animals only by the larger number of class II MHC-positive respiratory epithelial cells in the lower trachea and main bronchi. The distribution of monocytes/macrophages (ED1-positive cells) did not differ between the groups. After systemic treatment of SPF rats with interferon-gamma class II MHC molecules were newly induced in all respiratory epithelia and in the endothelium of large vessels. In addition, interferon-gamma sometimes led to pulmonary infiltration and caused class II-positive activated monocytes to accumulate in medium-sized pulmonary vessels and in alveolar capillaries. It is concluded that the microbial status does not qualitatively alter the distribution of class II MHC molecules and monocytes/macrophages in rat respiratory organs. Interferon-gamma can, however, provoke profound changes.

Animals↗
PubMed1992

Differential response of kidney and pancreas rejection to cyclosporine immunosuppression.

Immunological interferences between kidney and pancreas transplants were investigated in a genetically defined rat model of combined kidney and pancreas transplantation. Kidney and whole-pancreas grafts were transplanted microsurgically either as individual grafts or in a combined technique. Whole pancreas grafts were grafted into streptozotocin diabetic recipients (55 mg/kg bodyweight i.v.) three days after induction of diabetes. The exocrine secretion was suppressed by duct ligation. Rejection of the grafts was defined by recurrence of diabetes in pancreas-grafted recipients and renal failure after kidney transplantation. There were marked differences in the efficacy of identical short-term cyclosporine immunosuppression (15 mg/kg intramuscularly for 14 days): DA kidneys survived indefinitely in LEW rats (MST greater than 100 days), while DA pancreas allografts underwent prolonged but not permanent survival (P less than 0.01) either as individual grafts (MST 27.3 +/- 1,9 days) or when transplanted simultaneously together with the kidney (44 +/- 16 days) (P less than 0.01). LEW rats carrying a DA kidney for 100 days also rejected a subsequent donor-specific pancreas transplant within 30 days. The histological alterations in the kidney were more pronounced than after cyclosporine-induced DA kidney long-term survival alone. By contrast to the rejecting subsequently transferred pancreas, a metachronous second DA kidney was permanently accepted (greater than 100 days) without further immunosuppression after removal of the first graft, while unrelated LEW. 1U kidneys were acutely rejected. In summary, the results indicate that there are not only quantitative differences of kidney and pancreas allograft survival but also differences concerning the state of immunological unresponsiveness induced by identical cyclosporine immunosuppression. While CsA induces donor-specific immunological unresponsiveness after kidney transplantation, pancreas transplants are all eventually rejected after some differential prolongation of survival. Further investigations on the effects of different MHC and minor alloantigens may provide more insight into the complex immunological situation of individual and combined kidney and pancreas transplantation.

Animals↗
PubMed1991

Progressive deterioration of endocrine function after intraportal but not kidney subcapsular rat islet transplantation.

In inbred streptozocin-induced diabetic rats, the long-term function of different endocrine pancreatic isografts was compared. Isolated islets transplanted into the portal vein showed a progressive deterioration of function over time. In contrast, islets under the kidney capsule sustained a constant long-term function controlling all clinical signs of diabetes. Recipients of kidney subcapsular islets displayed normal growth rate, peripheral serum glucose and insulin levels, and metabolic parameters. However, their functional reserve was markedly reduced as revealed by diminished glucose tolerance and reduced insulin-secreting capacity after an intravenous glucose challenge. Vascularized whole-organ pancreatic grafts with portal venous drainage led to complete normalization of all parameters determined in this study. This study showed that the long-term function of islets transplanted under the kidney capsule is superior compared with islets transplanted into the portal vein.

Animals↗
PubMed1990

[Suppression of exocrine secretion does not lead to disruption of endocrine function of pancreas transplants].

The adequate management of the exocrine secretion of vascularized pancreas transplants is still controversial. Basically, the exocrine graft secretion may either be suppressed by obstruction of the pancreatic ducts or preserved by drainage into the recipient's enteric or urinary tract. In a model of isogenic pancreas transplantation in streptozotocin diabetic rats the impact of preserved versus suppressed exocrine secretion on the quality of endocrine graft function was investigated. Preservation of the exocrine secretion was accomplished by pancreaticoduodenal transplantation, while duct ligation was used to suppress the exocrine secretion. Endocrine graft function was monitored by determination of non-fasting blood glucose levels, intravenous glucose tolerance tests, peripheral insulin levels, water and food intake as well as urine and faeces production. Suppression of the exocrine graft secretion induced acinar atrophy, proliferation of pancreatic ducts, interstitial cell infiltration and fragmentation of islets of Langerhans, while drainage of the exocrine graft secretion completely preserved the architecture of the transplant. Despite the fundamental structural changes induces by exocrine suppression no deterioration of endocrine graft function was noted within the observation period of one year. Both techniques were equally effective in ameliorating the diabetic hyperglycemia, hypoinsulinemia, reduced glucose tolerance, polydipsia, polyphagia, polyuria and restored normal growth rate and general health of diabetic pancreas graft recipients. Thus it can be concluded that suppression of the exocrine secretion does not impair the quality of endocrine function of pancreas transplants.

Animals↗
PubMed1990

Comparison of graft morphology and endocrine function after vascularized whole-pancrease transplantation in the rat by different surgical techniques.

Graft morphology and endocrine function following vascularized pancreas transplantation by different surgical techniques were determined in streptozotocin-diabetic rats. Eight different surgical techniques were studied. Intestinal drainage of exocrine secretion was accomplished by pancreaticoduodenal transplantation or by utilizing only a patch of the donor duodenum for duodenojejunostomy. Following pancreaticoureterostomy and pancreaticocystostomy, the graft's exocrine secretion was drained to the recipient's urinary tract. The exocrine secretion was allowed to drain freely into the recipient's peritoneal cavity following transverse or longitudinal incision of the common bile duct. Exocrine secretion was suppressed either by duct ligation or by retrograde ductal injection of prolamine. Following enteric or urinary exocrine graft drainage, the architecture of both the endocrine and exocrine pancreas was perfectly preserved. Pancreatic juice had remarkably few adverse effects on the recipient's urinary tract. Obstruction of the exocrine secretion induced atrophy of the acinar cells, proliferation of small pancreatic ducts, and a typical fragmentation of the islets of Langerhans. Prolamine was biologically degraded within 28 days. Following free intraperitoneal drainage, spontaneous suppression of the exocrine graft function occurred early after transplantation. Metabolic signs of diabetes mellitus including hypoinsulinemia, hyperglycemia, polydipsia, polyuria, and impaired glucose tolerance were completely normalized by pancreas transplantation irrespective of the surgical technique used. Despite fundamental differences in graft architecture no alteration of endocrine graft function was noted following vascularized pancreas transplantation by different surgical techniques.

Animals↗
PubMed1990

Gamma interferon treatment in vivo provokes accumulation of activated monocytes in the venous circulation of rats.

Activated monocytes forming intravascular clumps in the veins of most organs appeared in LEW rats after a 3-day intravenous treatment with recombinant rat gamma interferon. Phenotyping in situ and in cytospot preparations of perfusates revealed that the cells coexpressed the rat monocyte/macrophage antigen ED1 and class II MHC molecules. In addition, most cells reacted with a rat CD11b antibody and weakly expressed determinants detected by the W3/13 and Ox22 reagents. Minor fractions of the activated monocytes were positive for rat CD4 and the Ox2 and ED3 determinants. Cell proliferation was assessed by double staining for bromodeoxyuridine (BrdUrd) incorporation and phenotypic markers. Of the ED 1-positive class II-positive cells, 80% were labeled with BrdUrd after 3 days of combined infusion with gamma interferon. Pulse labeling for 30 minutes revealed 8% BrdUrd-positive intravascular ED 1-positive class II-positive monocytes in situ on day 3 of treatment, which contrasted with almost-absent labeling of this cell population in normal LEW rats. It is concluded that interferon not only promotes activation but also intravascular division of monocytes or their immediate precursors. Interestingly, cells of identical morphology and phenotype were observed in the vasculature of rats during lethal graft-versus-host reactions. Activated monocytes may thus contribute to the pathologic consequences of cytokine treatment and severe systemic immune reactions in vivo.

Animals↗
PubMed1990

Identical pattern of acute rejection after isolated islet and vascularized whole-pancreas transplantation in the rat.

The course of acute rejection of major histocompatibility complex (MHC)-incompatible isolated rat pancreatic islets transplanted under the kidney capsule was monitored functionally and histologically from day 1 to 10. The patterns observed were compared to those of vascularized whole-pancreas transplants with preserved and suppressed exocrine secretion. In addition the morphologic reactions after isogenic transplantation of islets or whole-pancreas transplants are described. The sequential patterns of acute rejection were found to be essentially identical in isolated islet and whole-pancreas allografts. This was also true for the process of I-A-like class II MHC antigen induction. Endocrine cell necrosis and reduced insulin content of beta cells were detected in isolated islets but not in whole-organ isografts. Thus ischemic damage may have occurred to be transplanted islets on days 1 and 2 because connections to the renal vasculature were not demonstrated before day 3. Islet cell loss was, however, functionally compensated by beta cell proliferation beginning on day 4. From the first day after transplantation, an altered spacial distribution of insulin- and glucagon-containing cells was present in islet isografts. This phenomenon was, however, not unique to islets, but also occurred in duct-ligated whole-organ isografts on days 6 to 10.

Acute Disease↗
PubMed1989

Genetic control of rat heart allograft rejection: effect of different MHC and non-MHC incompatibilities.

We investigated the genetic control of heterotopic heart allograft rejection using a family of standard inbred, major histocompatibility complex (MHC)-congenic, and intra-MHC recombinant rat strains. Gene products of the various regions within the rat MHC differed markedly in their capacity to induce rejection. Isolated incompatibility at class I antigens encoded by the RTl.A and RTl.C regions failed to induce rejection within the observation period of 100 days, whereas class II antigens encoded by the RTl.B/D region provoked rapid rejection within 10 days. By comparison of the rejection times of isolated and combined incompatibilities a number of functional interactions could be demonstrated between individual MHC regions which either prolonged or shortened allograft survival. In contrast to rapid rejection of MHC-mismatched heart allografts, differences at non-MHC histocompatibility antigens were associated with graft survival beyond 100 days, although chronic rejection of variable severity was detected histologically. Disparity at non-MHC plus class I antigens, however, provoked acute heart allograft rejection.

Animals↗