Falsiporphyromonas endometrii gen. nov., sp. nov., isolated from the post-partum bovine uterus, and emended description of the genus Porphyromonas Shah and Collins 1988.

Two black-pigmented, anaerobic bacterial strains, designated LMM 40(T) and LMM 41, were isolated from the bovine post-partum endometrium of two Holstein cows. The 16S rRNA gene sequences of the two strains were identical and showed the highest similarity to the 16S rRNA gene sequence of the type strain of Porphyromonas crevioricanis (90.2%) but only 85.1% 16S rRNA gene sequence similarity to the type strain of the type species of the genus Porphyromonas, Porphyromonas asaccharolytica. The major fatty acid profiles of the two strains were similar to those of species of the genus Porphyromonas, containing iso-C(15 : 0) as the major component and moderate amounts of anteiso-C(15 : 0), iso-C(13 : 0), C(15 : 0) and C(16 : 0). Hydroxylated fatty acids, such as iso-C(14 : 0) 3-OH, iso-C(16 : 0) 3-OH and iso-C(17 : 0) 3-OH, were also detected. The quinone profiles were dominated by the menaquinones MK-8 and MK-9, while spermidine was the major polyamine. The polar lipid profiles contained major amounts of phosphatidylethanolamine, an unidentified phospholipid, an unidentified aminophospholipid and two unidentified lipids and minor amounts of phosphatidylglycerol, an unidentified aminolipid, a second unidentified aminophospholipid and an unidentified glycolipid. The cell-wall peptidoglycan contained meso-diaminopimelic acid. The genomic DNA G+C contents of LMM 40(T) and LMM 41 were 40.7 and 41.3 mol%, respectively. Based on a polyphasic approach, including phylogenetic analysis, physiological and biochemical tests as well as metabolic fingerprinting, it is proposed that the two strains are members of a novel genus and species, for which the name Falsiporphyromonas endometrii gen. nov., sp. nov. is proposed. The type strain of Falsiporphyromonas endometrii is LMM 40(T) ( = DSM 27210(T) = CCUG 64267(T)). An emended description of the genus Porphyromonas is also presented.

Apoptosis of T lymphocytes in liver and/or small bowel allografts during tolerance induction.

BACKGROUND: Apoptosis of parenchymal cells has been described during allograft rejection. Immunologically privileged tissue in the mouse has been found to prevent rejection by initiating apoptosis of infiltrating lymphocytes. The aim of this study was to investigate whether apoptosis may play a role in T-cell regulation during rejection and subsequent tolerance induction after liver transplantation (LTx) and combined liver/small bowel transplantation (LSBTx). METHODS: LTx and LSBTx (Brown Norway-->Lewis) were performed without immunosuppression. Cell migration, activation, and apoptosis were investigated by means of sequential histology, immunohistochemistry, and the terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling assay. Donor (Brown Norway) and third-party (Dark Agouti) cardiac allografts were transplanted into LSBTx recipients to determine specific tolerance. RESULTS: Transient acute cellular rejection occurred after LTx and LSBTx and was followed by specific tolerance. The kinetics of apoptosis were similar in liver allografts after LTx and LSBTx, but differed from the processes in small bowel allografts after LSBTx. Apoptosis of parenchymal cells in the grafted livers correlated directly with interleukin-2 receptor expression of the infiltrating T cells. During the late phase of rejection, a peak of apoptosis in the lymphocyte infiltrate was demonstrated, characterized as predominantly apoptotic CD8+ T lymphocytes. CONCLUSIONS: These results demonstrate that specific tolerance is achieved in both LTx and LSBTx after a transient rejection crisis. Apoptosis is involved in graft rejection and tolerance induction. Activation of T lymphocytes correlates with parenchymal cell apoptosis in the allograft. T-cell inactivation seems to result in apoptosis of cytotoxic T cells and tolerance, which appears to be unique to the liver allograft.