Developed and resolving lesions in porcine proliferative enteropathy: possible pathogenetic mechanisms.

Proliferative enteropathy, caused by Lawsonia intracellularis, offers the opportunity to examine bacterial mechanisms that influence epithelial cell proliferation. Ultrastructural features of developed and resolving lesions included the presence of enlarged intestinal crypts containing undifferentiated immature epithelial cells and an absence of goblet cells. Numerous intracytoplasmic bacteria, identified as L. intracellularis, were consistently present within affected cells. In recovering intestinal tissue, additional features were (1) the common presence of pale, swollen, protruding epithelial cells, (2) shrunken, degenerate epithelial cells, (3) apoptotic bodies in both epithelial cells and macrophages, (4) the reappearance of normal goblet cells, and (5) reduced numbers of L. intracellularis within lesions. Bacteria were released from cells via cytoplasmic and cellular protrusions into the intestinal lumen. It is speculated that the presence of the intracytoplasmic bacterium, L. intracellularis, may disrupt normal processes of cell growth, differentiation or apoptosis in the intestinal epithelium.

[1]  S. McOrist,et al.  Entry of the bacterium ileal symbiont intracellularis into cultured enterocytes and its subsequent release. , 1995, Research in Veterinary Science.

[2]  A. Wyllie,et al.  Apoptosis. The role of the endonuclease. , 1990, The American journal of pathology.

[3]  S. McOrist,et al.  Reproduction of porcine proliferative enteropathy with pure cultures of ileal symbiont intracellularis , 1993, Infection and immunity.

[4]  S. McOrist,et al.  Enterocyte proliferation and intracellular bacteria in animals. , 1994, Gut.

[5]  E. Kieff,et al.  Induction of bcl-2 expression by epstein-barr virus latent membrane protein 1 protects infected B cells from programmed cell death , 1991, Cell.

[6]  S. McOrist,et al.  Experimentally induced proliferative enteritis in hamsters: an ultrastructural study. , 1994, Research in veterinary science.

[7]  C. Potten,et al.  Further studies on the response of intestinal crypt cells of different hierarchical status to eighteen different cytotoxic agents. , 1987, British Journal of Cancer.

[8]  F. Nagengast,et al.  Intracolonic environment and the presence of colonic adenomas in man. , 1983, Gut.

[9]  G. Lawson,et al.  Experimental reproduction of porcine intestinal adenomatosis and necrotic enteritis , 1977, Veterinary Record.

[10]  J. Wojta,et al.  Bartonella bacilliformis stimulates endothelial cells in vitro and is angiogenic in vivo. , 1990, The American journal of pathology.

[11]  L. Gooding,et al.  Tumor necrosis factor can induce both apoptic and necrotic forms of cell lysis. , 1988, Journal of immunology.

[12]  Wagner Je,et al.  Experimental hamster enteritis: an electron microscopic study. , 1977 .

[13]  S. McOrist,et al.  Early Lesions of Proliferative Enteritis in Pigs and Hamsters , 1989, Veterinary pathology.

[14]  Gerard I. Evan,et al.  Induction of apoptosis in fibroblasts by c-myc protein , 1992, Cell.

[15]  S. Barns,et al.  Characterization of Lawsonia intracellularis gen. nov., sp. nov., the obligately intracellular bacterium of porcine proliferative enteropathy. , 1995, International journal of systematic bacteriology.

[16]  G. L. Coleman,et al.  Transmissible Murine Colonic Hyperplasia , 1978, Veterinary pathology.

[17]  A. Wyllie,et al.  Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics , 1972, British Journal of Cancer.

[18]  B. Goldin,et al.  The intestinal microflora and the colon cancer connection. , 1990, Reviews of infectious diseases.

[19]  R. Jacoby,et al.  Transmissible ileal hyperplasia of hamsters. II. Ultrastructure. , 1978, The American journal of pathology.

[20]  A. Raji,et al.  Adhesion to and invasion of cultured human cells by Bartonella bacilliformis , 1992, Infection and immunity.

[21]  S. McOrist,et al.  Intracellular bacteria of porcine proliferative enteropathy: cultivation and maintenance in vitro , 1993, Journal of clinical microbiology.

[22]  H. Stills.  Isolation of an intracellular bacterium from hamsters (Mesocricetus auratus) with proliferative ileitis and reproduction of the disease with a pure culture , 1991, Infection and immunity.

[23]  T. Dexter,et al.  Haemopoietic colony stimulating factors promote cell survival by suppressing apoptosis , 1990, Nature.

[24]  Gwyn T. Williams,et al.  Molecular regulation of apoptosis: Genetic controls on cell death , 1993, Cell.

[25]  M. Koury,et al.  Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells. , 1990, Science.

[26]  R. Schreiber,et al.  Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death , 1990, Nature.

[27]  A. Wyllie,et al.  Apoptosis: mechanisms and roles in pathology. , 1991, International review of experimental pathology.

[28]  S. Falkow,et al.  Attaching and effacing locus of a Citrobacter freundii biotype that causes transmissible murine colonic hyperplasia , 1993, Infection and immunity.

[29]  S. McOrist,et al.  Infection of cultured rat enterocytes by Ileal symbiont intracellularis depends on host cell function and actin polymerisation. , 1995, Veterinary microbiology.

[30]  D. Hicks,et al.  BCL-2 expression in human colorectal adenomas and carcinomas. , 1994, Oncogene.

[31]  C. Goodwin.  Gastric cancer and Helicobacter pylori: the whispering killer? , 1993, The Lancet.

[32]  S. Korsmeyer,et al.  BCL2 protein is topographically restricted in tissues characterized by apoptotic cell death. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[33]  S. McOrist,et al.  Synergism of ileal symbiont intracellularis and gut bacteria in the reproduction of porcine proliferative enteropathy , 1994, Veterinary Record.