scholarly journals The Role ofE. coliInfection in the Pathogenesis of Primary Biliary Cirrhosis

2010 ◽  
Vol 29 (6) ◽  
pp. 301-311 ◽  
Author(s):  
Dimitrios P. Bogdanos ◽  
Harold Baum ◽  
Diego Vergani ◽  
Andrew K. Burroughs
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Molecular Mimicry ◽  
Epidemiological Studies ◽  
Cross Reactivity ◽  
Biliary Cirrhosis ◽  
E Coli ◽  
Cellular Immune Responses ◽  
Experimental Findings ◽  
Tract Infections ◽  
Cellular Immune

Among various infectious agents possibly involved in the pathogenesis of primary biliary cirrhosis (PBC),Escherichia Coli (E. coli)has received special attention because of epidemiological and experimental evidence linking this bacterium with the disease's development. This review discusses early and more recent epidemiological studies associating recurrent urinary tract infections withE. coliand the development of PBC. We also critically review data provided over the years demonstrating disease-specific humoral and cellular immune responses againstE. coliantigens in patients with PBC. Finally, we assess the relevance of experimental findings reporting cross-reactive immunity between mimicking sequences ofE. coliand the major PBC mitochondrial antigens in the pathogenesis of the PBC. We also address the extent to which molecular mimicry and immunological cross-reactivity can be considered as a critical pathogenic process linking infection with self destruction.

scholarly journals E. coliInduced Experimental Model of Primary Biliary Cirrhosis: At Last

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Andreas L. Koutsoumpas ◽  
Daniel S. Smyk ◽  
Dimitrios P. Bogdanos
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Infected Animal ◽  
Infectious Agent ◽  
Epidemiological Studies ◽  
Cholestatic Liver Disease ◽  
Biliary Cirrhosis ◽  
E Coli ◽  
Intrahepatic Bile Ducts ◽  
Additional Support ◽  
Tract Infections

Recurrent urinary tract infections (UTI) have been considered potential triggers of primary biliary cirrhosis (PBC), an autoimmune cholestatic liver disease characterised by progressive destruction of intrahepatic bile ducts. Additional support for the link made between PBC and UTI was based on early observations of recurrent episodes of bacteriuria in female patients with PBC. A series of large epidemiological studies demonstrated a strong correlation between recurrent UTI and PBC, initiating a series of studies investigating the role ofEscherichia coli(E. coli, the most prevalent organism isolated in women with UTI) as a trigger of PBC. Immunological evidence of B- and T-cell cross-reactive responses implicating PBC-specific autoantigens andE. colimimics have been clearly demonstrated, adding support to the notion thatE. coliis a potential infectious inducer of PBC in susceptible individuals. One of the major limitations in proving theE. coli/PBC association was the lack of reliableE. coli-infected animal models of PBC. This review provides an overview of the evidence linking this infectious agent with PBC and discusses the pros and cons of a recently developedE. coli-infected animal model of PBC.

Cellular Immune Responses to Biliary Tract Antigens in Primary Biliary Cirrhosis and Chronic Active Hepatitis

1979 ◽  
Vol 56 (3) ◽  
pp. 15P-15P
Author(s):  
B. M. Wojcicka ◽  
P. Amoroso ◽  
I. G. McFarlane ◽  
A. L. W. F. Eddleston ◽  
R. Williams
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Immune Responses ◽  
Biliary Tract ◽  
Chronic Active Hepatitis ◽  
Biliary Cirrhosis ◽  
Cellular Immune Responses ◽  
Cellular Immune

Antibodies against the COOH-terminal region of E. coli ClpP protease in patients with primary biliary cirrhosis

2000 ◽  
Vol 33 (4) ◽  
pp. 528-536 ◽  
Author(s):  
Isabel Mayo ◽  
Paz Arizti ◽  
Albert Pares ◽  
Joaquin Oliva ◽  
Rita Alvarez Doforno ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Terminal Region ◽  
Biliary Cirrhosis ◽  
E Coli

scholarly journals Analysis of TCR antagonism and molecular mimicry of an HLA-A*0201-restricted CTL epitope in primary biliary cirrhosis

Hepatology ◽  
2002 ◽  
Vol 36 (4) ◽  
pp. 918-926 ◽  
Author(s):  
Hiroto Kita ◽  
Shuji Matsumura ◽  
Xiao-Song He ◽  
Aftab A. Ansari ◽  
Zhe-Xiong Lian ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Molecular Mimicry ◽  
Biliary Cirrhosis ◽  
Ctl Epitope

Molecular mimicry of mitochondrial and nuclear autoantigens in primary biliary cirrhosis

2003 ◽  
Vol 124 (7) ◽  
pp. 1915-1925 ◽  
Author(s):  
Shinji Shimoda ◽  
Minoru Nakamura ◽  
Hiromi Ishibashi ◽  
Akira Kawano ◽  
Takashi Kamihira ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Molecular Mimicry ◽  
Biliary Cirrhosis

scholarly journals Comparison of Escherichia coli Strains Recovered from Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

1998 ◽  
Vol 66 (7) ◽  
pp. 3059-3065 ◽  
Author(s):  
David E. Johnson ◽  
C. Virginia Lockatell ◽  
Robert G. Russell ◽  
J. Richard Hebel ◽  
Michael D. Island ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Virulence Factors ◽  
Bacterial Infections ◽  
Clinical Symptoms ◽  
Epidemiological Studies ◽  
In Vivo Studies ◽  
E Coli ◽  
Tract Infections

ABSTRACT Urinary tract infection, most frequently caused byEscherichia coli, is one of the most common bacterial infections in humans. A vast amount of literature regarding the mechanisms through which E. coli induces pyelonephritis has accumulated. Although cystitis accounts for 95% of visits to physicians for symptoms of urinary tract infections, few in vivo studies have investigated possible differences between E. coli recovered from patients with clinical symptoms of cystitis and that from patients with symptoms of pyelonephritis. Epidemiological studies indicate that cystitis-associated strains appear to differ from pyelonephritis-associated strains in elaboration of some putative virulence factors. With transurethrally challenged mice we studied possible differences using three each of the most virulent pyelonephritis and cystitis E. coli strains in our collection. The results indicate that cystitis strains colonize the bladder more rapidly than do pyelonephritis strains, while the rates of kidney colonization are similar. Cystitis strains colonize the bladder in higher numbers, induce more pronounced histologic changes in the bladder, and are more rapidly eliminated from the mouse urinary tract than pyelonephritis strains. These results provide evidence that cystitis strains differ from pyelonephritis strains in this model, that this model is useful for the study of the uropathogenicity of cystitis strains, and that it would be unwise to use pyelonephritis strains to study putative virulence factors important in the development of cystitis.

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