ORCID Profile
0000-0001-6306-3189
Current Organisations
Robert G Gish Consultants LLC
,
Loma Linda University
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Publisher: Elsevier BV
Date: 2017
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-1999
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-1999
Abstract: Microchimerism has been implicated in the etiology of autoimmune diseases. It has also been implicated in the induction/maintenance of fetal tolerance. We used polymerase chain reaction (PCR) analysis to determine whether microchimerism occurred in patients who subsequently developed primary biliary cirrhosis (PBC), and thus may be involved in its etiology. We performed PCR lification of sequences unique to both the X and Y chromosomes from the livers of 37 women with PBC and 39 female controls using WAVE technology a very sensitive technology based on an ion-pair reverse-phase high-performance liquid chromatography system. All patients were known to have had at least 1 son and it was confirmed that PBC was diagnosed after the birth of the son. Data were analyzed for both detection of the Y chromosome gene and the ratio of the yield of the Y chromosome PCR products to the X chromosome. The prevalence of Y chromosome detection in PBC was 26 of 37 (70%) compared with 28 of 39 (72%) in controls, and the ratio of Y chromosome to X chromosome was similar between the PBC and control groups, 0.402 +/- 0.143 vs. 0.271 +/- 0.055, respectively. Our results, using our more sensitive technology, showed that microchimerism is a very common event in human liver and supported the thesis that this may contribute to the induction/maintenance of fetal tolerance. However, although we cannot exclude the possibility that select fetal major histocompatibility complex (MHC) haplotypes might contribute to disease susceptibility, our data suggest that microchimerism by itself does not play a significant role in the development of PBC.
Publisher: Elsevier BV
Date: 10-1999
DOI: 10.1016/S0168-8278(99)80346-8
Abstract: A variety of data suggest that microbial infections and, in particular, atypical mycobacteria infections, may either initiate and/or be associated with the pathogenesis of primary biliary cirrhosis. To address this hypothesis, use was made of polymerase chain reaction techniques and primers specific for the 16s rRNA gene of Eubacteria, Archaeabacteria, Mycobacteria and Helicobacter to determine if such sequences were detectable in liver tissue specimens from 29 patients with primary biliary cirrhosis. Similar liver tissues from patients with primary sclerosing cholangitis, chronic hepatitis, alcoholic liver disease and otherwise normal donors were analyzed in parallel. Genomic DNA was extracted from each of these liver tissue specimens using sterile techniques to avoid possible laboratory contamination. The DNA was subjected to polymerase chain reaction lification using bacterial genus specific primers and the lified products cloned and sequenced. Sequence data were analyzed by searching for homology to existing genes. Sequences from primary biliary cirrhosis and control livers corresponded to those found in a variety of bacteria, but no consensus sequence was found in primary biliary cirrhosis specimens. Neither Archaeabacteria nor Mycobacteria products were detected in liver specimens of patients with primary biliary cirrhosis, and Helicobacter pylori DNA was detected in only one primary biliary cirrhosis patient. Although bacterial infection, particularly with intracellular organisms, has been suggested to play a role in the initiation of primary biliary cirrhosis, there is no evidence from this study to suggest an ongoing chronic infectious process.
Location: United States of America
No related grants have been discovered for Robert Gish.