Cirrhosis impairs serum bacteriostasis for Escherichia coli
Lister, P.D.; Mellencamp, M.A.; Preheim, L.C.
Journal of Laboratory and Clinical Medicine 120(4): 633-638
1992
ISSN/ISBN: 0022-2143 PMID: 1402339 Document Number: 392220
To study the effects of cirrhosis on serum inhibition of Escherichia coli, cirrhosis with ascites was induced in male Sprague-Dawley rats by intragastric administration of carbon tetrachloride. Heat-inactivated (56 degree C for 30 minutes) serum from cirrhotic rats (CRS) or that from control rats (NRS) was inoculated with 1 times 10-5 colony-forming units per millimeter (CFU/ml) of E. coli, and growth was measured after 24 hours. The mean growth of E. coli in CRS was significantly higher than growth in NRS: 3.5 +- 5.4 times 10-8 CFU/ml versus 1.2 +- 2.0 times 10-6 CFU/ml, respectively (p lt 0.01). Fifty-four percent of CRS samples (22/41) completely lacked bacteriostatic activity. These CRS samples were categorized as growth-supporting (G + CRS) because their growth exceeded the mean + 2 SD of NRS (5.2 times 10-6 CFU/ml). Serum bacteriostasis could be restored to G+CRS by adding purified rat apotransferrin (1 mg/ml), suggesting the presence of excess iron in G+CRS. However, serum iron concentration (SI) and total iron binding capacity (TIBC) were virtually the same in G+CRS (SI = 120 +- 22 mu-g/dl; TIBC = 351 +- 45 mu-g/dl) as in growth-inhibitory CRS (SI = 131 +- 16 mu-g/dl; TIBC = 347 +- 46 mu-g/dl) but were significantly less than NRS (SI = 208 +- 29 mu-g/dl; TIBC = 533 +- 57-mu-g/dl), p lt 0.01. The percent transferrin saturation was similar in all groups: 34% +- 6%; 38% +- 5% and 39% +- 9%, respectively. These results suggest that growth of E. coli in G+CRS is not due to excess iron or oversaturation of transferrin but may be related to abnormalities in transferrin or in other humoral factors that contribute to bacteriostasis.