Laboratory K-12 colonizing our guts?

David F. Spencer via (by DSpencer from Dal.CA)
Tue Jun 19 14:38:27 EST 2007

Trond Erik Vee Aune wrote:
> Dear all,
> Yesterday we started discussing the possibility of our recombinant 
> E.coli K-12 establishing themselves in our guts. I know there were some 
> controversy around this in the 70's, but I haven't been able to find out 
> what the conclusions were. Here are some specific questions:
> * Can our modern laboratory K-12 acutally establish themselves in our 
> guts, competing with our natural flora?
> * What if after an antibiotics cure when the natural flora is greatly 
> reduced?
> * Can expression of recombinant proteins from such bacteria cause 
> problems with human health)
> I would especially like any references to articles that handle these 
> questions.
> Best regards,
> Trond Erik

E.coli K-12 was the first of the primary E. coli isolates (1922, from 
the stool of a diptheria patient).
Here is a section from a good summary of E. coli, including K-12, taken 


  In order to evaluate K-12's potential to colonize the human intestine 
the following should be addressed: (1) the characteristics relevant to 
E. coli colonization of the human colon, and how K-12 compares to other 
E. coli in terms of these traits, and (2) data relevant to colonization 
potential of K-12 strains.

  The binding of an E. coli to the mucosal surface of the colon requires 
two factors. The first factor is the production of a specific glycocalyx 
or fimbriae from the surface of the bacterium. This specific glycocalyx 
recognizes a specific lectin on the surface of the enterocyte lining of 
the human colon. The glycocalyxes appear to bind to structures such as 
the mucus glycoproteins elaborated from the goblet cells of the 
intestine. In Gram-negative bacteria, the polysaccharide chains arising 
from the core of the lipopolysaccharides in the outer membrane appear to 
be the major ones which affect binding to the colon.

E. coli K-12 is defective in at least three cell wall characteristics. 
The outer membrane has a defective lipopolysaccharide core which affects 
the attachment of the O-antigen polysaccharide side chains (Curtiss, 
1978). Second, it does not have the type of glycocalyx required for 
attachment to the mucosal surface of the human colon (Edberg, 1991) as a 
result of the altered O-antigen properties noted above. Finally, K-12 
strains do not appear to express capsular (K) antigens, which are 
heat-labile polysaccharides important for colonization and virulence 
(Curtiss, 1978).

  K-12, thus, is not able to colonize the human intestinal tract under 
normal conditions, even after ingestion of billions of organisms 
(Anderson, 1975, Cohen et al., 1979., Levy and Marshall, 1981; Levy et. 
al, 1980, Smith, 1975). As noted above, K-12 is defective in cell wall 
components relevant to the ability to recognize and adhere to the 
mucosal surface of colonic cells (Curtiss, 1978). The normal flora in 
residence in the colon thus can easily exclude K-12, and prevent it from 
colonizing the human colon.


There was a lot of fuss in the 70's about the safety of plasmid 
transformed E. coli which resulted in the production of the cell 
chi_1776, an extremely enfeebled strain that was essentially impossible 
to actually work with.

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