Laboratory K-12 colonizing our guts?
Trond Erik Vee Aune
(by trondaun from nt.ntnu.no)
Wed Jun 20 01:19:37 EST 2007
Thank you very much,
This was perfect, exactly what I sought.
David F. Spencer wrote:
> 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
>> * Can expression of recombinant proteins from such bacteria cause
>> problems with human health)
>> I would especially like any references to articles that handle these
>> 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.
> [END QUOTE]
> 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.
Trond Erik Vee Aune
Department of Biotechnology, NTNU
- Must be sad being a dyslectic, agnostic insomniac, lying
awake during the night, wondering if there really is a dog
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