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Novel mucosal anti-microbial functions interfering with the plasmid-mediated virulence determinants of adherence and
Abstract:
Mucosal antibodies in vivo and in vitro interfere with the stability of plasmids coding for important virulence determinants in porcine enteropathogenic E. coli (EEC), such as the adhesion determinants K88ab and K88ac. The effector antibody is not directed against K88 antigens and is not serotype specific, but an antigen common to K88+ strains is implicated. Further lack of pathogen specificity is exemplified by antibody elimination of the more recently discovered K88ad plasmid. Antibodies that interfere with K88 plasmids do not affect K99, which now appears as an alternative adhesion factor in porcine enteropathogenic E. coli. This plasmid can be eliminated, however, by antibodies having K99 specificity. In extending the studies to drug-resistance plasmids, further evidence has emerged that mucosal antibodies may assist in host control of the reservoir of R factors in the intestinal microflora. A major effector mechanism is that secretory IgA and IgM antibodies from orally immunized pigs can block the transfer of R factors between donor and recipient strains of E. coli.
Insights
Mucosal antibodies can destabilize virulence plasmids in E. coli, impacting pathogen control. Secretory IgA and IgM antibodies also block the transfer of antibiotic resistance plasmids between bacteria.
Area of Science:
- Immunology
- Microbiology
- Veterinary Medicine
Background:
- Porcine enteropathogenic E. coli (EEC) utilizes virulence plasmids for adhesion, such as K88ab and K88ac.
- Mucosal antibodies play a role in host defense against enteric pathogens.
- Antibiotic resistance (R factors) poses a significant threat in intestinal microflora.
Purpose of the Study:
- To investigate the role of mucosal antibodies in controlling virulence and R factor plasmids in EEC.
- To identify the mechanisms by which antibodies affect plasmid stability and transfer.
Main Methods:
- In vivo and in vitro studies using porcine models.
- Analysis of antibody interactions with K88 and K99 adhesion plasmids.
- Investigation of secretory IgA and IgM antibody effects on R factor transfer.
Main Results:
- Mucosal antibodies interfere with the stability of K88 adhesion plasmids in EEC, independent of K88 antigen specificity.
- Antibodies specific to K99 can eliminate K99 plasmids, an alternative adhesion factor.
- Secretory IgA and IgM antibodies from immunized pigs block R factor transfer between E. coli strains.
Conclusions:
- Mucosal antibodies are crucial for controlling virulence factors and antibiotic resistance in porcine E. coli.
- Antibody-mediated plasmid elimination and transfer blocking represent key host defense mechanisms.
- Targeting mucosal immunity offers a potential strategy for managing EEC infections and antibiotic resistance.