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Infection and Immunity, March 2001, p. 1895-1901, Vol. 69, No. 3
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.3.1895-1901.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Role of Alginate O Acetylation in Resistance of
Mucoid Pseudomonas aeruginosa to Opsonic
Phagocytosis
Gerald B.
Pier,1,*
Fadie
Coleman,1
Martha
Grout,1
Michael
Franklin,2 and
Dennis E.
Ohman3,4
Channing Laboratory, Department of Medicine,
Brigham and Women's Hospital, Harvard Medical School, Boston,
Massachusetts 02115-58041; Department of
Microbiology, Montana State University, Bozeman, Montana
597172; Department of Microbiology and
Immunology, Medical College of Virginia Campus of Virginia Commonwealth
University, Richmond, Virginia 23298-06783; and
McGuire Veterans Affairs Medical Center, Richmond, Virginia
232494
Received 31 July 2000/Returned for modification 2 October
2000/Accepted 22 November 2000
Establishment and maintenance of chronic lung infections with
mucoid Pseudomonas aeruginosa in patients with cystic
fibrosis (CF) require that the bacteria avoid host defenses.
Elaboration of the extracellular, O-acetylated mucoid
exopolysaccharide, or alginate, is a major microbial factor in
resistance to immune effectors. Here we show that O acetylation of
alginate maximizes the resistance of mucoid P.
aeruginosa to antibody-independent opsonic killing and is the
molecular basis for the resistance of mucoid P.
aeruginosa to normally nonopsonic but alginate-specific antibodies found in normal human sera and sera of infected CF patients.
O acetylation of alginate appears to be critical for P.
aeruginosa resistance to host immune effectors in CF patients.
*
Corresponding author. Mailing address: Channing
Laboratory, 181 Longwood Ave., Boston, MA 02115-5804. Phone: (617) 525 2269. Fax: (617) 731-1541. E-mail:
gpier{at}channing.harvard.edu.
Infection and Immunity, March 2001, p. 1895-1901, Vol. 69, No. 3
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.3.1895-1901.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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