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Mucosal immune responses to capsular pneumococcal polysaccharides in immunized preschool children and controls with similar nasal pneumococcal colonization rates

ZHANG, QIBO PHD; ARNAOUTAKIS, KONSTANTINOS BSC; MURDOCH, CRAIG PHD; LAKSHMAN, RAMAN MRCPCH; RACE, GILLIAN BSC; BURKINSHAW, ROGER BSC; FINN, ADAM PHD, FRCPCH

Pediatric Infectious Disease Journal: April 2004 - Volume 23 - Issue 4 - pp 307-313
Original Studies

Background. Immunization with conjugate pneumococcal vaccines induces significant primary and memory IgG anti-polysaccharide (PS) responses in serum. It can also induce mucosal responses in infants especially after a polysaccharide booster. However, it is unclear whether it can prime for mucosal memory responses on nasal exposure to pneumococcus, which may be important in protection against pneumococcal invasion and/or carriage.

Methods. IgA and IgG to serotypes 4, 6B, 9V, 14, 18C, 19F and 23F (conjugate vaccine serotypes), 1 and 3 (nonvaccine serotypes) capsular PS were measured by immunoassay in saliva from 2- to 5-year-old children previously given three doses of 7-valent pneumococcal conjugate vaccine in infancy, followed by 23-valent PS vaccine at 13 months and from unvaccinated controls of similar age and sex. Salivary antibody responses were analyzed in relation to carriage of pneumococci assessed by bacterial culture of nasopharyngeal swab samples collected in the summer and winter of the year 2000.

Results. Rates of detectable IgG antibodies to all vaccine serotypes except 23F were higher in subjects than in controls. No such differences were observed for IgA antibodies except for serotype 6B. Nasal colonization rates were similar, and in both groups mucosal IgA responses were more common and larger than IgG responses.

Conclusions. The mucosal anti-capsular IgA responses observed could develop in response to colonization in preschool children, regardless of vaccination status, and contribute to the falling carriage rates observed with increasing age.

From the Department of Clinical Sciences South Bristol, University of Bristol Faculty of Medicine (QZ, KA, AF); the Division of Genomic Medicine, University of Sheffield Medical School (CM); and Sheffield Institute for Vaccine Studies, University of Sheffield (RL, GR, RB), Sheffield, UK.

Accepted for publication Dec. 3, 2003.

Address for reprints: Professor Adam Finn, Level 6, UBHT Education Centre, Upper Maudlin St., Bristol, BS2 8AE UK. Fax 44 117 342 1078; E-mail Adam.Finn@bristol.ac.uk.

© 2004 Lippincott Williams & Wilkins, Inc.