Infection and Immunity, October 2005, p. 6945-6951, Vol. 73, No. 10
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.10.6945-6951.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Nasal Colonization with Streptococcus pneumoniae Includes Subpopulations of Surface and Invasive Pneumococci
David E. Briles,1,2*
Lea Novak,3
Muneki Hotomi,1
Frederik W. van Ginkel,1,
and
Janice King1
Departments of Microbiology,1
Pediatrics,2
Pathology, University of Alabama at Birmingham, Birmingham, Alabama3
Received 20 December 2004/
Returned for modification 2 February 2005/
Accepted 23 May 2005
We demonstrated that during colonization with Streptococcus pneumoniae the nasal mucosal tissues of mice support two populations of pneumococci. Transparent-phase pneumococci can be readily washed from the outer surface, while a second population composed of primarily opaque-phase pneumococci is released only by homogenization of the nasal tissue. The fact that the opaque phase has previously been associated with invasion and the fact that opaque-phase pneumococci were released by homogenization of previously washed nasal tissue suggest that the opaque-phase pneumococci may have invaded the nasal tissue. Consistent with this hypothesis was our observation that there was inflammation in portions of the nasal mucosa of the colonized mice but not in the mucosa of noncolonized mice, but this observation did not prove the hypothesis. If the opaque-phase pneumococci released from the nasal tissue were from within the tissue and/or if resistance of the opaque-phase subpopulation to antibody, complement, and phagocytes is essential for long-term carriage, it seems likely that the virulence factors of S. pneumoniae that are necessary for killing humans exist to facilitate carriage. Although this speculation is unproven, the observation that there are separate populations of pneumococci during colonization may help guide future attempts to understand the biology of nasal colonization by this pathogen.
* Corresponding author. Mailing address: BBRB 658, 1530 3rd Avenue South, Birmingham, AL 35294-2170. Phone: (2050 934-6595. Fax: (205) 934-0605. E-mail: dbriles{at}uab.edu.
Editor: J. N. Weiser
Present address: Department of Pathobiology, Auburn University, Auburn, Ala.
Infection and Immunity, October 2005, p. 6945-6951, Vol. 73, No. 10
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.10.6945-6951.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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Copyright © 2005 by the American Society for Microbiology. All rights reserved.