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Infection and Immunity, February 2006, p. 830-838, Vol. 74, No. 2
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.2.830-838.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Nontypeable Haemophilus influenzae Adheres to Intercellular Adhesion Molecule 1 (ICAM-1) on Respiratory Epithelial Cells and Upregulates ICAM-1 Expression

Vasanthi Avadhanula,1,2 Carina A. Rodriguez,1 Glen C. Ulett,1 Lauren O. Bakaletz,4 and Elisabeth E. Adderson1,2,3*

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee,1 Departments of Molecular Sciences,2 Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee,3 Columbus Children's Research Institute and The Ohio State University, Columbus, Ohio4

Received 16 August 2005/ Returned for modification 13 October 2005/ Accepted 5 November 2005

Nontypeable Haemophilus influenzae (NTHI) is an important respiratory pathogen. NTHI initiates infection by adhering to the airway epithelium. Here, we report that NTHI interacts with intracellular adhesion molecule 1 (ICAM-1) expressed by respiratory epithelial cells. A fourfold-higher number of NTHI bacteria adhered to Chinese hamster ovary (CHO) cells transfected with human ICAM-1 (CHO-ICAM-1) than to control CHO cells (P ≤ 0.005). Blocking cell surface ICAM-1 with specific antibody reduced the adhesion of NTHI to A549 respiratory epithelial cells by 37% (P = 0.001) and to CHO-ICAM-1 cells by 69% (P = 0.005). Preincubating the bacteria with recombinant ICAM-1 reduced adhesion by 69% (P = 0.003). The adherence to CHO-ICAM-1 cells of NTHI strains deficient in the adhesins P5, P2, HMW1/2, and Hap or expressing a truncated lipooligosaccharide was compared to that of parental strains. Only strain 1128f–, which lacks the outer membrane protein (OMP) P5-homologous adhesin (P5 fimbriae), adhered less well than its parental strain. The numbers of NTHI cells adhering to CHO-ICAM-1 cells were reduced by 67% (P = 0.009) following preincubation with anti-P5 antisera. Furthermore, recombinant ICAM bound to an OMP preparation from strain 1128f+, which expresses P5, but not to that from its P5-deficient mutant, confirming a specific interaction between ICAM-1 and P5 fimbriae. Incubation of respiratory epithelial cells with NTHI increased ICAM-1 expression fourfold (P = 0.001). Adhesion of NTHI to the respiratory epithelium, therefore, upregulates the expression of its own receptor. Blocking interactions between NTHI P5 fimbriae and ICAM-1 may reduce respiratory colonization by NTHI and limit the frequency and severity of NTHI infection.

* Corresponding author. Mailing address: Room E8054, Mailstop 320, 332 N. Lauderdale St., Memphis, TN 38105. Phone: (901) 495-3459. Fax: (901) 495-3009. E-mail: Elisabeth.Adderson{at}stjude.org.

Editor: J. D. Clements

Infection and Immunity, February 2006, p. 830-838, Vol. 74, No. 2
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.2.830-838.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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