Nontypeable Haemophilus influenzae adheres to intercellular adhesion molecule 1 (ICAM-1) on respiratory epithelial cells and upregulates ICAM-1 expression

Avadhanula, Vasanthi, Rodriguez, Carina A., Ulett, Glen C., Bakaletz, Lauren O. and Adderson, Elisabeth E. (2006) Nontypeable Haemophilus influenzae adheres to intercellular adhesion molecule 1 (ICAM-1) on respiratory epithelial cells and upregulates ICAM-1 expression. Infection And Immunity, 74 2: 830-838. doi:10.1128/IAI.74.2.830-838.2006

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Author Avadhanula, Vasanthi
Rodriguez, Carina A.
Ulett, Glen C.
Bakaletz, Lauren O.
Adderson, Elisabeth E.
Title Nontypeable Haemophilus influenzae adheres to intercellular adhesion molecule 1 (ICAM-1) on respiratory epithelial cells and upregulates ICAM-1 expression
Journal name Infection And Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
Publication date 2006-02-01
Sub-type Article (original research)
DOI 10.1128/IAI.74.2.830-838.2006
Open Access Status File (Publisher version)
Volume 74
Issue 2
Start page 830
End page 838
Total pages 9
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Abstract 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.
Keyword Immunology
Infectious Diseases
Outer-membrane Proteins
Nf-kappa-b
Falciparum-infected Erythrocytes
Endothelial-cells
Gene-expression
Immune-system
Receptor
Binding
Lfa-1
P5
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Chemistry and Molecular Biosciences
 
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Created: Thu, 20 Sep 2007, 03:59:45 EST