Abstract
Nasal colonization is a major risk factor for S. aureus infections. The mechanisms responsible for colonization are still not well understood and involve several factors on the host and the bacterial side. One key factor is the cell wall teichoic acid (WTA) of S. aureus, which governs direct interactions with nasal epithelial surfaces. We report here the first receptor for the cell wall glycopolymer WTA on nasal epithelial cells. In several assay systems this type F-scavenger receptor, termed SREC-I, bound WTA in a charge dependent manner and mediated adhesion to nasal epithelial cells in vitro. The impact of WTA and SREC-I interaction on epithelial adhesion was especially pronounced under shear stress, which resembles the conditions found in the nasal cavity. Most importantly, we demonstrate here a key role of the WTA-receptor interaction in a cotton rat model of nasal colonization. When we inhibited WTA mediated adhesion with a SREC-I antibody, nasal colonization in the animal model was strongly reduced at the early onset of colonization. More importantly, colonization stayed low over an extended period of 6 days. Therefore we propose targeting of this glycopolymer-receptor interaction as a novel strategy to prevent or control S. aureus nasal colonization.
Highlights
The nasal cavity is the major reservoir of Staphylococcus aureus, which asymptomatically colonizes the anterior nares of 20% of the normal human population persistently [1,2]
SREC-I is expressed on nasal epithelial cells In differential pull down experiments of solubilized membrane proteins from epithelial cells with cell wall preparations from wildtype S. aureus, a mutant without wall teichoic acid (WTA) and a mutant with structurally altered WTA, SREC-I was found as a potential WTA binding partner
We evaluated the presence of SREC-I by reverse transcriptase PCR (RT-PCR), FACS analysis and confocal microscopy in these cells
Summary
The nasal cavity is the major reservoir of Staphylococcus aureus, which asymptomatically colonizes the anterior nares of 20% of the normal human population persistently [1,2]. If carriers are infected with S. aureus, the strain found in the nose is usually responsible for the infection [1,2]. Since S. aureus is able to cause a variety of severe diseases, the carrier status is an important risk factor in both the community and the healthcare system [1,3]. Some studies showed that S. aureus colonizes mostly the anterior parts of the nares and interacts very efficiently with squamous, keratinized cells [4]. S. aureus is even able to persist intracellularly in nasal epithelial cells of patients suffering from recurrent sinusitis [5]
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