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Pseudomonas aeruginosa-dependent upregulation of TLR2 influences host responses to a secondary Staphylococcus aureus infection

Authors
Shin, Hee-SungLee, Jung-HoonPaek, Se-HwanJung, Yong WooHa, Un-Hwan
Issue Date
Nov-2013
Publisher
OXFORD UNIV PRESS
Keywords
Pseudomonas aeruginosa; Staphylococcus aureus; secondary infection; TLR2
Citation
PATHOGENS AND DISEASE, v.69, no.2, pp.149 - 156
Indexed
SCIE
SCOPUS
Journal Title
PATHOGENS AND DISEASE
Volume
69
Number
2
Start Page
149
End Page
156
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/101689
DOI
10.1111/2049-632X.12074
ISSN
2049-632X
Abstract
The clinical impact of polymicrobial infections has received increasing attention from the medical community. However, the potential effects of Pseudomonas aeruginosa infection on the development of host responses against Gram-positive bacteria, such as Staphylococcus aureus, are unknown. Here, P.aeruginosa infection was found to induce the expression of Toll-like receptor 2 (TLR2), which plays a dominant role in sensing pathogen-associated molecular patterns (PAMPs) expressed by Gram-positive bacteria. P.aeruginosa-dependent upregulation of TLR2 was not mediated by flagellin, or by the type III (T3SS) or type VI (T6SS) secretion systems, but was upregulated by lipopolysaccharide (LPS). Upregulation of TLR2 influenced the magnitude of proinflammatory responses to the secondary S.aureus infection, but there was no clear effect on phagocytosis of S.aureus by macrophages. Taken together, the results of this study demonstrate that P.aeruginosa infection results in the upregulation of TLR2 expression, subsequently enhancing innate immune responses against a secondary S.aureus infection. The clinical impact of polymicrobial infections has increasingly recognized in recent years. In this study the impact of a P.aeruginosa infection on a secondary S.aureus was studied. The findings are intriguing since it was demonstrated that the primary P.aeruginosa infection upregulated TLR2 expression thereby enhancing innate immune responses against the secondary S.aureus infection.
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