scholarly journals Shift from toll-like receptor 2 (TLR-2) toward TLR-4 dependency in the erosive stage of chronic streptococcal cell wall arthritis coincident with TLR-4-mediated interleukin-17 production

2008 ◽  
Vol 58 (12) ◽  
pp. 3753-3764 ◽  
Author(s):  
Shahla Abdollahi-Roodsaz ◽  
Leo A. B. Joosten ◽  
Monique M. Helsen ◽  
Birgitte Walgreen ◽  
Peter L. van Lent ◽  
...  
Keyword(s):  
Cell Wall ◽  
Interleukin 17 ◽  
Toll Like Receptor ◽  
Streptococcal Cell Wall ◽  
Toll Like Receptor 2 ◽  
Streptococcal Cell Wall Arthritis

scholarly journals Toll-Like Receptor 2 Pathway Drives Streptococcal Cell Wall-Induced Joint Inflammation: Critical Role of Myeloid Differentiation Factor 88

2003 ◽  
Vol 171 (11) ◽  
pp. 6145-6153 ◽  
Author(s):  
Leo A. B. Joosten ◽  
Marije I. Koenders ◽  
Ruben L. Smeets ◽  
Marleen Heuvelmans-Jacobs ◽  
Monique M. A. Helsen ◽  
...  
Keyword(s):  
Cell Wall ◽  
Critical Role ◽  
Joint Inflammation ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Streptococcal Cell Wall ◽  
Differentiation Factor ◽  
Toll Like Receptor 2 ◽  
Myeloid Differentiation Factor

scholarly journals Membrane-Associated Proteins of a Lipopolysaccharide-Deficient Mutant of Neisseria meningitidis Activate the Inflammatory Response through Toll-Like Receptor 2

2001 ◽  
Vol 69 (4) ◽  
pp. 2230-2236 ◽  
Author(s):  
Robin R. Ingalls ◽  
Egil Lien ◽  
Douglas T. Golenbock
Keyword(s):  
Cell Wall ◽  
Inflammatory Response ◽  
Neisseria Meningitidis ◽  
Parental Strain ◽  
Host Responses ◽  
Deficient Mutant ◽  
Toll Like Receptor ◽  
Gram Negative ◽  
Negative Cell ◽  
Toll Like Receptor 2

ABSTRACT The recent isolation of a lipopolysaccharide (LPS)-deficient mutant of Neisseria meningitidis has allowed us to explore the roles of other gram-negative cell wall components in the host response to infection. The experiments in this study were designed to examine the ability of this mutant strain to activate cells. Although it was clearly less potent than the parental strain, we found the LPS-deficient mutant to be a capable inducer of the inflammatory response in monocytic cells, inducing a response similar to that seen with Staphylococcus aureus. Cellular activation by the LPS mutant was related to expression of CD14, a high-affinity receptor for LPS and other microbial products, as well as Toll-like receptor 2, a member of the Toll family of receptors recently implicated in host responses to gram-positive bacteria. In contrast to the parental strain, the synthetic LPS antagonist E5564 did not inhibit the LPS-deficient mutant. We conclude that even in the absence of LPS, the gram-negative cell wall remains a potent inflammatory stimulant, utilizing signaling pathways independent of those involved in LPS signaling.

scholarly journals GM-CSF neutralisation suppresses inflammation and protects cartilage in acute streptococcal cell wall arthritis of mice

2006 ◽  
Vol 66 (4) ◽  
pp. 452-457 ◽  
Author(s):  
C Plater-Zyberk ◽  
L A B Joosten ◽  
M M A Helsen ◽  
J Hepp ◽  
P A Baeuerle ◽  
...  
Keyword(s):  
Cell Wall ◽  
Streptococcal Cell Wall ◽  
Gm Csf ◽  
Streptococcal Cell Wall Arthritis

DIFFERENT ROLES OF TUMOUR NECROSIS FACTOR α AND INTERLEUKIN 1 IN MURINE STREPTOCOCCAL CELL WALL ARTHRITIS

Cytokine ◽  
1998 ◽  
Vol 10 (9) ◽  
pp. 690-702 ◽  
Author(s):  
Sandra Kuiper ◽  
Leo A.B. Joosten ◽  
Alison M. Bendele ◽  
Carl K. Edwards III ◽  
Onno J. Arntz ◽  
...  
Keyword(s):  
Cell Wall ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Tumour Necrosis Factor Α ◽  
Streptococcal Cell Wall ◽  
Factor Α ◽  
Streptococcal Cell Wall Arthritis ◽  
Necrosis Factor

scholarly journals Toll-Like Receptor 2 Modulates the Proinflammatory Milieu in Staphylococcus aureus-Induced Brain Abscess

2005 ◽  
Vol 73 (11) ◽  
pp. 7428-7435 ◽  
Author(s):  
Tammy Kielian ◽  
Anessa Haney ◽  
Patrick M. Mayes ◽  
Sarita Garg ◽  
Nilufer Esen
Keyword(s):  
Staphylococcus Aureus ◽  
Brain Abscess ◽  
Complex Nature ◽  
Interleukin 17 ◽  
Immune Recognition ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Proinflammatory Mediators ◽  
Brain Abscesses ◽  
Toll Like Receptor 2

ABSTRACT Toll-like receptor 2 (TLR2) is a pattern recognition receptor (PRR) that plays an important role in innate immune recognition of conserved structural motifs on a wide array of pathogens, including Staphylococcus aureus. To ascertain the functional significance of TLR2 in the context of central nervous system (CNS) parenchymal infection, we evaluated the pathogenesis of S. aureus-induced experimental brain abscess in TLR2 knockout (KO) and wild-type (WT) mice. The expression of several proinflammatory mediators, including inducible nitric oxide synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly attenuated in brain abscesses of TLR2 KO mice compared to WT mice during the acute phase of infection. Conversely, interleukin-17 (IL-17), a cytokine produced by activated and memory T cells, was significantly elevated in lesions of TLR2 KO mice, suggesting an association between innate and adaptive immunity in brain abscess. Despite these differences, brain abscess severity in TLR2 KO and WT animals was similar, with comparable mortality rates, bacterial titers, and blood-brain barrier permeability, implying a role for alternative PRRs. Expression of the phagocytic PRRs macrophage scavenger receptor type AI/AII and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was increased in brain abscesses of both TLR2 KO and WT mice compared to uninfected animals. However, LOX-1 induction in brain abscesses of TLR2 KO mice was significantly attenuated compared to WT animals, revealing that the TLR2-dependent signal(s) influence LOX-1 expression. Collectively, these findings reveal the complex nature of gram-positive bacterial recognition in the CNS which occurs, in part, through engagement of TLR2 and highlight the importance of receptor redundancy for S. aureus detection in the CNS.

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