Toll-like receptor 4 agonists adsorbed to aluminium hydroxide adjuvant attenuate ovalbumin-specific allergic airway disease: role of MyD88 adaptor molecule and interleukin-12/interferon-γ axis

2008 ◽  
Vol 38 (10) ◽  
pp. 1668-1679 ◽  
Author(s):  
J. Bortolatto ◽  
É. Borducchi ◽  
D. Rodriguez ◽  
A. C. Keller ◽  
E. Faquim-Mauro ◽  
...  
Keyword(s):  
Aluminium Hydroxide ◽  
Airway Disease ◽  
Interferon Γ ◽  
Allergic Airway Disease ◽  
Interleukin 12 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Adaptor Molecule

Stimulation of toll-like receptor 4 expression in human mononuclear phagocytes by interferon-γ: a molecular basis for priming and synergism with bacterial lipopolysaccharide

Blood ◽  
2002 ◽  
Vol 99 (9) ◽  
pp. 3427-3431 ◽  
Author(s):  
Daniela Bosisio ◽  
Nadia Polentarutti ◽  
Marina Sironi ◽  
Sergio Bernasconi ◽  
Kensuke Miyake ◽  
...  
Keyword(s):  
Surface Expression ◽  
Interferon Γ ◽  
Mononuclear Phagocytes ◽  
Bacterial Lipopolysaccharide ◽  
Interleukin 12 ◽  
Mrna Levels ◽  
Adapter Protein ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tlr4 Mrna

Abstract In human monocytes and macrophages, interferon-γ (IFNγ) augmented mRNA and surface expression of toll-like receptor 4 (TLR4), a crucial component of the signaling receptor complex for bacterial lipopolysaccharide (LPS). Expression of the accessory component MD-2 and of the adapter protein MyD88 was also increased. LPS increased TLR4 mRNA levels, but concomitantly decreased its surface expression. IFNγ counteracted the LPS-induced downregulation of TLR4. IFNγ-primed monocytes showed increased responsiveness to LPS in terms of phosphorylation of the interleukin-1 receptor–associated kinase (IRAK; immediately downstream of the MyD88 adapter protein), NF-kB DNA binding activity, and, accordingly, of cytokine (tumor necrosis factor α [TNFα] and interleukin-12 [IL-12]) production. These results suggest that enhanced TLR4 expression underlies the long-known priming by IFNγ of mononuclear phagocytes for pathogen recognition and killing as well as its synergism with LPS in macrophage activation.

scholarly journals The role of Toll-like receptor 4 versus interleukin-12 in immunity to respiratory syncytial virus

2004 ◽  
Vol 34 (4) ◽  
pp. 1146-1153 ◽  
Author(s):  
Stephan Ehl ◽  
Ruth Bischoff ◽  
Tobias Ostler ◽  
Simone Vallbracht ◽  
Jürgen Schulte-Mönting ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Interleukin 12 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Syncytial Virus

scholarly journals Cleavage of Fibrinogen by Proteinases Elicits Allergic Responses Through Toll-Like Receptor 4

Science ◽  
2013 ◽  
Vol 341 (6147) ◽  
pp. 792-796 ◽  
Author(s):  
Valentine Ongeri Millien ◽  
Wen Lu ◽  
Joanne Shaw ◽  
Xiaoyi Yuan ◽  
Garbo Mak ◽  
...  
Keyword(s):  
Allergic Disease ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Airway Disease ◽  
Airway Epithelial Cells ◽  
Allergic Airway Disease ◽  
Airway Epithelial ◽  
Toll Like Receptor ◽  
Defensive Strategy ◽  
Toll Like Receptor 4

Proteinases and the innate immune receptor Toll-like receptor 4 (TLR4) are essential for expression of allergic inflammation and diseases such as asthma. A mechanism that links these inflammatory mediators is essential for explaining the fundamental basis of allergic disease but has been elusive. Here, we demonstrate that TLR4 is activated by airway proteinase activity to initiate both allergic airway disease and antifungal immunity. These outcomes were induced by proteinase cleavage of the clotting protein fibrinogen, yielding fibrinogen cleavage products that acted as TLR4 ligands on airway epithelial cells and macrophages. Thus, allergic airway inflammation represents an antifungal defensive strategy that is driven by fibrinogen cleavage and TLR4 activation. These findings clarify the molecular basis of allergic disease and suggest new therapeutic strategies.

Investigating the Role of Relaxin in the Regulation of Airway Fibrosis in Animal Models of Acute and Chronic Allergic Airway Disease

2005 ◽  
Vol 1041 (1) ◽  
pp. 194-196 ◽  
Author(s):  
ISHANEE MOOKERJEE ◽  
MIMI L.K. TANG ◽  
NATASHA SOLLY ◽  
GEOFFREY W. TREGEAR ◽  
CHRISHAN S. SAMUEL
Keyword(s):  
Animal Models ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Airway Fibrosis

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia

Contrasting effects of the Toll-like receptor 4 in determining ovarian follicle endowment and fertility in female adult mice

Zygote ◽  
2021 ◽  
pp. 1-7
Author(s):  
Júlio Panzera Gonçalves ◽  
Breno Augusto Magalhães ◽  
Paulo Henrique Almeida Campos-Junior
Keyword(s):  
Ovarian Follicle ◽  
Cumulus Cells ◽  
Toll Like Receptor ◽  
Female Reproduction ◽  
Toll Like Receptor 4 ◽  
Genetic Ablation ◽  
Adult Mice ◽  
Cumulus Oocyte Complex ◽  
Estrous Cyclicity

Abstract Toll-like receptor 4 (TLR4) is best known for its role in bacteria-produced lipopolysaccharide recognition. Regarding female reproduction, TLR4 is expressed by murine cumulus cells and participates in ovulation and in cumulus–oocyte complex (COC) expansion, maternal–fetal interaction and preterm labour. Despite these facts, the role of TLR4 in ovarian physiology is not fully understood. Therefore, the aim of the present study was to investigate the effects of TLR4 genetic ablation on mice folliculogenesis and female fertility, through analysis of reproductive crosses, ovarian responsiveness and follicular quantification in TLR4−/− (n = 94) and C57BL/6 mice [wild type (WT), n = 102]. TLR4-deficient pairs showed a reduced number of pups per litter (P = 0.037) compared with WT. TLR4−/− mice presented more primordial, primary, secondary and antral follicles (P < 0.001), however there was no difference in estrous cyclicity (P > 0.05). A lower (P = 0.006) number of COC was recovered from TLR4−/− mice oviducts after superovulation, and in heterozygous pairs, TLR4−/− females also showed a reduction in the pregnancy rate and in the number of fetuses per uterus (P = 0.007) when compared with WT. Altogether, these data suggest that TLR4 plays a role in the regulation of murine folliculogenesis and in determining ovarian endowment. TLR4 deficiency may affect ovulation and pregnancy rates, potentially decreasing fertility, therefore the potential side effects of its blockade have to be carefully investigated.

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