scholarly journals Trichophyton rubrum Elicits Phagocytic and Pro-inflammatory Responses in Human Monocytes Through Toll-Like Receptor 2

2019 ◽  
Vol 10 ◽  
Author(s):  
Giovanna Azevedo Celestrino ◽  
Ana Paula Carvalho Reis ◽  
Paulo Ricardo Criado ◽  
Gil Benard ◽  
Maria Gloria Teixeira Sousa
Keyword(s):  
Trichophyton Rubrum ◽  
Inflammatory Responses ◽  
Human Monocytes ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Varicella-Zoster Virus Activates Inflammatory Cytokines in Human Monocytes and Macrophages via Toll-Like Receptor 2

2005 ◽  
Vol 79 (20) ◽  
pp. 12658-12666 ◽  
Author(s):  
Jennifer P. Wang ◽  
Evelyn A. Kurt-Jones ◽  
Ok S. Shin ◽  
Michael D. Manchak ◽  
Myron J. Levin ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Cell Line ◽  
Human Monocyte ◽  
Human Cell Line ◽  
Mouse Cell ◽  
Human Monocytes ◽  
Toll Like Receptor ◽  
Herpes Simplex Viruses ◽  
Varicella Zoster ◽  
Toll Like Receptor 2

ABSTRACT The pattern recognition receptor Toll-like receptor 2 (TLR2) has been implicated in the response to several human viruses, including herpes simplex viruses (types 1 and 2) and cytomegalovirus. We demonstrated that varicella-zoster virus (VZV) activates inflammatory cytokine responses via TLR2. VZV specifically induced interleukin-6 (IL-6) in human monocytes via TLR2-dependent activation of NF-κB, and small interfering RNA designed to suppress TLR2 mRNA reduced the IL-6 response to VZV in human monocyte-derived macrophages. Unlike other herpesviruses, the cytokine response to VZV was species specific. VZV did not induce cytokines in murine embryonic fibroblasts or in a mouse cell line, although VZV did activate NF-κB in a human cell line expressing a murine TLR2 construct. Together, these results suggest that TLR2 may play a role in the inflammatory response to VZV infection.

scholarly journals Protective effect of Lactobacillus reuteri DSM 17938 against experimental necrotizing enterocolitis is mediated by Toll-like receptor 2

2018 ◽  
Vol 315 (2) ◽  
pp. G231-G240 ◽  
Author(s):  
Thomas K. Hoang ◽  
Baokun He ◽  
Ting Wang ◽  
Dat Q. Tran ◽  
J. Marc Rhoads ◽  
...  
Keyword(s):  
T Cells ◽  
Necrotizing Enterocolitis ◽  
Immune Modulation ◽  
Lactobacillus Reuteri ◽  
Inflammatory Responses ◽  
Cow Milk ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory

Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to reduce the incidence and severity of necrotizing enterocolitis (NEC). It is unclear if preventing NEC by LR 17938 is mediated by Toll-like receptor 2 (TLR2), which is known to mediate proinflammatory responses to bacterial cell wall components. NEC was induced in newborn TLR2−/− or wild-type (WT) mice by the combination of gavage-feeding cow milk-based formula and exposure to hypoxia and cold stress. Treatment groups were administered formula supplemented with LR 17938 or placebo (deMan-Rogosa-Sharpe media). We observed that LR 17938 significantly reduced the incidence of NEC and reduced the percentage of activated effector CD4+T cells, while increasing Foxp3+ regulatory T cells in the intestinal mucosa of WT mice with NEC, but not in TLR2−/− mice. Dendritic cell (DC) activation by LR 17938 was mediated by TLR2. The percentage of tolerogenic DC in the intestine of WT mice was increased by LR 17938 treatment during NEC, a finding not observed in TLR2−/− mice. Furthermore, gut levels of proinflammatory cytokines IL-1β and IFN-γ were decreased after treatment with LR 17938 in WT mice but not in TLR2−/− mice. In conclusion, the combined in vivo and in vitro findings suggest that TLR2 receptors are involved in DC recognition and DC-priming of T cells to protect against NEC after oral administration of LR 17938. Our studies further clarify a major mechanism of probiotic LR 17938 action in preventing NEC by showing that neonatal immune modulation of LR 17938 is mediated by a mechanism requiring TLR2. NEW & NOTEWORTHY Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to protect against necrotizing enterocolitis (NEC) in neonates and in neonatal animal models. The role of Toll-like receptor 2 (TLR2) as a sensor for gram-positive probiotics, activating downstream anti-inflammatory responses is unclear. Our current studies examined TLR2 −/− mice subjected to experimental NEC and demonstrated that the anti-inflammatory effects of LR 17938 are mediated via a mechanism requiring TLR2.

scholarly journals Essential Calcium-binding Cluster ofLeptospiraLipL32 Protein for Inflammatory Responses through the Toll-like Receptor 2 Pathway

2013 ◽  
Vol 288 (17) ◽  
pp. 12335-12344 ◽  
Author(s):  
Yueh-Yu Lo ◽  
Shen-Hsing Hsu ◽  
Yi-Ching Ko ◽  
Cheng-Chieh Hung ◽  
Ming-Yang Chang ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Inflammatory Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Leptospira surface adhesin (Lsa21) induces Toll like receptor 2 and 4 mediated inflammatory responses in macrophages

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Syed M. Faisal ◽  
Vivek P. Varma ◽  
M. Subathra ◽  
Sarwar Azam ◽  
Anil K. Sunkara ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Relationship between Arg753Gln Toll-like receptor 2 and Asp299Gly Toll-like receptor 4 genetic variations and susceptibility to colorectal cancer in Southern Iran

2018 ◽  
Vol 70 (4) ◽  
pp. 775-779 ◽  
Author(s):  
Seyed Hosseini ◽  
Zahra Mojtahedi ◽  
Zahra Beizavi ◽  
Hajar Khazraei ◽  
Mozhdeh Zamani
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Inflammatory Responses ◽  
Tumor Stage ◽  
Nucleotide Polymorphisms ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Southern Iran ◽  
Toll Like Receptor 2 ◽  
Colorectal Cancer Patients

Variations in Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) encoding genes have been associated with tumorigenesis through the disruption of immune and inflammatory responses. The aims of this study were to evaluate the two single nucleotide polymorphisms (SNPs) of the genes Arg753Gln TLR2 (rs5743708) and Asp299Gly TLR4 (rs4986790) in colorectal cancer patients in southern Iran. Colorectal cancer patients and healthy controls were included in this study (150 Persian subjects in each group). Blood samples were used for genotyping by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The association between these SNPs and colorectal cancer and clinicopathological factors, including age, gender, tumor stage and differentiation were also investigated. A significant association was found between Arg753Gln TLR2 SNP and colorectal cancer. This SNP was significantly more frequent in male patients. However, there was no association between Asp299Gly TLR4 and colorectal cancer. Therefore, Arg753Gln TLR2 SNP can be considered as a risk factor for colorectal cancer incidence in southern Iran, especially in men. Further investigations in other populations are recommended in order to assess the association of this SNP with colorectal cancer.

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