Toll‐like receptor (TLR) 2 and TLR4 deficiencies exert differential <i>in vivo</i> effects against <i>Schistosoma japonicum</i>

Zhang, M.; Gao, Yali; Du, Xiu‐Fang; Zhang, D.; Ji, Minjun; Wu, Genghua

doi:10.1111/j.1365-3024.2010.01265.x

Cited by 31 publications

(27 citation statements)

References 34 publications

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“…However, the expression and distribution of TLR2 and TLR4 in response to the infection of C. sinensis in vivo have not yet been reported so far. The results of present study showed that the transcripts of both TLR2 and TLR4 gene were increased on day 28 PI, which is interestingly consistent with the increased in cytokines including Th1 and Th2 types immune responses, suggesting that TLR2 and TLR4 might be engaged in the production of cytokines such as IL-4, IL-10, IFN-γ, and TNF-α in mice with C. sinensis infection [36]. In addition, TLR2-mediated immune response via inflammatory/anti-inflammatory cytokines may be involved in the imbalance of oxidants/antioxidants in patients re-infected by O. viverrini [37].…”

Section: Discussionsupporting

confidence: 73%

Expression of Toll-like receptor (TLR) 2 and TLR4 in the livers of mice infected by Clonorchis sinensis

Yan

et al. 2015

J Infect Dev Ctries

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Introduction: Clonorchis sinensis is one of the most important foodborne pathogens in humans, and can cause biliary diseases such as gallstones, cholecystitis, cholangitis, and cholangiocarcinoma. Toll-like receptors (TLRs) as sensors are crucial to initiating both innate and adaptive immune defenses against pathogens. However, little is known about the hepatic expression of TLRs of hosts induced by C. sinensis infection. Methodology: In the present study, the expression and distribution of TLR2 and TLR4 were investigated in a mouse model of clonorchiasis on days 28, 56, 84, and 112 post-infection (PI) using real-time quantitative reverse transcription polymerase chain reaction (PCR) and immunohistochemically staining, respectively. The levels of cytokines that are mediated by TLR2 and TLR4 were also evaluated using a cytometric bead array. Results: Results showed that the transcripts of TLR2 and TLR4 were upregulated on day 28 PI in C. sinensis-infected mice compared with non-infected ones (p < 0.01). In addition, their proteins were strongly immunohistochemically positive in the cytoplasm and membrane of endothelial cells, fibroblasts, and biliary epithelium cells of C. sinensis-infected mice. The levels of interleukin (IL)-4, IL-10, tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) were increased with activation of TLR2 and TLR4. Conclusions: The expression of TLR2 and TLR4 is upregulated against C. sinensis infection, which suggests that TLR2 and TLR4 might be involved in immune responses during C. sinensis infection.

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Section: Discussionsupporting

confidence: 73%

Expression of Toll-like receptor (TLR) 2 and TLR4 in the livers of mice infected by Clonorchis sinensis

Yan

et al. 2015

J Infect Dev Ctries

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“…The normal cercaria antigen (NCA) (40 ng/μL), attenuated cercaria antigen (ACA) (40 ng/μL), soluble egg antigen (SEA) (40 ng/μL) and soluble worm anti-gen (SWAP) (40 ng/μL) were prepared as before[19]. The concentrations of antigens were assayed using Bicinchoninic Acid Protein Assay Kit (Pierce, Rockford, IL, USA).…”

Section: Methodsmentioning

confidence: 99%

Schistosoma japonicum infection induces macrophage polarization

Xu¹,

Zhang²,

Chen³

et al. 2014

J Biomed Res

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The role of macrophages (Mφ) as the first line of host defense is well accepted. These cells play a central role in orchestrating crucial functions during schistosomal infection. Thus, understanding the functional diversity of these cells in the process of infection as well as the mechanisms underlying these events is crucial for developing disease control strategies. In this study, we adopted a Mφ polarization recognition system. M1 macrophage was characterized by expressing CD16/32, IL-12 and iNOS. M2 macrophage was characterized by expressing CD206, IL-10 and arg-1. In vivo (mouse peritoneal macrophages of different infection stages were obtained) and in vitro (different S. japonicum antigens were used to stimulate RAW264.7) were characterized by using the above mentioned system. NCA and ACA stimulated RAW264.7 express significantly higher levels of IL-12 while significantly higher levels of IL-10 were detected after soluble egg antigen (SEA) stimulation. The results showed that dramatic changes of antigen in the microenvironment before and after egg production led to macrophage polarization. Furthermore, through TLR blocking experiments, the TLR4 signaling pathway was found to play a role in the process of macrophage polarization toward M1. Our data suggest that macrophage polarization during S. japonicum infection had significant effects on host immune responses to S. japonicum.

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“…The first TLR2 agonists identified were bacterial lipoproteins (3). In practice, TLR2 has been reported to recognize a wider range of pathogens than any other TLR, including fungi (4), protozoans (5), worms (6), Mycoplasma (7), Gram-positive and -negative bacteria (8,9), DNA viruses (10), and RNA viruses (11), as well as host molecules such as HMGB1 (12). However, concern is growing that many reported TLR2 agonists are artifacts of possible contamination, cellular debris, or merely molecules that sensitize cells to be activated by authentic TLR2 agonists (13,14).…”

Section: Importancementioning

confidence: 99%

MyD88-Dependent Immunity to a Natural Model of Vaccinia Virus Infection Does Not Involve Toll-Like Receptor 2

Davies

Sei

Siciliano

et al. 2014

J Virol

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Although the pattern recognition receptor Toll-like receptor 2 (TLR2) is typically thought to recognize bacterial components, it has been described to alter the induction of both innate and adaptive immunity to a number of viruses, including vaccinia virus (VACV). However, many pathogens that reportedly encode TLR2 agonists may actually be artifactually contaminated during preparation, possibly with cellular debris or merely with molecules that sensitize cells to be activated by authentic TLR2 agonists. In both humans and mice, the most relevant natural route of infection with VACV is through intradermal infection of the skin. Therefore, we examined the requirement for TLR2 and its signaling adaptor MyD88 in protective immunity to VACV after intradermal infection. We find that although TLR2 may recognize virus preparations in vitro and have a minor role in preventing dissemination of VACV following systemic infection with large doses of virus, it is wholly disposable in both control of virus replication and induction of adaptive immunity following intradermal infection. In contrast, MyD88 is required for efficient induction of CD4 T cell and B cell responses and for local control of virus replication following intradermal infection. However, even MyD88 is not required to induce local inflammation, inflammatory cytokine production, or recruitment of cells that restrict virus from spreading systemically after peripheral infection. Thus, an effective antiviral response does require MyD88, but TLR2 is not required for control of a peripheral VACV infection. These findings emphasize the importance of studying relevant routes of infection when examining innate sensing mechanisms. IMPORTANCEVaccinia virus (VACV) provides the backbone for some of the most widely used and successful viral vaccine vectors and is also related to the human pathogens Cantagalo virus and molluscum contagiosum virus that infect the skin of patients. Therefore, it is vital to understand the mechanisms that induce a strong innate immune response to the virus following dermal infection. Here, we compare the ability of the innate sensing molecule Toll-like receptor 2 (TLR2) and the signaling molecule MyD88 to influence the innate and adaptive immune response to VACV following systemic or dermal infection.

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Toll‐like receptor (TLR) 2 and TLR4 deficiencies exert differential in vivo effects against Schistosoma japonicum

Cited by 31 publications

References 34 publications

Expression of Toll-like receptor (TLR) 2 and TLR4 in the livers of mice infected by Clonorchis sinensis

Expression of Toll-like receptor (TLR) 2 and TLR4 in the livers of mice infected by Clonorchis sinensis

Schistosoma japonicum infection induces macrophage polarization

MyD88-Dependent Immunity to a Natural Model of Vaccinia Virus Infection Does Not Involve Toll-Like Receptor 2

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