Contribution of Toll-like receptors 2 and 4 in an oral Yersinia enterocolitica mouse infection model

Sing, Andreas; Tvardovskaia, Natalia; Rost, D; Kirschning, Carsten J.; Wagner, Hermann; Heesemann, Jürgen

doi:10.1078/1438-4221-00277

Cited by 24 publications

(25 citation statements)

References 27 publications

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“…In mice, V antigen is an immunomodulator (TNF- and IFN- downregulation and IL-10 induction) both in vivo and in vitro [78][79][80][81][82][83][84]. Such effects would depend on TLR2 stimulation [85]. In our study, the agonistic interaction of rV with TLR2 was confirmed.…”

Section: Cellular Immune Responses To Y Pestissupporting

confidence: 72%

Role of immune response in Yersinia pestis infection

Amedei

Niccolai

Marino

et al. 2011

J Infect Dev Ctries

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Yersinia pestis (Y. Pestis) is an infamous pathogen causing plague pandemics throughout history and is a selected agent of bioterrorism threatening public health. Y. pestis was first isolated by Alexandre Yersin in 1894 in Hong Kong and in the following years from all continents. Plague is enzootic in different rodents and their fleas in Africa, North and South America, and Asia, including the Middle/Far East and ex-USSR countries. Comprehending the multifaceted interaction between Y. pestis and the host immune system will enable us to design more effective vaccines. Innate immune response and both components (humoral and cellular) of adaptive immune response contribute to host defense against Y. pestis infection, but the bacterium possesses different mechanisms to counteract the immune response. The review aims to analyze the role of immune response versus Yersinia pestis infection and to highlight the various stratagems adopted by Y. pestis to escape the immunological defenses.

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Section: Cellular Immune Responses To Y Pestissupporting

confidence: 72%

Role of immune response in Yersinia pestis infection

Amedei

Niccolai

Marino

et al. 2011

J Infect Dev Ctries

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“…In order to determine the susceptibility of TLR2 Ϫ/Ϫ mice to Y. pseudotuberculosis, we performed i.p. infections of TLR2 Ϫ/Ϫ mice that were derived from a different Tlr2 construction than that used in the previous studies (48,50,51) and which had been completely backcrossed into the C57BL/6J background (54). Surprisingly, these animals had levels of Y. pseudotuberculosis CFU similar to those in TLR2 ϩ/ϩ mice in both the liver and spleen at 4 days after i.p.…”

Section: Y Pseudotuberculosis Infection Induces Tnf-␣ Ifn-␥mentioning

confidence: 86%

“…Sing et al (50,51) reported that treatment of macrophages with recombinant Y. enterocolitica LcrV activates the transcription factor NF-B and induces the expression of IL-10 in a TLR2-dependent manner. The induction of IL-10 was linked to a single residue within the LcrV N terminus (K42) (48).…”

mentioning

confidence: 99%

Growth of Yersinia pseudotuberculosis in Mice Occurs Independently of Toll-Like Receptor 2 Expression and Induction of Interleukin-10

Auerbuch

Isberg

2007

Infect Immun

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Pathogenic Yersinia translocates effector proteins into target cells via a type III secretion system (TTSS), modulating the host immune response. A component of the TTSS translocon, LcrV, has been implicated in preventing inflammation through Toll-like receptor 2 (TLR2) by inducing expression of the anti-inflammatory cytokine interleukin-10 (IL-10). TLR2 ؊/؊ mice were reported to be less susceptible to the enteropathogen Yersinia enterocolitica. To determine whether TLR2 also plays a role in recognition of the enteropathogen Yersinia pseudotuberculosis and whether this results in an immune response that is detrimental to the host, we evaluated the macrophage cytokine response to live Y. pseudotuberculosis and analyzed the susceptibility of TLR2 ؊/؊ mice to enteropathogenic Yersinia. We find that Yersinia induction of macrophage IL-10 occurs independently of TLR2 and LcrV and is blocked by the TTSS. In particular, the TTSS effector protein YopJ, which inhibits production of the inflammatory cytokine tumor necrosis factor alpha (TNF-␣), also inhibits IL-10 expression. Consistent with these results, IL-10 is undetectable in Y. pseudotuberculosis-infected mouse tissues until advanced stages of infection. In addition, we find that TLR2 ؊/؊ mice (derived independently from those used in previous studies) do not display altered susceptibility to enteropathogenic Yersinia compared to wild-type mice. Tissue levels of IL-10, as well as the inflammatory cytokines TNF-␣, IL-6, and gamma interferon and the chemokine macrophage chemotactic protein 1, are similar in TLR2 ؉/؉ and TLR2 ؊/؊ mice during enteropathogenic Yersinia infection. Therefore, the absence of TLR2 alone does not affect the cytokine response of macrophages to, or the in vivo growth and survival of, enteropathogenic Yersinia.

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“…Whereas it is difficult to provide direct functional evidence in human SpA and thereby to demonstrate the biologic significance of our findings, animal studies have indicated the importance of TLR-4 in the early inflammatory cytokine response of phagocytes upon infection with SpA-associated gram-negative bacteria such as Salmonella, Yersinia, and Chlamydia (22)(23)(24)(25)60). Accordingly, the role of bacterial products such as streptococcal cell wall and LPS in the induction and/or perpetuation of experimental arthritis is critically dependent on TLR-2 and TLR-4, respectively, and the associated adaptor molecule, myeloid differentiation factor 88 (35,36).…”

Section: De Rycke Et Almentioning

confidence: 92%

Tumor necrosis factor α blockade treatment down‐modulates the increased systemic and local expression of toll‐like receptor 2 and toll‐like receptor 4 in spondylarthropathy

Rycke¹,

Vandooren²,

Kruithof³

et al. 2005

Arthritis & Rheumatism

119

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Results. Expression of TLR-4, but not TLR-2, was increased on PBMCs from patients with SpA, whereas both TLRs were increased in RA patients. TLR expression was particularly increased on the CD163؉ macrophage subset. Infliximab reduced TLR-2 and TLR-4 expression on monocytes of SpA and RA patients, leading to lower levels than in controls and to impaired TNF␣ production upon LPS stimulation. In inflamed synovium, the expression of both TLRs and of CD163 was significantly higher in patients with SpA than in those with RA or OA. Paralleling the systemic effect, TLRs in synovium were down-regulated following treatment with infliximab as well as etanercept, indicating a class effect of TNF␣ blockers.Conclusion. Inflammation in SpA is characterized by increased TLR-2 and TLR-4 expression, which is sharply reduced by TNF␣ blockade. These findings suggest a potential role of innate immunity-mediated inflammation in SpA and provide an additional clue regarding the mechanism of action as well as the potential side effects of TNF␣ blockade.

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Contribution of Toll-like receptors 2 and 4 in an oral Yersinia enterocolitica mouse infection model

Cited by 24 publications

References 27 publications

Role of immune response in Yersinia pestis infection

Role of immune response in Yersinia pestis infection

Growth of Yersinia pseudotuberculosis in Mice Occurs Independently of Toll-Like Receptor 2 Expression and Induction of Interleukin-10

Tumor necrosis factor α blockade treatment down‐modulates the increased systemic and local expression of toll‐like receptor 2 and toll‐like receptor 4 in spondylarthropathy

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