Immunohistological Characterization of the Cellular Immune Response against Yersinia enterocolitica in Mice: Evidence for the Involvement of T Lymphocytes

Autenrieth, Ingo B.; Hantschmann, Peer; B, Heymer; Heesemann, Jürgen

doi:10.1016/s0171-2985(11)80241-x

Cited by 60 publications

(46 citation statements)

References 41 publications

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“…Histopathology data are summarized in Tables 1 and 2. The histopathology of earlier time points of Y. enterocolitica infection has been described (2,6,12). Interestingly, as previously reported for earlier time points, mice infected orally with the rovA mutant did not have a strong inflammatory response even at the 24-day time point in any of the tissues.…”

Section: Regulon Is Required After Oral Infection 3513supporting

confidence: 67%

The rovA Mutant of Yersinia enterocolitica Displays Differential Degrees of Virulence Depending on the Route of Infection

et al. 2003

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Yersinia enterocolitica is an invasive enteric pathogen that causes significant inflammatory disease. Recently, we identified and characterized a global regulator of virulence (rovA). When mice are infected orally with the rovA mutant they are attenuated by 50% lethal dose (LD 50 ) analysis and have altered kinetics of infection. Most significantly, mice orally infected with the rovA mutant have greatly reduced inflammation in the Peyer's patches compared to those infected with wild-type Y. enterocolitica. However, we present data here indicating that when the rovA mutant bacteria are delivered intraperitoneally (i.p.), they are significantly more virulent than when delivered orally. The i.p. LD 50 for the rovA mutant is only 10-fold higher than that of the wild-type Y. enterocolitica, and there are significant inflammatory responses to the rovA mutant that are evident in the liver and spleen. Altogether, these data suggest that the RovA regulon may be required for the early events of the infection that occur in the Peyer's patches. Furthermore, these data suggest that the RovA regulon may be dispensable for Y. enterocolitica systemic disease and inflammatory responses if the Peyer's patches are bypassed.

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Section: Regulon Is Required After Oral Infection 3513supporting

confidence: 67%

The rovA Mutant of Yersinia enterocolitica Displays Differential Degrees of Virulence Depending on the Route of Infection

et al. 2003

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“…Although several studies with detailed histologic approaches analyzed the inflammatory response of the infected mucosa to infection by Y. enterocolitica (2,4), it is still unclear which pathogen and host signals may trigger and promote this reaction. Epithelial cells, the first cells to encounter yersiniae upon orogastric infection, are attributed a key role in generating signals to the underlying mucosa, thereby initiating the host's immune response.…”

Section: Discussionmentioning

confidence: 99%

Yersinia enterocoliticaInvasin Protein Triggers Differential Production of Interleukin-1, Interleukin-8, Monocyte Chemoattractant Protein 1, Granulocyte-Macrophage Colony-Stimulating Factor, and Tumor Necrosis Factor Alpha in Epithelial Cells: Implications for Understanding the Early Cytokine Network inYersiniaInfections

2000

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“…The early control of infection with Yersinia is mediated by mechanisms of innate immunity, involving macrophages, NK cells and neutrophils [7][8][9]. This early response is followed by an adaptive immune response, and the resolution of the infection is mediated by CD4 + Th1 cells that produce cytokines such as IFN-c and IL-2 [8,9].…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to Yersinia pseudotuberculosis Infection is Linked to the Pattern of Macrophage Activation

Tansini

Medeiros

2009

Scand J Immunol

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T helper 1 cells play a crucial role in the clearance of Yersinia pseudotuberculosis infection. By producing cytokines and presenting antigens to T cells, activated macrophages can orientate the adaptive immune response. The pathway used by macrophages to metabolize arginine has been employed as an important parameter to discriminate their activation state. In this study, the pattern of macrophage activation in Y. pseudotuberculosis-infected BALB ⁄ c (Yersinia-susceptible) and C57BL ⁄ 6 (Yersinia-resistant) mice and their immunostimulatory capacity were analysed. In the early phase of infection, macrophages obtained from C57BL ⁄ 6 mice produced higher levels of NO, lower arginase activity, and larger amounts of IL-12 and TNF-a than macrophages from BALB ⁄ c mice. On the other hand, macrophages derived from BALB ⁄ c mice produced higher levels of IL-10 and TGF-b than C57BL ⁄ 6 mice. The Y. pseudotuberculosis infection leads to a fall in the macrophage immunostimulatory capacity of both strains of mice, with T-cell proliferation significantly reduced 12 h after infection. Moreover, we observed in the supernatant of co-culture of macrophages from infected mice with T lymphocytes from heat-killed Yersiniaimmunized mice lower IFN-c production by cells from BALB ⁄ c mice than by C57BL ⁄ 6 mice, and IL-4 was produced only by BALB ⁄ c mice on the first-and third-day post-infection. These results suggest that the pattern of macrophage activation is associated with susceptibility and resistance to Y. pseudotuberculosis infection in BALB ⁄ c and C57BL ⁄ 6 mice.

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Immunohistological Characterization of the Cellular Immune Response against Yersinia enterocolitica in Mice: Evidence for the Involvement of T Lymphocytes

Cited by 60 publications

References 41 publications

The rovA Mutant of Yersinia enterocolitica Displays Differential Degrees of Virulence Depending on the Route of Infection

The rovA Mutant of Yersinia enterocolitica Displays Differential Degrees of Virulence Depending on the Route of Infection

Susceptibility to Yersinia pseudotuberculosis Infection is Linked to the Pattern of Macrophage Activation

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