CD29 x inversin

Last update 08 May 2025

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Related Targets

CD29inversin

100 Clinical Results associated with CD29 x inversin

100 Translational Medicine associated with CD29 x inversin

0 Patents (Medical) associated with CD29 x inversin

Literatures (Medical) associated with CD29 x inversin

01 Feb 2016·International Journal of Medical MicrobiologyQ3 · MEDICINE

Role of β1 integrins and bacterial adhesins for Yop injection into leukocytes in Yersinia enterocolitica systemic mouse infection

Q3 · MEDICINE

Article

Author: Schütz, Monika ; Siegfried, Alexandra ; Deuschle, Eva ; Autenrieth, Stella E ; Spaeth, Tanja ; Keller, Birgit ; Autenrieth, Ingo B ; Drechsler-Hake, Doreen ; Böttcher, Ralph T ; Manncke, Birgit ; Köberle, Martin ; Reber, Julia ; Bohn, Erwin

Injection of Yersinia outer proteins (Yops) into host cells by a type III secretion system is an important immune evasion mechanism of Yersinia enterocolitica (Ye). In this process Ye invasin (Inv) binds directly while Yersinia adhesin A (YadA) binds indirectly via extracellular matrix (ECM) proteins to β1 integrins on host cells. Although leukocytes turned out to be an important target of Yop injection by Ye, it was unclear which Ye adhesins and which leukocyte receptors are required for Yop injection. To explain this, we investigated the role of YadA, Inv and β1 integrins for Yop injection into leukocytes and their impact on the course of systemic Ye infection in mice. Ex vivo infection experiments revealed that adhesion of Ye via Inv or YadA is sufficient to promote Yop injection into leukocytes as revealed by a β-lactamase reporter assay. Serum factors inhibit YadA- but not Inv-mediated Yop injection into B and T cells, shifting YadA-mediated Yop injection in the direction of neutrophils and other myeloid cells. Systemic Ye mouse infection experiments demonstrated that YadA is essential for Ye virulence and Yop injection into leukocytes, while Inv is dispensable for virulence and plays only a transient and minor role for Yop injection in the early phase of infection. Ye infection of mice with β1 integrin-depleted leukocytes demonstrated that β1 integrins are dispensable for YadA-mediated Yop injection into leukocytes, but contribute to Inv-mediated Yop injection. Despite reduced Yop injection into leukocytes, β1 integrin-deficient mice exhibited an increased susceptibility for Ye infection, suggesting an important role of β1 integrins in immune defense against Ye. This study demonstrates that Yop injection into leukocytes by Ye is largely mediated by YadA exploiting, as yet unknown, leukocyte receptors.

01 Aug 2015·Cellular MicrobiologyQ3 · BIOLOGY

Yersinia enterocolitica exploits different pathways to accomplish adhesion and toxin injection into host cells

Q3 · BIOLOGY

Article

Author: Fehrenbacher, Birgit ; Genth, Harald ; Haas, Rainer ; Jiménez‐Soto, Luisa F. ; Katava, Nenad ; Schade, Jessica ; Autenrieth, Ingo B. ; Mössner, Sara ; Siegfried, Alexandra ; Retta, Saverio F. ; Meyer, Hannelore ; Zent, Roy ; Bohn, Erwin ; Braunsdorf, Christina ; Deuschle, Eva ; Böttcher, Ralph T. ; Schaller, Martin ; Mühlenkamp, Melanie ; Schütz, Monika ; Keller, Birgit ; Griesinger, Tanja

The current paradigm suggests that Yersinia enterocolitica (Ye) adheres to host cells via the outer membrane proteins Yersinia adhesin A (YadA) or invasin (Inv) to facilitate injection of Yops by the type III secretion system. In this process Inv binds directly to β1 integrins of host cells while YadA may bind indirectly via extracellular matrix proteins to β1 integrins. Here we challenged this paradigm and investigated the requirements for Yop injection. We demonstrate that Inv- but not YadA-mediated adhesion depends on β1 integrin binding and activation, and that tight adhesion is a prerequisite for Yop injection. By means of novel transgenic cell lines, shRNA approaches and RGD peptides, we found that YadA, in contrast to Inv, may use a broad host cell receptor repertoire for host cell adhesion. In the absence of β1 integrins, YadA mediates Yop injection by interaction with αV integrins in cooperation with yet unknown cofactors expressed by epithelial cells, but not fibroblasts. Electron microscopic and flow chamber studies revealed that a defined intimate contact area between Ye and host cells resulting in adhesion forces resisting shear stress is required for Yop injection. Thus, the indirect binding of YadA to a broad extracellular matrix (ECM) binding host cell receptor repertoire of different cell types makes YadA a versatile tool to ensure Yop injection. In conclusion, given the differential expression of the outer membrane proteins Inv and YadA in the course of Ye infection and differential expression of integrins by various host cell populations, the data demonstrate that Ye is flexibly armed to accomplish Yop injection in different host cell types, a central event in its immune evasion strategy.

01 Dec 2004·Infection and ImmunityQ2 · MEDICINE

Yersinia enterocolitica Adhesin A Induces Production of Interleukin-8 in Epithelial Cells

Q2 · MEDICINE

Article

Author: Skurnik, Mikael ; Schmid, Yvonne ; Bühler, Oliver T. ; Autenrieth, Ingo B. ; Grassl, Guntram A. ; Bohn, Erwin

ABSTRACT The major invasive factor of Yersinia enterocolitica , the invasin (Inv) protein, induces proinflammatory host cell responses, including interleukin-8 (IL-8) secretion from human epithelial cells, by engagement of β1 integrins. The Inv-triggered β1 integrin signaling involves the small GTPase Rac; the activation of MAP kinases, such as p38, MEK1, and JNK; and the activation of the transcription factor NF-κB. In the present study, we demonstrate that Y. enterocolitica YadA, which is a major adhesin of Y. enterocolitica with pleiotropic virulence effects, induces IL-8 secretion in epithelial cells. The abilites of YadA and Inv to promote adhesion to and invasion of HeLa cells and to induce IL-8 production by the cells were investigated by expression of YadA and Inv in Escherichia coli . While YadA mediates efficacious adhesion to HeLa cells, it mediates marginal invasion compared with Inv. Both YadA and Inv trigger comparable levels of IL-8 production. Conformational changes of the YadA head domain by mutation of NSVAIG-S motifs, which abolish collagen binding, also abolish adhesion of Yersinia to HeLa cells and YadA-mediated IL-8 secretion. Furthermore, experiments in which blocking antibodies against β1 integrins were used demonstrate that β1 integrins are crucial for YadA-mediated IL-8 secretion. Inhibitor studies demonstrate the involvement of small GTPases and MAP kinases, such as p38, MEK1, and JNK, indicating that β1 integrin-dependent signaling mediated by Inv or YadA involves similar signaling pathways. These data present YadA, in addition to Inv, YopB, and Yersinia lipopolysaccharide, as a further inducer of proinflammatory molecules by which Y. enterocolitica might promote inflammatory tissue reactions.

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