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The Wnt/β-catenin signaling pathway controls the inflammatory response in infections caused by pathogenic bacteria.

Silva-García O, Valdez-Alarcón JJ, Baizabal-Aguirre VM - Mediators Inflamm. (2014)

Bottom Line: During bacterial infection, different signaling transduction pathways control the expression of a wide range of genes that orchestrate a number of molecular and cellular events to eliminate the invading microorganisms and regulate inflammation.The inflammatory response must be tightly regulated because uncontrolled inflammation may lead to tissue injury.Among the many signaling pathways activated, the canonical Wnt/β-catenin has been recently shown to play an important role in the expression of several inflammatory molecules during bacterial infections.

View Article: PubMed Central - PubMed

Affiliation: Centro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Km. 9.5 s/n Carretera Morelia-Zinapécuaro, La Palma, Tarímbaro, 58893 Morelia, MICH, Mexico.

ABSTRACT
Innate immunity against pathogenic bacteria is critical to protect host cells from invasion and infection as well as to develop an appropriate adaptive immune response. During bacterial infection, different signaling transduction pathways control the expression of a wide range of genes that orchestrate a number of molecular and cellular events to eliminate the invading microorganisms and regulate inflammation. The inflammatory response must be tightly regulated because uncontrolled inflammation may lead to tissue injury. Among the many signaling pathways activated, the canonical Wnt/β-catenin has been recently shown to play an important role in the expression of several inflammatory molecules during bacterial infections. Our main goal in this review is to discuss the mechanism used by several pathogenic bacteria to modulate the inflammatory response through the Wnt/β-catenin signaling pathway. We think that a deep insight into the role of Wnt/β-catenin signaling in the inflammation may open new venues for biotechnological approaches designed to control bacterial infectious diseases.

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Related in: MedlinePlus

Frizzled receptors reduce inflammation. In epithelial cells and macrophages, Mycobacterium tuberculosis induces NF-κB-dependent expression of IL-8, TNFα, and IFNγ (left panel) through TLR signaling. In turn, TNFα and IFNγ stimulation increases Fzd1, Wnt6, and Wnt5a expression at the membrane cell surface (middle panel). Finally, the binding of Wnt3a, Wnt5a, or Wnt6 to Fzd1 (right panel) induces stabilization of β-catenin, inhibiting the NF-κB pathway. This interaction of β-catenin with NF-κB decreases the expression of proinflammatory molecules such as TNFα.
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fig4: Frizzled receptors reduce inflammation. In epithelial cells and macrophages, Mycobacterium tuberculosis induces NF-κB-dependent expression of IL-8, TNFα, and IFNγ (left panel) through TLR signaling. In turn, TNFα and IFNγ stimulation increases Fzd1, Wnt6, and Wnt5a expression at the membrane cell surface (middle panel). Finally, the binding of Wnt3a, Wnt5a, or Wnt6 to Fzd1 (right panel) induces stabilization of β-catenin, inhibiting the NF-κB pathway. This interaction of β-catenin with NF-κB decreases the expression of proinflammatory molecules such as TNFα.

Mentions: Mycobacterium tuberculosis is able to interfere with some components of the Wnt/β-catenin pathway such as Fzd1, which is upregulated by TNFα and synergistically enhanced by IFNγ [8]. Presence of Wnt3a in the lungs of mice infected with M. tuberculosis affects the ability of macrophages to produce TNFα by increasing β-catenin transcriptional activity [8]. It is proposed that the upregulation of Fzd1 constitutes a mechanism by which Wnt3a represses inflammation, leading to a negative loop of inflammatory control in mice macrophages during M. tuberculosis infection (Figure 4).


The Wnt/β-catenin signaling pathway controls the inflammatory response in infections caused by pathogenic bacteria.

Silva-García O, Valdez-Alarcón JJ, Baizabal-Aguirre VM - Mediators Inflamm. (2014)

Frizzled receptors reduce inflammation. In epithelial cells and macrophages, Mycobacterium tuberculosis induces NF-κB-dependent expression of IL-8, TNFα, and IFNγ (left panel) through TLR signaling. In turn, TNFα and IFNγ stimulation increases Fzd1, Wnt6, and Wnt5a expression at the membrane cell surface (middle panel). Finally, the binding of Wnt3a, Wnt5a, or Wnt6 to Fzd1 (right panel) induces stabilization of β-catenin, inhibiting the NF-κB pathway. This interaction of β-catenin with NF-κB decreases the expression of proinflammatory molecules such as TNFα.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4127235&req=5

fig4: Frizzled receptors reduce inflammation. In epithelial cells and macrophages, Mycobacterium tuberculosis induces NF-κB-dependent expression of IL-8, TNFα, and IFNγ (left panel) through TLR signaling. In turn, TNFα and IFNγ stimulation increases Fzd1, Wnt6, and Wnt5a expression at the membrane cell surface (middle panel). Finally, the binding of Wnt3a, Wnt5a, or Wnt6 to Fzd1 (right panel) induces stabilization of β-catenin, inhibiting the NF-κB pathway. This interaction of β-catenin with NF-κB decreases the expression of proinflammatory molecules such as TNFα.
Mentions: Mycobacterium tuberculosis is able to interfere with some components of the Wnt/β-catenin pathway such as Fzd1, which is upregulated by TNFα and synergistically enhanced by IFNγ [8]. Presence of Wnt3a in the lungs of mice infected with M. tuberculosis affects the ability of macrophages to produce TNFα by increasing β-catenin transcriptional activity [8]. It is proposed that the upregulation of Fzd1 constitutes a mechanism by which Wnt3a represses inflammation, leading to a negative loop of inflammatory control in mice macrophages during M. tuberculosis infection (Figure 4).

Bottom Line: During bacterial infection, different signaling transduction pathways control the expression of a wide range of genes that orchestrate a number of molecular and cellular events to eliminate the invading microorganisms and regulate inflammation.The inflammatory response must be tightly regulated because uncontrolled inflammation may lead to tissue injury.Among the many signaling pathways activated, the canonical Wnt/β-catenin has been recently shown to play an important role in the expression of several inflammatory molecules during bacterial infections.

View Article: PubMed Central - PubMed

Affiliation: Centro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Km. 9.5 s/n Carretera Morelia-Zinapécuaro, La Palma, Tarímbaro, 58893 Morelia, MICH, Mexico.

ABSTRACT
Innate immunity against pathogenic bacteria is critical to protect host cells from invasion and infection as well as to develop an appropriate adaptive immune response. During bacterial infection, different signaling transduction pathways control the expression of a wide range of genes that orchestrate a number of molecular and cellular events to eliminate the invading microorganisms and regulate inflammation. The inflammatory response must be tightly regulated because uncontrolled inflammation may lead to tissue injury. Among the many signaling pathways activated, the canonical Wnt/β-catenin has been recently shown to play an important role in the expression of several inflammatory molecules during bacterial infections. Our main goal in this review is to discuss the mechanism used by several pathogenic bacteria to modulate the inflammatory response through the Wnt/β-catenin signaling pathway. We think that a deep insight into the role of Wnt/β-catenin signaling in the inflammation may open new venues for biotechnological approaches designed to control bacterial infectious diseases.

Show MeSH
Related in: MedlinePlus