Transforming growth factor beta production during rat cytomegalovirus infection.

Haagmans, Bart L.; Teerds, K. J.; Raaij, A.J.M. van den Eijnden-van; Horzinek, Marian C.; Schijns, Virgil E. C. J.

doi:10.1099/0022-1317-78-1-205

Cited by 24 publications

(22 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TGF-β in neurons has also been reported in mice with experimental allergic encephalomyelitis (Fujinami, 2006;Issazadeh et al, 1998) and in rats with spinal cord injury (O'Brien et al, 1994). Although in vivo induction of TGF-β1 specifically in CNS neurons by virus infections has not been reported, TGF-β1 is produced or activated in other cell types by several virus infections [reviewed in (Fitzpatrick and Bielefeldt-Ohmann, 1999)], including Epstein-Barr virus (Xu et al, 2000), cytomegalovirus (Haagmans et al, 1997;Michelson et al, 1994), herpes simplex virus (Méndez-Samperio et al, 2000), human T-lymphotropic virus (HTLV)-I, human immunodeficiency virus (HIV) (Lotz and Seth, 1993;Wahl et al, 1991;Yamamoto et al, 1999), influenza virus (Schultz-Cherry andHinshaw, 1996) and yellow fever virus (Quaresma et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…In vitro TGF-β1 production has been shown in several cell types, including splenocytes (Haagmans et al, 1997;Méndez-Samperio et al, 2000) and astrocytes (Michelson et al, 1994;Morganti-Kossmann et al, 1992;Yong, 1996). Using ELISAs, we found induction of TGF-β1 protein in spleen MNCs in GDVII virus infection, but not in the other TMEV infections.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

Tsunoda

Libbey

Fujinami

2007

Journal of Neuroimmunology

View full text Add to dashboard Cite

GDVII and DA strains of Theiler's murine encephalomyelitis virus (TMEV) differ in VP2 puff B. One week after GDVII virus infection, SJL/J mice had large numbers of TUNEL + apoptotic cells with a relative lack of T cell infiltration in the brain. DA viruses with mutation in puff B induced higher levels of apoptosis than wild-type DA virus, but levels of inflammation in brains were similar between DA and DA virus mutants. The difference in inflammation among TMEVs could be due to TGF-β1 expression that was seen only in GDVII virus infection and negatively correlated with CD3 + T cell infiltration.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

Tsunoda

Libbey

Fujinami

2007

Journal of Neuroimmunology

View full text Add to dashboard Cite

show abstract

“…TGF-␤1 was released in increasing amounts from splenocytes infected with rat CMV in vitro. 25 TGF-␤1 protein was increased in alveoli and stromal cells in rat lungs, spleen, and liver after radiation-induced immune suppression of CMV-infected rats. 25 Furthermore, CMVinfected murine astrocytes increased TGF-␤1 transcription and protein levels.…”

mentioning

confidence: 98%

“…25 TGF-␤1 protein was increased in alveoli and stromal cells in rat lungs, spleen, and liver after radiation-induced immune suppression of CMV-infected rats. 25 Furthermore, CMVinfected murine astrocytes increased TGF-␤1 transcription and protein levels. 26 In human kidney allografts, CMV proteins and DNA were associated with locally increased TGF-␤1 in tubuli and arterial endothelium long after viral clearance from the blood.…”

mentioning

confidence: 98%

Induction of an Epithelial Integrin αvβ6 in Human Cytomegalovirus-Infected Endothelial Cells Leads to Activation of Transforming Growth Factor-β1 and Increased Collagen Production

Tabata

Kawakatsu

Maidji

et al. 2008

The American Journal of Pathology

View full text Add to dashboard Cite

Human cytomegalovirus (CMV) infection is a major cause of morbidity in immunosuppressed individuals, and congenital CMV infection is a leading cause of birth defects in newborns. Infection with pathogenic viral strains alters cell-cell and cell-matrix interactions, affecting extracellular matrix remodeling and endothelial cell migration. The multifunctional cytokine transforming growth factor (TGF)-␤1 regulates cell proliferation, differentiation, and extracellular matrix remodeling. Secreted as a latent protein complex, TGF-␤1 requires activation before binding to receptors that phosphorylate intracellular effectors. TGF-␤1 is activated by integrin ␣v␤6, which is strongly induced in the epithelium by injury and inflammation but has not previously been found in endothelial cells. Here , we report that CMV infection induces integrin ␣v␤6 expression in endothelial cells , leading to activation of TGF-␤1 , signaling through its receptor ALK5 , and phosphorylation of its intracellular effector Smad3. Infection of endothelial cells was also found to stimulate collagen synthesis through a mechanism dependent on both TGF-␤1 and integrin ␣v␤6. Immunohistochemical analysis showed integrin ␣v␤6 up-regulation in capillaries proximal to foci of CMV infection in lungs , salivary glands , uterine decidua , and injured chorionic villi of the placenta , demonstrating both its induction in endothelium and upregulation in epithelium in vivo. Our results suggest that activation of TGF-␤1 by integrin ␣v␤6 contributes to pathological changes and may impair endothelial cell functions in tissues that are chronically infected with CMV.

show abstract

“…Recent work by Haagmans et al (1997) has provided evidence for the induction of transforming growth factor (TGF)-β1 in the BM and in a variety of tissues by rat CMV infection. Likewise, Lagneaux et al (1996) reported an in vitro induction of TGF-β1 in human BM stroma by human CMV.…”

Section: Introductionmentioning

confidence: 99%

Evidence against a key role for transforming growth factor-beta1 in cytomegalovirus-induced bone marrow aplasia.

Dobonici

Podlech

Steffens

et al. 1998

Journal of General Virology

View full text Add to dashboard Cite

During immunodeficiency after sublethal haematoablative treatment, cytomegalovirus (CMV) infection interferes with haematopoietic reconstitution and can cause lethal bone marrow (BM) aplasia. The in vivo model of murine CMV infection has identified the BM stroma as the principal target site of CMV in the haematopoietic cord. The infected cell type is the reticular stromal cell which forms the stromal network and produces essential haemopoietins, such as stem-cell factor (SCF). The expression of SCF was found to be reduced in the infected stroma, but the stromal network was not disrupted and the number of infected stromal cells was too low to explain the functional deficiency. These facts call for a negatively regulating cytokine that is induced by the infection and that potentiates the direct effect of infection by down-regulating haemopoietins in un-

show abstract

Transforming growth factor beta production during rat cytomegalovirus infection.

Cited by 24 publications

References 45 publications

TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

TGF-β1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus

Induction of an Epithelial Integrin αvβ6 in Human Cytomegalovirus-Infected Endothelial Cells Leads to Activation of Transforming Growth Factor-β1 and Increased Collagen Production

Evidence against a key role for transforming growth factor-beta1 in cytomegalovirus-induced bone marrow aplasia.

Contact Info

Product

Resources

About