Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

Magalhães-Santos, Isis Fernandes; Andrade, Sônia Gumes

doi:10.1590/s0074-02762005000500017

Cited by 16 publications

(7 citation statements)

References 30 publications

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“…Particularly, the RA strain of T. cruzi has been proven to promote neuromyopathic inflammatory lesions in acutely infected mice, with predominance of CD8+ T cells in leukocyte infiltrates [19] . In agreement with previous findings [16,31,32] , acute myocarditis and intense rhabdomyolysis developed during the initial phase of experimental Chagas' disease. Muscle cells may be actively involved in the recruitment of mononuclear cells from the bloodstream and in the cross-talk between infiltrating leukocytes and myocytes, mediated by active transcription and release of cytokines and chemokines by both cell types, creating the conditions for ongoing inflammation [33] .…”

Section: Discussionsupporting

confidence: 93%

“…In the present study, during the parasitic phase of infection, we found early induction of muscular expression for CCL5/CCR5 and CXCL9/ CXCR3, accompanied by the severity of parasite burden and myopathy. These molecules, together with IFN-␥ , TNF-␣ and TGF-␤ , might participate in the selective recruitment of CD8+ T lymphocytes involved in the immunopathogenesis of muscle inflammation observed in experimental acute Chagas' disease [31] . Further studies may provide additional insights into the recognition of those components of the cytokine/chemokine network which are essential for parasite control in the infected host and/or contribute to T. cruzi -dependent inflammatory damage to skeletal muscles.…”

Section: Discussionmentioning

confidence: 99%

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Timing of Expression of Inflammatory Mediators in Skeletal Muscles from Mice Acutely Infected with the RA Strain of <i>Trypanosoma cruzi</i>

Cutrullis

Postan²,

Petray³

et al. 2009

Pathobiology

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Objective: Chagas’ disease is caused by persistent Trypanosoma cruzi infection in muscle cells that ultimately results in chronic inflammation and tissue destruction. The goal of this study was to determine the expression of different chemokines and their receptors, as well as proinflammatory cytokines and inducible nitric oxide synthase, in muscles from mice acutely infected with T. cruzi. Methods: Histological, semiquantitative reverse transcriptase polymerase chain reaction and immunohistochemical studies were performed on skeletal muscle and myocardium of BALB/c mice infected with T. cruzi, RA strain. Results: Early induction of muscular mRNA expression for CCL5/CCR5 and CXCL9/CXCR3, as well as for iNOS, IFN-γ, TNF-α and MIF, was demonstrated accompanied by progressive increases in parasitism and leukocyte recruitment. Protein overexpression for MIF and CCL5/CCR5 was also verified in the infected muscles. Conclusions: In muscles from acutely T. cruzi RA-infected mice, upregulated gene expression of proinflammatory chemokines, chemokine receptors, cytokines and iNOS is associated with the severity of parasite burden and myopathic alterations. Compared to the heart, striated muscles displayed differential timing of expression of several inflammatory mediators throughout acute infection. Our findings suggest that enhanced early production of these factors could contribute to T. cruzi-dependent inflammatory damage to skeletal muscles.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Timing of Expression of Inflammatory Mediators in Skeletal Muscles from Mice Acutely Infected with the RA Strain of <i>Trypanosoma cruzi</i>

Cutrullis

Postan²,

Petray³

et al. 2009

Pathobiology

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“…TGF-b is a strong profibrogenic cytokine implicated in the genesis of fibrosis associated with chagasic cardiomyopathy fibrosis (Araujo-Jorge et al, 2002;Magalhaes-Santos and Andrade, 2005). It is also known to promote ECM accumulation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of extracellular matrix expression and distribution in Trypanosoma cruzi-infected cardiomyocytes

Calvet

Oliveira

Araújo-Jorge

et al. 2009

International Journal of Medical Microbiology

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“…However, recent studies using these dental materials indicate that their beneficial effects on the dentin–pulp complex relate to their ability to sterilize the infection while releasing bioactive components locally from the dentin . Data demonstrating that necrotic cells release low‐levels of pro‐inflammatory mediators may indicate that pulpal injury resulting from calcium hydroxide and MTA treatment initiates a relatively mild acute immune cell response, which may also promote reparative events . In addition, increased cytokine release, including IL‐1α, ‐1β, ‐2, ‐6, and ‐8, from mineralizing cells following MTA exposure has also been demonstrated and such a material‐induced inflammatory response may also contribute to clinical repair .…”

Section: Interplay Between Dental Tissue Inflammation and Regenerationmentioning

confidence: 99%

Molecular mediators of pulp inflammation and regeneration

Cooper¹,

Smith²

2013

Endodontic Topics

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Dental tissue infection results in immune and inflammatory responses mediated by molecular and cellular events that, if unchecked, result in tissue breakdown. The tooth, like other tissues and organs within the body, will attempt to repair and regenerate its own hard and soft tissues given the appropriate conditions and environment. However, unchecked infection and inflammation will have a significant impact on the natural regenerative responses of the dental tissues. Thus far, there have been limited studies addressing the inter‐relationship between these two processes, which are clearly linked by molecular and cellular events. Indeed, locally derived growth factors, cytokines, and chemokines, which are all sequestrated within the dental tissue extracellular matrix and are also expressed by pulpal cells, immune cells, and/or necrotic host tissue, will have considerable impact on the cellular events within the tissue. In addition to the molecular signaling, there will be important cellular interactions that will occur as stem cells, resident or recruited to the pulp, have known immuno‐modulatory activity with significant implications for regenerative events. In this review, we aim to explore how the pulpal tissue responds to the invading bacteria and the signaling mechanisms that are now being described and are important in regulating both the immune/inflammatory and regenerative responses.

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Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

Cited by 16 publications

References 30 publications

Timing of Expression of Inflammatory Mediators in Skeletal Muscles from Mice Acutely Infected with the RA Strain of <i>Trypanosoma cruzi</i>

Timing of Expression of Inflammatory Mediators in Skeletal Muscles from Mice Acutely Infected with the RA Strain of <i>Trypanosoma cruzi</i>

Regulation of extracellular matrix expression and distribution in Trypanosoma cruzi-infected cardiomyocytes

Molecular mediators of pulp inflammation and regeneration

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