Prevalence of CD8+αβ T cells in  -elicited myocarditis is associated with acquisition of CD62LLowLFA-1HighVLA-4High activation phenotype and expression of IFN-γ-inducible adhesion and chemoattractant molecules

Santos, Paula V.A. dos; Roffê, Ester; Santiago, Helton da Costa; Torres, Renata A.; Marino, Ana Paula M.P.; Paiva, Cláudia N.; Silva, Andréa Alice; Gazzinelli, Ricardo T.; Lannes-Vieira, Joseli

doi:10.1016/s1286-4579(01)01461-7

Cited by 95 publications

(152 citation statements)

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“…Samples of the perilesional area (aortic root and adjacent cardiac muscle) were cryopreserved for the study of the presence of CD4 ϩ , CD8 ϩ , and F4/80 ϩ cells. Serial 5-m-thick sections starting from the root of aorta were prepared, fixed in cold acetone, and stained with immunoperoxidase as previously described (11). Cells from three sections were counted for each animal.…”

Section: Measurement Of Mcp-1 and Inos Expression By Rt-pcrmentioning

confidence: 99%

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

Portugal¹,

Fernandes²,

César³

et al. 2004

Infect Immun

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Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-␥) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-␥ and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.Atherosclerotic lesions are characterized by progressive accumulation of lipids, macrophages, natural killer (NK) cells, T and B cells, smooth muscle cells, and fibroproliferative elements in the intima of arteries (30). However, hypercholesterolemia and, mainly, high serum levels of low-density lipoprotein (LDL) are considered an absolute prerequisite for lesion establishment. Several genetic and environmental risk factors have been found to contribute to the development of atherosclerosis (2,22,27,33). Among these factors, the immune system is one of the most important. Innate and adaptive immune responses modulate both the rate of lesion progression and composition of atherosclerotic lesions. ApoE knockout (KO) mice crossed into a recombination activating gene (Rag)-deficient background, which lack B and T lymphocytes, had an 80% decrease in the extension of atherosclerotic lesions (32). In addition, crosses of ApoE KO mice with different types of B-or T-cell-deficient mice also decreased atherosclerotic lesions (2,22,40). Inflammatory cytokines and chemokines, such as gamma interferon (IFN-␥), tumor necrosis factor alpha (TNF-␣), TNF-␤, interleukin-12 (IL-12), IL-1␤, and monocyte chemoattractant protein 1 (MCP-1), increase the influx of monocyte into the endothelium, an important step in fatty streak formation (21,24,39). Therefore, atherosclerosis is now considered a chronic inflammatory disease, and systemic infections are thought to play an important role in initiating and/or perpetuating the pathophysiology of aortic lesions. In fact, some studies indicate that bacterial and viral pathogens could be responsible for atherosclerotic development (35). Sunnemark et al. (37) have shown that the combination of an infection of the protozoan parasite Trypanosoma cruzi with an atherogenic diet induced atherosclerotic lesions in the aorta of atherosclerosis-resistant CBA/...

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Section: Measurement Of Mcp-1 and Inos Expression By Rt-pcrmentioning

confidence: 99%

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

Portugal¹,

Fernandes²,

César³

et al. 2004

Infect Immun

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“…Further, increased levels of CCL5/RANTES, CCL3/MIP-1α, CCL4/ MIP-1β, CCL2/MCP-1 and the CXC chemokines CXCL10/ IP-10 and CXCL9/MIG mRNA have been detected in the heart tissue of acutely and chronically T. cruzi-infected mice (Talvani et al 2000, Aliberti et al 2001, dos Santos et al 2001, Marino et al 2004, implicating a potential role for these molecules in Chagas disease.…”

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confidence: 95%

“…Studying C3H/He mice chronically infected with the Colombiana strain of T. cruzi we showed the prevalence of CD8 + T cells in the inflamed heart (dos Santos et al 2001). Further, recently we have shown that the establishment of the CD8 + T cells predominance in the cardiac tissue of T. cruziinfected mice is a rather precocious process, being detected during the early acute phase (Marino et al 2003a).…”

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“…Trying to understand the molecular mechanisms involved in T. cruzi-elicited myocarditis with prevalence of CD8 + T cells, we have investigated the expression of inflammatory CC-chemokines in the heart of Colombiana straininfected C3H/He mice. Interestingly, increased expression of CCL2, CCL3, CCL4 and CCL5 was observed during the acute and chronic phases (dos Santos et al 2001, Marino et al 2004). These CC-chemokines are described to attract activated leukocytes, preferentially CD8 + T cells (Sallusto 1998, Cook et al 1999.…”

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CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis

Marino

Silva

Santos

et al. 2005

Mem. Inst. Oswaldo Cruz

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“…Using C3H/HeJ mice infected with the Colombiana strain of T. cruzi we showed the prevalence of CD8 + T cells (CD4:CD8 ratio of 1:3) in the inflamed heart of chronically Trypanosoma cruzi-infected experimental animals. Akin chagasic patients, amastigote forms and parasite antigens were scarce in the chronically inflamed myocardium and associated with the presence of rare IL-4 producing cells, while large amounts of the pro-inflammatory cytokines IFN-γ and TNF-α were detected , dos Santos et al 2001. Thus, our results led us to consider that the infection of C3H/HeJ mice with the Colombiana strain of T. cruzi reproduces several aspects of the chagasic chronic myocarditis and is an appropriate model to study the molecular mechanisms involved in the recruitment and accumulation of inflammatory cells into the cardiac tissue leading to the establishment of chronic CD8-mediated T. cruzi-elicited myocarditis.…”

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confidence: 99%

Trypanosoma cruzi-elicited CD8+ T cell-mediated myocarditis: chemokine receptors and adhesion molecules as potential therapeutic targets to control chronic inflammation?

Lannes-Vieira

2003

Mem. Inst. Oswaldo Cruz

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Prevalence of CD8+αβ T cells in -elicited myocarditis is associated with acquisition of CD62LLowLFA-1HighVLA-4High activation phenotype and expression of IFN-γ-inducible adhesion and chemoattractant molecules

Cited by 95 publications

References 54 publications

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis

Trypanosoma cruzi-elicited CD8+ T cell-mediated myocarditis: chemokine receptors and adhesion molecules as potential therapeutic targets to control chronic inflammation?

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