Lymphocyte Muscarinic Cholinergic Activity and PGE2Involvement in ExperimentalTrypanosoma cruziInfection

Sterin‐Borda, Leonor; Gorelik, Gabriela; Goren, Nora; Cappa, Stella Gonzalez; Celentano, Ana M.; Borda, Enri

doi:10.1006/clin.1996.0167

Cited by 29 publications

(31 citation statements)

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“…Previous studies have shown that the release of eicosanoids during infection with T. cruzi regulates host responses and controls disease progression (10,(27)(28)(29)(30)(31). PGs, together with NO and TNF-␣, participate in a complex circuit that controls lymphoproliferative and cytokine responses in T. cruzi infection (28).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

Malvezi

Silva

Freitas

et al. 2014

Antimicrob Agents Chemother

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fThe intracellular protozoan parasite Trypanosoma cruzi is the etiologic agent of Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzymes during T. cruzi invasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib) caused marked inhibition of T. cruzi infection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO and interleukin-1␤ and decreased production of transforming growth factor ␤ (TGF-␤) by cells. Taken together, these results indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruzi activity in cardiac cells, and they provide a better understanding of the influence of TGF-␤-interfering therapies on the innate inflammatory response to T. cruzi infection and may represent a very pertinent target for new therapeutic treatments of Chagas disease.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

Malvezi

Silva

Freitas

et al. 2014

Antimicrob Agents Chemother

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“…Pharmacological antagonists of COX-1 (aspirin, ASA), COX-2 (celecoxib), or both (indomethacin) have been found to increase mortality and parasitemia (parasite load in peripheral blood and cardiac tissue) regardless of which mouse or T. cruzi strains were used [9–13]. Moreover, evidence suggests that administration of NSAIDs may enhance mortality in chagasic patients [12]. Conversely, others have found that inhibition of PG synthesis/release reduces parasitemia and extends survival of mice infected with T. cruzi [14–17].…”

Section: Introductionmentioning

confidence: 99%

Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry ofTrypanosoma cruziin Mouse Peritoneal Macrophages

Malvezi

Silva

Yamauchi

et al. 2014

Mediators of Inflammation

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The intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzyme during T. cruzi invasion. Pharmacological antagonist for COX-1, aspirin (ASA), caused marked inhibition of T. cruzi infection when peritoneal macrophages were pretreated with ASA for 30 min at 37°C before inoculation. This inhibition was associated with increased production of IL-1β and nitric oxide (NO∙) by macrophages. The treatment of macrophages with either NOS inhibitors or prostaglandin E2 (PGE2) restored the invasive action of T. cruzi in macrophages previously treated with ASA. Lipoxin ALX-receptor antagonist Boc2 reversed the inhibitory effect of ASA on trypomastigote invasion. Our results indicate that PGE2, NO∙, and lipoxins are involved in the regulation of anti-T. cruzi activity by macrophages, providing a better understanding of the role of prostaglandins in innate inflammatory response to T. cruzi infection as well as adding a new perspective to specific immune interventions.

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“…In previous work we demonstrated that, in T. cruzi infection, elevated PGE 2 levels are able to modulate tolerance to chronic Chagas' disease [31]. One of the major sources of PGE 2 are CD8 + T cells [32], which release large amount of PGE 2 when they are activated by M 2 mAChR autoantibodies [33]. This antibody-host immune competent cell recognition modulates immune response allowing to parasite to survive, leading to disease chronicity [32,33].…”

Section: Discussionmentioning

confidence: 93%

“…One of the major sources of PGE 2 are CD8 + T cells [32], which release large amount of PGE 2 when they are activated by M 2 mAChR autoantibodies [33]. This antibody-host immune competent cell recognition modulates immune response allowing to parasite to survive, leading to disease chronicity [32,33]. The existence of nicotinic cholinergic anti-inflammatory and protective mechanism by which stimulation of the vagus nerve and cholinergic agonist inhibiting cytokine synthesis by macrophages has been described [34,35].…”

Section: Discussionmentioning

confidence: 99%

Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

Ganzinelli

Borda

Joensen

et al. 2009

International Journal of Cardiology

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Lymphocyte Muscarinic Cholinergic Activity and PGE2Involvement in ExperimentalTrypanosoma cruziInfection

Cited by 29 publications

References 0 publications

Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry ofTrypanosoma cruziin Mouse Peritoneal Macrophages

Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

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