Immunological and non-immunological effects of cytokines and chemokines in the pathogenesis of chronic Chagas disease cardiomyopathy

Cunha‐Neto, Edécio; Nogueira, L.; Teixeira, Priscila Camillo; Ramasawmy, Rajendranath; Drigo, Sandra A.; Goldberg, Anna Carla; Fonseca, Simone Gonçalves; Bilate, Angelina M.; Kalil, Jorge

doi:10.1590/s0074-02762009000900032

Cited by 96 publications

(88 citation statements)

References 73 publications

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“…These cytokines activate Natural Killer (NK) cells, which are important sources for the synthesis of other cytokines, such as IFN-γ and TNF-α, responsible factors for the activation of macrophages and consequent destruction of intra-and extracellular microorganisms [20][21][22]. On the other hand, the production of IL-4 and IL-10 inhibits the activation of macrophages and the differentiation of Th1 cells, inducing differentiation of Th2 cells, more commonly observed in bacterial infections [23,24].…”

Section: Evolution Of Chagas' Disease and The Related Immune Responsementioning

confidence: 99%

Renal Disfunction in Chagas Disease

Miguel¹,

Filho²,

Mendes³

et al. 2017

J Bacteriol Parasitol

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Background: Chagas' disease has a wide distribution in South America, having several forms of transmission. The disease's evolution varies according to the parasite/host relationship, presenting diversified progression through the acute, indeterminate and chronic forms. In the cardiac form, there are several clinical and laboratory alterations due to the involvement of several organs, including the kidneys. Actually, a lot of mechanisms are employed for the control and detection of renal damage. It has been proven that before the cardiac inflammatory changes were established, alterations in renal function could be observed due to elevated levels of urea, creatinine and other alterations compatible with the clinical picture of uremia. As well it was possible to verify an anemic state in laboratory animals, thus, it could be a condition known as cardio-anemic-renal syndrome described in patients with heart failure. Although there are studies correlating clinical and laboratory findings of renal dysfunction in Chagas' disease, there is still a need to elucidate some pathways of interaction between chagasic physiopathogeny and renal function.

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Section: Evolution Of Chagas' Disease and The Related Immune Responsementioning

confidence: 99%

Renal Disfunction in Chagas Disease

Miguel¹,

Filho²,

Mendes³

et al. 2017

J Bacteriol Parasitol

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“…62,63 Moreover, BNP levels represent a strong predictor of the risk of stroke or death in longitudinal studies and might have a role in the clinical evaluation of patients with Chagas cardiomyopathy. 64 Levels of other biomarkers, such as cardiac muscle troponin T and several inflammatory cytokines (tumor necrosis factor and interferon-γ), correlate with the severity of cardiac disease and are candidate biomarkers to be used in clinical practice 65,66 However, in HIV-coinfected patients, biomarkers have not been evaluated. Most probably, these patients present reactivation of chronic infection, so they develop severe clinical manifestations, due to low CD4+ T cell counts.…”

Section: Chagas Diseasementioning

confidence: 99%

Diagnosing Neglected Tropical Diseases in HIV Coinfection

Lindoso

Lima²,

Cunha³

et al. 2015

Human Parasitic Diseases

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“…The acute phase of Chagas' disease is characterized by an exacerbated production of inflammatory cytokines, including IL-12, TNF-α, and IFN-γ, and chemokines such as CCL2, CCL3, CCL4, CCL5, and CXCL10 (72,73). CCL5 and CCL2, which bind to the Duffy antigen, have been singled out from these inflammatory mediators.…”

Section: Darc and Chagas' Diseasementioning

confidence: 99%

“…Clinical data suggest that the inflammatory infiltrate plays an important role in the development and progression of Chagas' disease, as mononuclear infiltrate is associated with greater cardiomyocyte destruction and local fibrosis in CCC (76,77). Development of this myocardiopathy involves three possible pathogenic mechanisms: cardiac dysautonomia, microcirculation changes, and tissue damage resulting from the inflammatory and immune responses (73).…”

Section: Darc and Chagas' Diseasementioning

confidence: 99%

“…An increase in plasmatic TNF-α and IFN-γ levels occurs; this is also observed in patients with the indeterminate form of the disease. Individuals with CCC present high TNF-α and CCL2 levels in the circulation in relation to those with the indeterminate form (73). It is important to point out the inflammatory chemokines whose receptor is DARC; these include CXCL8/IL-8, CCL5/ RANTES, CCL11/eotaxin, and CCL2/MCP-1.…”

Section: Darc and Chagas' Diseasementioning

confidence: 99%

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Chagas' disease and Duffy antigen/receptor for chemokine (DARC): a mini-review

Oliveira¹,

Mattos²,

Cavasini³

2011

J. Venom. Anim. Toxins incl. Trop. Dis

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Duffy gene (FY) codifies the transmembrane glycoprotein Duffy (gp-Fy) of 35 to 43 kDa which is moderately immunogenic. This glycoprotein is polymorphic, and constitutes the antigens of the Duffy histo-blood system which were designated receptors for chemokines and denominated DARC (Duffy antigen/receptor for chemokine). This receptor has an important role in the regulation of chemokine levels in the circulation, as it binds and adsorbs them on the surface of red cells as a reservoir. It plays a "sink" role, which can contribute to homeostasis by removing inflammatory chemokines from circulation as well as maintaining them in plasmatic levels. Chronic Chagas' cardiopathy (CCC) is the most frequent form of the disease. It is an inflammatory disease, in which infiltrated inflammatory cells play an important role in the development and progress of the infection. High chemokine levels in the plasma have been associated with the disease severity in patients with heart failure. In this context, the profile of DARC expression could play an important function as a receptor for chemokines in Chagas' disease, in patients with CCC, as it can modulate damage from this inflammatory disease.Key words: DARC antigen, Duffy blood-group system, Chagas' disease, Chagas' cardiomyopathy. Review ARticle INTRODUCTIONThe Duffy gene (FY) codifies the moderately immunogenic transmembrane glycoprotein Duffy (gp-Fy) of 35 to 43 kDa (1). This glycoprotein is polymorphic, and constitutes the antigens of the Duffy histo-blood system, which are codified by FYA and FYB alleles of the FY gene playing a codominant role. The FYA and FYB alleles differ due to substitution of the base G by another A in the 125 nucleotide, which develops a common polymorphism in the Caucasian population. This single nucleotide polymorphism (SNP) results in the substitution of amino acid glycine by asparagine in position 42 (2).Although this polymorphism originates distinct glycoproteins called Fya and Fyb antigens, both have moderate immunogenicity.They can be identified with the use of antiFya and anti-Fyb anti-sera, allowing the characterization of four erythrocyte phenotypes: Fy(a+b-), Fy(a-b+), Fy(a+b+) and Fy(a-b-) (3, 4). Negative phenotype Duffy [Fy(a-b-)] is the result of a variant FYB allele (FYB-33), which presents a single point mutation where there is a T to C substitution in nucleotide -33 (-33T>C), also known as the GATA-BOX, located in the promoter region of the FY gene (5, 6).The differential distribution of DARC antigenic determinant between ethnic groups is a characteristic of this histo-blood system. As an example, FYA is prevalent in European, Chinese, Japanese, and Malaysian populations, but rarely in African population. And on the other hand, in Caucasians, FYB is widely found compared to Asian and African populations (7, 8 (25)(26)(27)(28). Genetic mechanisms for the Duffy-negative phenotype in erythrocytes have preserved its expression in the endothelium determining an important role in inflammation physiopathology (16, 19).Antigens...

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Immunological and non-immunological effects of cytokines and chemokines in the pathogenesis of chronic Chagas disease cardiomyopathy

Cited by 96 publications

References 73 publications

Renal Disfunction in Chagas Disease

Renal Disfunction in Chagas Disease

Diagnosing Neglected Tropical Diseases in HIV Coinfection

Chagas' disease and Duffy antigen/receptor for chemokine (DARC): a mini-review

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