Response of Adipose Tissue to Early Infection With Trypanosoma cruzi (Brazil Strain)

Nagajyothi, Fnu; Desruisseaux, Mahalia S.; Machado, Fabiana S.; Upadhya, Rajendra; Zhao, Dazhi; Schwartz, Gary J.; Teixeira, Mauro Martins; Albanese, Chris; Lisanti, Michael P.; Chua, Streamson C.; Weiss, Louis M.; Scherer, Philipp E.; Tanowitz, Herbert B.

doi:10.1093/infdis/jir840

Cited by 67 publications

(98 citation statements)

References 45 publications

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“…The studies of Shoemaker and colleagues in the 1970s suggested preference for BAT in T. cruzi (Tulahuen strain) infected mice [34, 35]. However, we have found that as early as 15 days after infection of mice with T. cruzi (Brazil strain), there is a significant parasite load in both BAT and WAT as compared with other organs such the heart and spleen [36]. Macrophages and parasites are found in adipose tissue in mice chronically infected with T. cruzi , and the parasite persisted for over 300 days [15].…”

Section: Discussionmentioning

confidence: 83%

“…Previously, we have demonstrated both by Western blotting and PCR analyses that T. cruzi infection of mice results in the increased expression of proinflammatory cytokines and chemokines including IL-1β [15, 36]. At both 30 and 90 days of infection there is a greater increase in proinflammatory cytokines and chemokines in BAT than in WAT (Nagajyothi et al, unpublished observations), and thus the observed reduction in Cx43 expression in BAT obtained from T. cruzi -infected mice may be explained in part by the increased expression of pro-inflammatory mediators such as IL-1β.…”

Section: Discussionmentioning

confidence: 99%

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Adipocytes in both brown and white adipose tissue of adult mice are functionally connected via gap junctions: implications for Chagas disease

Burke

Nagajyothi

Thi

et al. 2014

Microbes and Infection

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Adipose tissue serves as a host reservoir for the protozoan Trypanosoma cruzi, the causative organism in Chagas disease. Gap junctions interconnect cells of most tissues, serving to synchronize cell activities including secretion in glandular tissue, and we have previously demonstrated that gap junctions are altered in various tissues and cells infected with T. cruzi. Herein, we examined the gap junction protein connexin 43 (Cx43) expression in infected adipose tissues. Adipose tissue is the largest endocrine organ of the body and is also involved in other physiological functions. In mammals, it is primarily composed of white adipocytes. Although gap junctions are a prominent feature of brown adipocytes, they have not been explored extensively in white adipocytes, especially in the setting of infection. Thus, we examined functional coupling in both white and brown adipocytes in mice. Injection of electrical current or the dye Lucifer Yellow into adipocytes within fat tissue spread to adjacent cells, which was reduced by treatment with agents known to block gap junctions. Moreover, Cx43 was detected in both brown and white fat tissue. At thirty and ninety days post-infection, Cx43 was downregulated in brown adipocytes and upregulated in white adipocytes. Gap junction-mediated intercellular communication likely contributes to hormone secretion and other functions in white adipose tissue and to nonshivering thermogenesis in brown fat, and modulation of the coupling by T. cruzi infection is expected to impact these functions.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Adipocytes in both brown and white adipose tissue of adult mice are functionally connected via gap junctions: implications for Chagas disease

Burke

Nagajyothi

Thi

et al. 2014

Microbes and Infection

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show abstract

“…Comparison among CCHD groups showed that CCHD III cases were older 1 and presented higher proportion of patients with hypertension. 2 The CCHD I group showed lower levels of systolic 3 and diastolic 4 blood pressure, whereas CCHD III showed increased levels of anti-B13 5 and Atherogenic Index. 6 …”

Section: Introductionmentioning

confidence: 94%

“…1 It has been described recently that T. cruzi infection might be a risk factor for high blood pressure 2 and that it might induce cholesterol homeostasis disruption. 3 In this respect, Nagajyothi et al 4,5 have observed in an experimental murine model that T. cruzi infection promotes an important decrease of serum levels of low-density lipoprotein-cholesterol (LDL-c) and triglycerides (TG). On the other hand, even though both hypertension and atherogenic dyslipidemia (AD) are well-known risk factors for coronary artery disease, heart failure and stroke, their influence on the severity of CCHD is not known.…”

Section: Introductionmentioning

confidence: 99%

The potential influence of atherogenic dyslipidemia on the severity of chronic Chagas heart disease

Peverengo

Rodeles

Vicco

et al. 2016

Rev. Assoc. Med. Bras.

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Introduction: chronic Chagas heart disease (CCHD) is the most common manifestation of American Trypanosomiasis, causing about 50,000 deaths annually. Several factors bear correlation with the severity of CCHD. However, to our knowledge, the assessment on the contribution of major cardiovascular risk factors (CRF), such as hypertension and atherogenic dyslipidemia (AD) to CCHD severity is scarce, despite their well-established role in coronary artery disease, heart failure and stroke. Objective: to explore the potential relationship of blood pressure and AD with the clinical profile of patients with CCHD. Methods: we performed a cross-sectional study in T. cruzi seropositive patients categorized according to a standard CCHD classification. All individuals were subjected to complete clinical examination. Autoantibodies induced by T. cruzi were assessed by ELISA. Results: we observed that Atherogenic index (AI) levels rose significantly in relation to the severity of the CCHD stage, with CCHD III cases showing the highest values of AI. Furthermore, those patients with globally dilated cardiomyopathy with reduced ejection fraction showed higher levels of AI. In regard to autoantibodies, anti-B13 also showed relation with the severity of the disease. Conclusion: we observed that AI correlated with CCHD stages and contributed, in association with anti-B13 antibodies and age, to the prediction of systolic heart failure.

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“…Whether the fat tissue plays a role in human Chagas disease progression or in the severity of CCC has not been properly elucidated. There is evidence on the possible contribution of adipose tissue to T. cruzi-induced pathology in mice, but many of them are focused in the acute phase of infection [15][16][17][18][19]. Nevertheless, when considering that the adipose tissue seems to be one of the main reservoirs of T. cruzi during the chronic phase of disease [20], the possibility that a disbalance between certain fat inflamed-derived metabolic factors (like TNF-α, IL-6, leptin and adiponectin) as contributing to cardiomyopathy progression and severity, sounds likely.…”

Section: Introductionmentioning

confidence: 99%

Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy

González

Villar

D’Attilio

et al. 2018

Neuroimmunomodulation

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Individuals who are infected with Trypanosoma cruzi develop chronic Chagas cardiomyopathy (CCC), which is a complication involving a series of immune pathogenetic mechanisms, although an association between immune and metabolic alterations was more recently proposed. Accordingly, we investigated the immuno-metabolic response in chagasic patients and their possible influence on CCC pathogenesis. To this end, T. cruzi-seropositive (asymptomatic or with CCC) and sero-negative individuals were studied. Serum tumour necrosis factor (TNF)-α, interleukin (IL)-6, adipocytokines and the expression of their receptors in peripheral blood mononuclear cell (PBMC) were evaluated, together with other factors influencing the immune response. CCC patients showed major metabolic and hormonal abnormalities, in parallel with increased IL-6 and leptin serum levels. TNF-α receptor s, leptin and adiponectin receptors (ObR and Adipo-Rs respectively), as well as PPAR-γ expression in PBMCs from CCC patients were compatible with a counteracting response leading to an unfavourable immune-metabolic profile. These results suggest that persistently increased levels of immune-metabolic pro-inflammatory mediators along with the adverse endocrine anti-inflammatory response of CCC individuals, may contribute to the underlying mechanisms dealing with myocardial tissue damage.

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Response of Adipose Tissue to Early Infection With Trypanosoma cruzi (Brazil Strain)

Cited by 67 publications

References 45 publications

Adipocytes in both brown and white adipose tissue of adult mice are functionally connected via gap junctions: implications for Chagas disease

Adipocytes in both brown and white adipose tissue of adult mice are functionally connected via gap junctions: implications for Chagas disease

The potential influence of atherogenic dyslipidemia on the severity of chronic Chagas heart disease

Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy

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