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1.
J Gastroenterol Hepatol ; 32(11): 1832-1838, 2017 Nov.
Article in English | MEDLINE | ID: mdl-28387430

ABSTRACT

BACKGROUND AND AIM: Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection. METHODS: Immunohistochemistry to CD4+ and CD8+ T-cells, γ-interferon, transforming growth factor-ß, interleukin (IL)-4, IL-6, IL-13, and IL-17 was performed in esophageal samples of 40 chronically HIV+ patients under highly active antiretroviral therapy (16 with Candida esophagitis, 12 virologically non-supressed with blood CD4 count < 500, and 12 virologically suppressed with blood CD4 count > 500; the latter two groups without esophageal candidiasis). The controls were 12 HIV-negative healthy individuals. RESULTS: Esophageal CD4+ T-cell expression in HIV+ patients did not differ from the control group (P = 0.50). Mucosal CD8+ T-cell expression was significantly increased in HIV+ patients (P = 0.0018). Candida esophagitis and virologically non-supressed HIV+ patients with CD4 < 500 showed an increased expression of IL-17 and IL-6 with fewer expressions of γ-interferon, more attenuated in the latter group. Transforming growth factor-ß was increased only in virologically suppressed HIV+ patients with CD4 > 500. IL-4 and IL-13 were similar to the control group. CONCLUSION: In contrast to CD8+ T-cell expression, esophageal CD4+ T-cell expression does not reflect the HIV+ patient's immunological status. T-helper 17 (Th17) response seems to play a role in the esophageal mucosa of virologically non-supressed HIV+ patients with blood CD4 < 500. Candida esophagitis showed a Th1/Th17 response but seems to be dominantly regulated by the Th17 pathway.


Subject(s)
Candidiasis/complications , Esophageal Mucosa/immunology , Esophagitis/microbiology , HIV Infections/complications , Opportunistic Infections/complications , Adult , CD4-Positive T-Lymphocytes , CD8-Positive T-Lymphocytes , Candidiasis/immunology , Esophagitis/immunology , Female , HIV Infections/immunology , Humans , Interleukin-17 , Interleukin-6 , Male , Middle Aged , Opportunistic Infections/immunology , Transforming Growth Factor beta
2.
JOP ; 15(3): 237-42, 2014 May 27.
Article in English | MEDLINE | ID: mdl-24865534

ABSTRACT

CONTEXT: Several mechanisms are involved in the development of the local and systemic response in acute pancreatitis. Cardiovascular system may be affected throughout the clinical course of acute pancreatitis. The aim was to evaluate local myocardial cytokine production, as well as, functional and histological myocardial alterations in severe acute pancreatitis. METHODS: The animals were divided into three groups: Group 1: control; Group 2: sham; Group 3: severe acute pancreatitis. Echocardiographic assessment of cardiac function, serum levels of amylase and cytokines (TNF-α, IL-6 and IL-10), and mRNA expression of TNF-α, IL-6 and TGF-ß were measured. Myocardial tissue alterations were analysed by histological examination. RESULTS: The serum TNF-α and IL-10 levels were significant higher in AP 2h group. The mRNA IL-6 levels from group AP 2h were statistically higher. The mRNA TNF-α level from sham group and AP 2h were statistically lower. Significant changes in the left ventricular diameter were found in AP 2h and AP 12h groups. There were statistical changes for vacuolar degeneration, picnosis and loss of nucleus, and lymphocytes. CONCLUSION: We found cardiac and histological changes compatible with the inflammatory process triggered by SAP with the promotion of local myocardial cytokine production.


Subject(s)
Cytokines/immunology , Heart Diseases/immunology , Myocardium/immunology , Pancreatitis/immunology , Acute Disease , Amylases/blood , Animals , Biopsy , Cytokines/genetics , Cytokines/metabolism , Echocardiography , Heart Diseases/metabolism , Heart Diseases/pathology , Heart Function Tests , Inflammation Mediators/blood , Interleukin-10/genetics , Interleukin-10/immunology , Interleukin-10/metabolism , Interleukin-6/genetics , Interleukin-6/immunology , Interleukin-6/metabolism , Male , Myocardium/metabolism , Pancreatitis/metabolism , Pancreatitis/pathology , RNA, Messenger/metabolism , Rats, Wistar , Severity of Illness Index , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/immunology , Tumor Necrosis Factor-alpha/metabolism
3.
J Heart Lung Transplant ; 26(11): 1091-6, 2007 Nov.
Article in English | MEDLINE | ID: mdl-18022073

ABSTRACT

BACKGROUND: Chagas' disease is endemic in many Latin American countries. In the last decades, millions of people from these countries have migrated to the United States, changing the scenario of acute Chagas' disease associated with blood transfusion in North America. METHODS AND RESULTS: We report the case of a chagasic patient who developed intracranial hypertension and focal neurologic signs 7 months after heart transplantation. Immunosuppression after transplantation was achieved with prednisone, cyclosporine A, and mycophenolate mofetil. Cranial magnetic resonance imaging revealed a right temporoparietal mass lesion with surrounding edema. Trypanosoma cruzi was observed in the cerebrospinal fluid by Giemsa method, and autopsy disclosed a cerebral chagoma with amastigote forms of T cruzi, with neither associated myocarditis nor systemic infection. CONCLUSION: In chagasic patients who undergo heart transplantation and immunosuppression, the risk of late reactivation of Chagas' disease by means of an isolated cerebral mass lesion must be considered.


Subject(s)
Chagas Cardiomyopathy/surgery , Chagas Disease/complications , Chagas Disease/diagnosis , Encephalitis/diagnosis , Encephalitis/etiology , Heart Transplantation/adverse effects , Animals , Brain/parasitology , Brain/pathology , Humans , Immunosuppression Therapy/methods , Magnetic Resonance Imaging , Male , Middle Aged , Recurrence , Trypanosoma cruzi/pathogenicity
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