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Now showing 1 - 8 of 8
  • Publication
    PPBP and DEFA1/DEFA3 genes in hyperlipidaemia as feasible synergistic inflammatory biomarkers for coronary heart disease
    (2017-04-19) Yaowapa Maneerat; Kriengchai Prasongsukarn; Surachet Benjathummarak; Wilanee Dechkhajorn; Mahidol University; Phramongkutklao College of Medicine
    blood mononuclear cells using DNA microarrays. Eight selected genes expressed only in H and CHD groups were validated by real-time quantitative reverse transcription PCR and plasma protein determination. Results: α-defensin (DEFA1/DEFA3), pro-platelet
  • Publication
    Roles of partially purified antigens from gnathostoma spinigerum larvae on antibody production by human b cell culture
    (2011-07-01) Kasem Somthana; Yuki Eshita; Ratchanok Kumsisri; Paron Dekumyoy; Jitra Waikagul; Thareerat Kalambaheti; Yaowapa Maneerat; Mahidol University; Oita University; Rangsit University
    filtration chromatography, could be used for serodiagnosis. Using DNA microarray analysis, significant gene expression related to immunoreactivity was examined in peripheral blood mononuclear cells (PBMC) cocultured with Gnath Ag. Antigenicity
  • Publication
    Increased alpha-defensin expression is associated with risk of coronary heart disease: A feasible predictive inflammatory biomarker of coronary heart disease in hyperlipidemia patients
    (2016-07-18) Yaowapa Maneerat; Kriengchai Prasongsukarn; Surachet Benjathummarak; Wilanee Dechkhajorn; Urai Chaisri; Mahidol University; Pramongkutklao Hospital
    and the development of CHD, and whether it was a useful predictive indicator for CHD risk. Methods: First, DNA microarray analysis was performed on peripheral blood mononuclear cells (PBMCs) from Thai control, hyperlipidemia and CHD male patients (n = 7). Gene
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    PublicationOpen Access
    Increased alpha-defensin expression is associated with risk of coronary heart disease: a feasible predictive inflammatory biomarker of coronary heart disease in hyperlipidemia patients
    (2016) Yaowapa Maneerat; Kriengchai Prasongsukarn; Surachet Benjathummarak; Wilanee Dechkhajorn; Urai Chaisri; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
    and the development of CHD, and whether it was a useful predictive indicator for CHD risk. Methods: First, DNA microarray analysis was performed on peripheral blood mononuclear cells (PBMCs) from Thai control, hyperlipidemia and CHD male patients (n = 7). Gene
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    PublicationOpen Access
    PPBP and DEFA1/DEFA3 genes in hyperlipidaemia as feasible synergistic inflammatory biomarkers for coronary heart disease.
    (2017) Yaowapa Maneerat; Kriengchai Prasongsukarn; Surachet Benjathummarak; Wilanee Dechkhajorn; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology; Mahidol University. Faculty of Tropical Medicine. Center of Excellence for Antibody Research; Pramongkutklao Hospital and College of Medicine
    cells using DNA microarrays. Eight selected genes expressed only in H and CHD groups were validated by real-time quantitative reverse transcription PCR and plasma protein determination. Results: α-defensin (DEFA1/DEFA3), pro-platelet basic protein
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    PublicationOpen Access
    Third-stage Gnathostoma spinigerum larva excretory secretory antigens modulate function of Fc gamma receptor I-mediated monocytes in peripheral blood mononuclear cell culture
    (2016) Surachet Benjathummarak; Ratchanok Kumsiri; Supaporn Nuamtanong; Thareerat Kalambaheti; Jitra Waikagul; Nareerat Viseshakul; Yaowapa Maneerat; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
    Background: Third (infective)-stage Gnathostoma spinigerum larvae (L3) mainly cause human gnathostomiasis. G. spinigerum L3 migrate throughout the subcutaneous tissues, vital organs, and central nervous system and can cause various pathogenesis including sudden death. Interestingly, G. spinigerum L3 can survive and evade host cellular immunity for months or years. The effects of G. spinigerum excretory-secretory (ES) products involved in larval migration and immune-evasive strategies are unknown. Monocytes are innate immune cells that act as phagocytic and antigenpresenting cells and also play roles against helminthic infections via a complex interplay between other immune cells. Fc gamma receptor I (FcγRI) is a high-affinity receptor that is particularly expressed on monocytes, macrophages, and dendritic cells. The cross-linking of FcγRI and antigen-antibody complex initiates signal transduction cascades in phagocytosis, cytokine production, and antibody-dependent cell-mediated cytotoxicity (ADCC). This study investigated whether ES antigen (ESA) from G. spinigerum L3 affects monocyte functions. Results: Cultures of normal peripheral blood mononuclear cells (PBMC) separated from healthy buffy coats were used as a human immune cell model. ESA was prepared from G. spinigerum L3 culture. Using Real-Time quantitative reverse transcription-polymerase chain reaction (qRT-PCR), the effect of ESA to down-regulate FcγRI mRNA expression in monocytes during 90 min of observation was not well delineated. Flow cytometry analysis revealed a significant phenotypic-decreased FcγRI expression on the monocyte surface at 12 hours (h) of cultivation with the ESA (p = 0.033). Significantly reduced monocyte-mediated phagocytosis capacity was consistently observed after 12 h of ESA pretreatment (p = 0.001). Conclusions: Our results suggest that G. spinigerum ESA modulates monocyte function via depletion of FcγRI expression. This study provides preliminary information for future in-depth studies to elucidate mechanisms of the immune-evasive strategy of G. spinigerum larvae.
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    PublicationOpen Access
    Phenotypic alterations in human saphenous vein culture induced by tumor necrosis factor-alpha and lipoproteins: a preliminary development of an initial atherosclerotic plaque model
    (2013) Kriengchai Prasongsukarn; Urai Chaisri; Peenutchanee Chartburus; Kamolwan Wetchabut; Surachet Benjathummarak; Vasant Khachansaksumet; Yaowapa Maneerat; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
    Background: Atherosclerosis is a chronic progressive inflammatory disease of blood vessels particularly the arteries. The development of atherosclerotic plaques or atherogenesis is a complex process that is influenced by cardiovascular risk factors such as vascular inflammation and dyslipidemia. This study demonstrates the ability of tumor necrosis factor-alpha (TNF-α) and low density lipoproteins (LDL) to induce atherosclerotic plaque in human saphenous vein (HSV) organ culture. Methods: Normal HSV segments, from male patients who had coronary bypass graft, were cultured in DMEM containing 5% heat inactivated fetal bovine serum. TNF-α (5 ng/ml) was applied in combination with native LDL (nLDL) or oxidized LDL (oxLDL) at the dose of 50 μg/ml for 14 days. The phenotypic changes of the organ cultures characteristic of initial atherosclerotic plaques were evaluated. The effect of anti-atherogenic agent, 17-β estradiol (E2), was also determined. Results: Histologic, histomorphometric, and immunohistochemical examinations revealed that HSV rings stimulated with TNF-α + nLDL or TNF-α + oxLDL can exhibit the essential morphological features of atherogenesis, including fibrous cap formation, cholesterol clefts, evident thickening of the intimal layer, increased proliferation of smooth muscle cells (SMC) and migration to the subendothelial layer, significant SMC foam cell formation, and increased expression of adhesion molecules in the vascular wall. Addition of E2 (50 nM) to the culture significantly modulated the critical changes. Consistently, mRNA profiling of the HSV model revealed that 50 of 84 genes of atherosclerosis were up-regulated. Conclusions: Phenotypic changes characteristic of the initial development of atherosclerotic plaques can be induced in HSV organ culture.
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    PublicationOpen Access
    Activation of nuclear factor kappa B in peripheral blood mononuclear cells from malaria patients
    (2012-06-10) Chuchard Punsawad; ชูชาติ พันธ์สวัสดิ์; Srivicha Krudsood; ศรีวิชา ครุฑสูตร; Yaowapa Maneerat; เยาวพา มณีรัตน์; Urai Chaisri; อุไร ไชยศรี; Noppadon Tangpukdee; นพดล ตั้งภักดี; Emsri Pongponratn; เอี่ยมศรี พงศ์พนรัตน์; Kwannan Nantavisai; Rachanee Udomsangpetch; รัชนีย์ อุดมแสงเพ็ชร; Parnpen Viriyavejakul; พรรณเพ็ญ วิริยเวชกุล; Parnpen Viriyavejakul; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology; Mahidol University. Faculty of Tropical Medicine. Department of Tropical Hygiene; Mahidol University. Faculty of Tropical Medicine. Department of Clinical Tropical Medicine; Mahidol University. Faculty of Science. Department of Pathobiology.
    BACKGROUND: Malaria parasites and their products can activate a specific immune response by stimulating cytokine production in the host's immune cells. Transcription nuclear factor kappa B (NF-κB) is an important regulator for the control of many pro-inflammatory genes, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). The activation and expression of NF-κB p65 in peripheral blood mononuclear cells (PBMCs) of malaria patients were investigated and correlated with the levels of IL-10 and TNF to study the nature of NF-κB p65 and its linkage to inflammatory cytokines. METHODS: The sample group comprised 33 patients admitted with malaria caused by Plasmodium vivax (n = 11), uncomplicated Plasmodium falciparum (n = 11), and complicated Plasmodium falciparum (n = 11). Peripheral blood was collected at admission and on day 7 for PBMC isolation. Healthy subjects were used as a control group. The expressions of NF-κB p65 in the PBMCs from malaria patients and the plasma levels of IL-10 and TNF were measured by using enzyme-linked immunosorbent assay (ELISA). The immunofluorescence technique was used to determine NF-κB nuclear translocation. RESULTS: At admission, patients with P. vivax and uncomplicated P. falciparum had significantly elevated phospho-NF-κB p65 levels in the PBMCs compared with those of healthy controls. However, patients with complicated P. falciparum malaria had decreased levels of phospho-NF-κB p65. On day 7 post-treatment, significantly increased phospho-NF-κB p65 was found in the PBMCs of patients with complicated P. falciparum, compared with healthy controls. The plasma level of IL-10 was elevated in day 0 in patients with complicated P. falciparum malaria and was found to be negatively correlated with phospho-NF-κB p65 level (rs = -0.630, p = 0.038). However, there was no correlation between phospho-NF-κB p65 expression and TNF level in patients with complicated P. falciparum malaria. CONCLUSIONS: This is the first report demonstrating alterations in NF-κB p65 activity in the PBMCs of malaria patients. The altered lower features of NF-κB p65 in the PBMCs of patients with complicated P. falciparum at admission could be due to a suppressive effect of high IL-10 associated with complicated P. falciparum malaria.