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Helminth Infections, Type-2 Immune Response, and Metabolic Syndrome
Author(s) -
Aprilianto E. Wiria,
Erliyani Sartono,
Taniawati Supali,
Maria Yazdanbakhsh
Publication year - 2014
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1004140
Subject(s) - immune system , helminths , immunology , biology , helminth infections
Metabolic syndrome (MetS), a disorder of energy utilization andstorage, manifests as a cluster of conditions such as hypertension,dyslipidemia, abdominal obesity, and altered glucose metabolism,which increases the risk of type-2 diabetes (T2D) and cardiovas-cular diseases (CVD). A lifestyle that consists of overeating, high-calorie food intake, and no or irregular physical activity is a riskfactor for developing MetS. Therefore, treatment for MetScomprises regular physical activity, diet modification to reduceweight and/or blood glucose, and the use of lipid-lowering drugs.Recently, evidence is emerging that innate and/or adaptiveinflammatory responses might be associated with MetS [1]. Obesepeople with MetS have higher concentrations of circulatinginflammatory markers [2]. Nevertheless, the incidence of CVDis also found to be higher in patients with inflammatory diseasessuch as asthma [3] or rheumatoid arthritis [4]. It has been shownin vitro that an inflammatory milieu, with pro-inflammatorycytokines and high levels of interleukin (IL) 17 and tumor necrosisfactor (TNF), can lead to the development of a prothrombotic statein human endothelial cells [5]. Several studies have shown thatcontrolling inflammation might be linked to improved MetS. AT2D drug, thiazolidinedione (pioglitazone), can improve insulinsensitivity by activation of peroxisome proliferator-activatedreceptor (PPAR) c, a type-2 nuclear receptor that regulates fatty-acid storage and glucose metabolism [6]. It was noted that theexpression of PPARc in Foxp3+CD4+ regulatory T cells (Treg) invisceral adipose tissue was essential for the restoration ofinsulin sensitivity in obese mice after pioglitazone treatment[6]. In addition, subcutaneous injection of adjuvant-freeapolipoprotein B100-derived peptides, as atherosclerosis-relat-ed antigens, can induce accumulation of atherosclerosis-specific Treg in lymph nodes and prevent development andprogression of atherosclerosis in C57BL/6J apoE

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