Adipose tissue is composed mainly by adipocytes and stromal-vascular fraction, which are composed by different cell types including macrophages. There are three types of adipose tissue: brown (BrAT), white (WAT), and beige (BeAT). BrAT is less abundant and is implicated in lipid oxidation and energy balance; BeAT has the pathway of adaptive thermogenesis, and WAT is endocrine in nature and lipid storage site and is implicated as an endocrine organ that secretes hormones and different molecules. These molecules are pro-inflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, adiponectin, and others, are involved with the development of adipose tissue inflammation and obesity. This pathological condition, together with other factors such as oxidative stress, may develop insulin resistance and the pathogenesis of type 2 diabetes mellitus (T2DM).

Entamoeba histolytica invades the intestine and other organs during the pathogenesis of amoebiasis. In the early stages, the host organism responds with an inflammatory infiltrate composed mostly of neutrophils. It has been reported that these immune cells, activated by E. histolytica, exert a protective role by releasing proteolytic enzymes and generating reactive oxygen/nitrogen species (ROS/RNS) and antimicrobial peptides. It is now known that neutrophils also produce neutrophil extracellular traps (NETs), which are able to damage and kill pathogens. Studies have shown that intracellular protozoan pathogens, including Toxoplasma gondi, Plasmodium falciparum and Leishmania spp, induce neutrophils to release NETs and are damaged by them. However, the action of this mechanism has not been explored in relation to E. histolytica trophozoites. Through scanning electron, epifluorescence microscopy and viability assays, we show for first time that during in vitro interaction with E. histolytica trophozoites, human neutrophils released NETs that covered amoebas and reduced amoebic viability. These NETs presented histones, myeloperoxidase and decondensed chromatin. The results suggest that NETs participate in the elimination of the parasite.

Liver fibrosis occurs in the presence of continuous insults, including toxic or biological agents. Novel treatments must focus on ceasing the progression of cellular damage, promoting the regeneration of the parenchyma and inhibition of the fibrotic process. The present study analyzed the effect of bone morphogenetic protein (BMP)-7 gene therapy with or without co-treatment with doxazosin in a model of liver cirrhosis in hamsters. The serum alanine aminotransferase, aspartate aminotransferase and albumin levels were analyzed spectrophotometrically. Tissue hepatic samples were analyzed by hematoxylin and eosin for parenchymal structure and Sirius red for collagen fiber content. BMP-7 and α-smooth muscle actin (SMA)-positive cells were detected by immunohistochemistry. BMP-7 and collagen type I content in hepatic tissue were analyzed by western blotting, and tissue inhibitor of metalloproteinases (TIMP)-2 and matrix metalloproteinase (MMP)-13 expression levels were detected by reverse transcription-quantitative polymerase chain reaction. The present study detected a significant reduction of collagen type I deposits in the group treated with adenoviral-transduction with BMP-7 and doxazosin. In animals with BMP-7 and doxazosin therapy, α-SMA-positive cells were 31.7 and 29% significantly decreased compared with animals with placebo, respectively. Adenoviral-BMP-7 transduction and/or doxazosin treatments actively induced decrement in type I collagen deposition via increased MMP-13 and reduced TIMP-2 expression. In conclusion, the adenovirus-BMP-7 gene therapy and the doxazosin therapy are potential candidates for the diminution of fibrosis in the liver, although combination of both therapies does not improve the individual anti-fibrotic effect once cirrhosis is established.

Educational programs are a fundamental part of the global efforts to increase PID diagnosis and care. To be successful, such programs should include public relations, reach for first-contact physicians, and aim to develop an efficient referral network with molecular diagnostic capability. Enhancing medical knowledge on PID is a successful strategy to improve early diagnosis and treatment.

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