Background The parasite Entamoeba histolytica is the causal agent of amoebiasis, a worldwide emerging disease. Amebic brain abscess is a form of invasive amebiasis that is both rare and frequently lethal. This condition always begins with the infection of the colon by E. histolytica trophozoites, which subsequently travel through the bloodstream to extraintestinal tissues. Case presentation We report a case of a 71-year-old female who reported an altered state of consciousness, disorientation, sleepiness and memory loss. She had no history of hepatic or intestinal amoebiasis. A preliminary diagnosis of colloidal vesicular phase neurocysticercosis was made based on nuclear magnetic resonance imaging (NMRI). A postsurgery immunofluorescence study was positive for the 140 kDa fibronectin receptor of E. histolytica, although a serum analysis by ELISA was negative for IgG antibodies against this parasite. A specific E. histolytica 128 bp rRNA gene was identified by PCR in biopsy tissue. The final diagnosis was cerebral amoebiasis. The patient underwent neurosurgery to eliminate amoebic abscesses and was then given a regimen of metronidazole, ceftriaxone and dexamethasone for 4 weeks after the neurosurgery. However, a rapid decline in her condition led to death. Conclusions The present case of an individual with a rare form of cerebral amoebiasis highlights the importance of performing immunofluorescence, NMRI and PCR if a patient has brain abscess and a poorly defined diagnosis. Moreover, the administration of corticosteroids to such patients can often lead to a rapid decline in their condition.

No abstract

Entamoeba histolytica is an invasive enteric protozoan, whose infections are associated to high morbidity and mortality rates. However, only less than 10% of infected patients develop invasive amebiasis. The ability of E. histolytica to adapt to the intestinal microenvironment could be determinant in triggering pathogenic behavior. Indeed, during chronic inflammation, the vagus nerve limits the immune response through the anti-inflammatory reflex, which includes acetylcholine (ACh) as one of the predominant neurotransmitters at the infection site. Consequently, the response of E. histolytica trophozoites to ACh could be implicated in the establishment of invasive disease. The aim of this study was to evaluate the effect of ACh on E. histolytica virulence. Methods include binding detection of ACh to plasma membrane, quantification of the relative expression of virulence factors by RT-PCR and western blot, evaluation of the effect of ACh in different cellular processes related to E. histolytica pathogenesis, and assessment of the capability of E. histolytica to migrate and form hepatic abscesses in hamsters. Results demonstrated that E. histolytica trophozoites bind ACh on their membrane and show a clear increase of the expression of virulence factors, that were upregulated upon stimulation with the neurotransmitter. ACh treatment increased the expression of L220, Gal/GalNAc lectin heavy subunit (170 kDa), amebapore C, cysteine proteinase 2 (ehcp-a2), and cysteine proteinase 5 (ehcp-a5). Moreover, erythrophagocytosis, cytotoxicity, and actin cytoskeleton remodeling were augmented after ACh treatment. Likewise, by assessing the formation of amebic liver abscess, we found that stimulated trophozoites to develop greater hamster hepatic lesions with multiple granulomas. In conclusion, ACh enhanced parasite pathogenicity by upregulating diverse virulence factors, thereby contributing to disease severity, and could be linked to the establishment of invasive amebiasis.

Entamoeba histolytica is an intestinal parasite that causes dysentery and amebic liver abscess. E. histolytica has the capability to invade host tissue by union of virulence factor Gal/GalNAc lectin; this molecule induces an adherence-inhibitory antibody response as well as to protect against amebic liver abscess (ALA). The present work showed the effect of the immunization with PEΔIII-LC3-KDEL3 recombinant protein. In vitro, this candidate vaccine inhibited adherence of E. histolytica trophozoites to HepG2 cell monolayer, avoiding the cytolysis, and in a hamster model, we observed a vaccine-induced protection against the damage to tissue liver and the inhibition of uncontrolled inflammation. PEΔIII-LC3-KDEL3 reduced the expression of TNF-α, IL-1β, and NF-κB in all immunized groups at 4- and 7-day postinfection. The levels of IL-10, FOXP3, and IFN-γ were elevated at 7 days. The immunohistochemistry assay confirmed this result, revealing an elevated quantity of +IFN-γ cells in the liver tissue. ALA formation in hamsters immunized was minimal, and few trophozoites were identified. Hence, immunization with PEΔIII-LC3-KDEL3 herein prevented invasive amebiasis, avoided an acute proinflammatory response, and activated a protective response within a short time. Finally, this recombinant protein induced an increase of serum IgG.

Background: The α and β adrenoblockers have been tested as an alternative treatment for chronic liver lesions such as fibrosis and cirrhosis in animal models, as well as their possible participation during the regeneration of the damage caused by liver cirrhosis in a hamster model. However, it was observed that doxazosin caused slight morphological changes in hepatocytes, while that curcumin showed protection to the hepatic parenchyma. Regardless, the pharmacokinetic effects of these 𝛼/𝛽 adrenoblockers on the hepatocytes' cell viability, possibly involved in the hepatic parenchyma's repopulation during cirrhosis reversal, are unknown. The present study aimed to elucidate the protective effect of curcumin on the possible side effects of doxazosin, tamsulosin, and carvedilol on the HepG2 cell line, drugs already tested with antifibrotic activity.Methods: HepG2 cells were exposed to 0.1, 0.5, 10, and 25 µM of doxazosin, carvedilol, and tamsulosin for 24, 48, and 72 h, for curcumin, cells were pretreated with 1 µM for 1 h before exposure to α and β adrenoblockers. The cell viability was assessed by MTT assay. The morphological changes were determined using hematoxylin and eosin (H&E) staining, scanning electron microscope (SEM), and acridine orange (AO) staining. Results: We observed that the doxazosin decreases cell viability dependently time and dose; carvedilol and tamsulosin increase cell proliferation. However, curcumin induces regulation of these effects in HepG2 cell line, increasing or maintaining viability compared to control. The pretreatment with curcumin regulated AST levels (aspartate aminotransferase) and ALT (alanine aminotransferase) in cells exposed to α and β adrenoblockers. The SEM and H&E staining provided evidence that doxazosin, carvedilol, and tamsulosin induced morphological changes in HepG2 cell line, depending on time and dose, approximately 80% of the cells treated with drugs were balonized, and curcumin protected these effects, maintaining the morphology in 90% of the treated cells.Conclusions: The present study demonstrates that curcumin protected the HepG2 cells against cytotoxicity and morphological changes induced by the α and β adrenoblockers attenuating secondary effects for possible oxidative stress. In this way, it is concluded that these treatments with antifibrotic effect, in co-treatment with curcumin, will not affect the possible repopulation process of the liver parenchyma during the reversion of fibrosis.