Amoebae of the genus Acanthamoeba are etiological agents of granulomatous amoebic encephalitis (GAE). Recently, through an in vivo GAE model, Acanthamoeba trophozoites were immunolocalized in contact with the peripheral nervous system (PNS) cells—Schwann cells (SC). In this study, we analyzed in greater detail the in vitro early morphological events (1, 2, 3, and 4 h) during the interaction of A. culbertsoni trophozoites (ATCC 30171) with SC from Rattus norvegicus (ATCC CRL-2941). Samples were processed for scanning and transmission electron microscopy as well as confocal microscopy. After 1 h of interaction, amoebae were observed to be adhered to the SC cultures, emitting sucker-like structures associated with micro-phagocytic channels. In addition, evidence of necrosis was identified since edematous organelles as well as multivesicular and multilamellar bodies characteristics of autophagy were detected. At 2 h, trophozoites migrated beneath the SC culture in which necrosis and autophagy persisted. By 3 and 4 h, extensive lytic zones were observed. SC necrosis was confirmed by confocal microscopy. We reported for the first time the induction of autophagic and necrotic processes in PNS cells, associated in part with the contact-dependent pathogenic mechanisms of A. culbertsoni trophozoites.

Skin infections have been associated with Acanthamoeba, nevertheless the events during skin invasion and UV-B light effects on it are unknown. The early morphological events of Acanthamoeba castellanii skin invasion are shown in SKH-1 mice that were chronically UV-B light irradiated. Mice that developed skin lesions (group 1) were topical and intradermally inoculated with A. castellanii trophozoites and sacrificed 48 h or 18 days later. Mice that showed no skin lesions (group 2) were intradermally inoculated and sacrificed 24, 48 or 72 h later. Mice ventral areas were considered controls with and without trophozoites intradermally inoculated. Skin samples were processed by histological and immunohistochemistry techniques. In group 1, trophozoites were immunolocalized in dermal areas, hair cysts, sebaceous glands, and blood vessels, and collagen degradation was observed. One of these mice shown trophozoites in the spleen, liver, and brain. In group 2, few trophozoites nearby collagenolytic activity zones were observed. In control samples, nor histological damage and no trophozoites were observed. Adherence and collagenolytic activity by A. castellanii were corroborated in vitro. We can infer that UV-B light irradiated skin could favor A. castellanii invasiveness causing damage in sites as far away as the brain, confirming the invasive capacity and pathogenic potential of these amphizoic amoebae.

: In traditional Mexican medicine, Solanum melongena is used to treat obesity, diabetes mellitus, hypertension, asthma, bronchitis, arthritis, and hypercholesterolemia. This study examined the effect of treatment with ethanolic extract (EE) from the fruit of S. melongena on kidney damage on metabolic syndrome (MS). Male Wistar rats were maintained for 12 weeks on a diet of 20% fructose in drinking water and chow to develop MS. After administering EE of S. melongena (100 and 200 mg/kg/day, orally) for 6 weeks, the histological study of the kidney cortex and determination by Western blot of the renal expression of angiotensin II AT1 receptor and cytokine transforming growth factor beta 1 (TGF-β1) were realized. The rats fed with high fructose developed MS and showed kidney damage characterized by proliferative glomerulonephritis and necrosis; this damage was reduced by S. melongena treatment and associated with decreased expression of AT1 receptor for angiotensin II and cytokine TGF-β1, controlling renal damage in this animal model. In rats affected by MS through high fructose feeding, the treatment with EE of S. melongena showed a renoprotective effect through decreased expression of AT1 receptor for angiotensin II and cytokine TGF-β1, causes of glomerulonephritis.