RESUMO
A 31-year-old female daily user of contact lenses sought medical attention, reporting blurred vision and irritation of the left eye. Slit-lamp examination revealed hyperemia and an irregular corneal epithelium surface, and empirical treatment was started. A corneal scrape was obtained and examined for the presence of fungi, bacteria, and Acanthamoeba spp. The results of the microbial culture revealed growth of Acanthamoeba spp. and Candida albicans. The Acanthamoeba isolate was characterized by cyst morphology as belonging to group II according to Pussard and Pons. Sequencing of the diagnostic fragment 3 (DF3) region located on the 18S ribosomal DNA identified the isolate as genotype T4. The patient was treated with chlorhexidine 0.02% and polyhexamethylene biguanide (PHMB) 0.02% drops for 5 months until the infection resolved. Lately, rare cases of polymicrobial keratitis associated with Acanthamoeba and Candida albicans have been reported. Cases of co-infection are more difficult to treat, since the specific treatment depends on precise identification of the agents involved.
Assuntos
Ceratite por Acanthamoeba/diagnóstico , Acanthamoeba/isolamento & purificação , Candida albicans/isolamento & purificação , Candidíase/diagnóstico , Córnea/patologia , Córnea/parasitologia , Acanthamoeba/genética , Ceratite por Acanthamoeba/tratamento farmacológico , Ceratite por Acanthamoeba/parasitologia , Adulto , Biguanidas/uso terapêutico , Candidíase/tratamento farmacológico , Clorexidina/uso terapêutico , Lentes de Contato , DNA Ribossômico/genética , Feminino , Genótipo , Humanos , RNA Ribossômico 18S/genéticaRESUMO
Considerando que a SAA é uma proteína de fase aguda e que uma concentração elevada desta proteína é observada em pacientes obesos e com resistência à insulina, estimulou-se pré-adipócitos murinos 3T3-L1 a baixas concentrações de rSAA durante o processo de proliferação e diferenciação. Ensaios de incorporação de [metil-3H]-timidina, ciclo e viabilidade celular por citometria de fluxo foram realizados, assim como genes adipogênicos foram determinados durante a fase de diferenciação. Ainda, investigou-se a participação da rSAA metabolismo da glicose, bem como a expressão do seu receptor GLUT4 e os perfis de lipólise. Como resultados, obteve-se que a rSAA causou um aumento na proliferação celular assim como na porcentagem de células na fase S. Este efeito foi dose dependente e mediado via sinalização da ERK1/2. Ainda, rSAA inibiu a diferenciação por meio da diminuição da expressão de fatores transcrição (PPARγ, C/EBPß e C/EBPα) e proteínas adipogênicas (FABP4 e perilipina). Em relação à captação de 2-desoxi-[1,2-3H]-D-glicose, a rSAA preveniu este processo, corroborando com os resultados de expressão diminuída receptor GLUT4. Ainda, o aumento da lipólise provocada pela rSAA, favorece resistência à insulina no modelo estudado. Portanto, conclui-se que a SAA aumenta a proliferação mas inibe a diferenciação de células 3T3-L1 sugerindo papel importante desta proteína no processo de adipogênese
Considering that SAA is an acute phase protein and increased serum levels are associated with chronic hyperglycemia, insulin resistance and obesity, we first examined the possibility that rSAA could affect proliferation and differentiation 3T3-L1 preadipocytes. 3T3-L1 adipocytes were treated with recombinant human SAA and [methyl-3H]-thymidine incorporation, flow cytometric analysis of cell cycle and viability were performed. Also, gene expression profiles of adipogenic factor were performed during differentiation protocol as well as glucose uptake, GLUT4 gene expression and lipolysis assay. rSAA caused an increment in cell proliferation consisted with FACS analysis with a percentage of cells in the S phase. Cell proliferation was mediated by ERK1/2 signaling pathway and in dose-dependent manner. Also, SAA inhibited differentiation process by decreasing adipogenic genes PPARγ, C/EBPß, C/EBPα, and proteins FABP4, and perilipin expression. Also, rSAA prevented 2-deoxy-[1,2-3H]-glucose uptake and GLUT4 expression. In addiction, lipolysis was increased favoring insulin resistance in 3T3L1 adipogenic model. In conclusion, it was demonstrated that rSAA enhances proliferation but prevents differentiation in 3T3-L1 adipocytes, supporting a even more complex participation, than previously expected, of inflammatory proteins the adipogenic process