RESUMO
The original article was published on July19, 2017 and corrected on May 15, 2018. The revised version of the article includes a funding source for Dr. Maija Kiuru's participation in this case report, awarded by the National Cancer Institute, National Institutes of Health grant K12CA138464. This change appears in the revised online PDF copy of this article.
Assuntos
Acrodermatite/patologia , Deficiências Nutricionais/patologia , Nutrição Parenteral Total/efeitos adversos , Pênfigo/diagnóstico , Dermatopatias Vesiculobolhosas/patologia , Zinco/deficiência , Acrodermatite/diagnóstico , Acrodermatite/etiologia , Idoso , Deficiências Nutricionais/diagnóstico , Deficiências Nutricionais/etiologia , Diagnóstico Diferencial , Feminino , Humanos , Dermatopatias Vesiculobolhosas/diagnóstico , Dermatopatias Vesiculobolhosas/etiologiaRESUMO
Acquired zinc deficiency can develop as a consequence of poor nutritional intake or from dependence on total parenteral nutrition. Acquired zinc deficiency dermatitis classically manifests with erosions and scaly plaques in a periorificial and acral distribution. We present a case of a woman on parenteral nutrition who presented with bullous acrodermatitis mimicking pemphigus foliaceus histopathologically. This case highlights clinical and histopathologic variants of zinc deficiency that may lead to a delay in diagnosis.
Assuntos
Acrodermatite/diagnóstico , Nutrição Parenteral/efeitos adversos , Pênfigo/diagnóstico , Zinco/deficiência , Neoplasias Abdominais/secundário , Acrodermatite/etiologia , Acrodermatite/patologia , Idoso , Diagnóstico Diferencial , Feminino , Humanos , Neoplasias Ovarianas/patologia , Pênfigo/patologiaAssuntos
Antineoplásicos/efeitos adversos , Deleção Cromossômica , Exantema/induzido quimicamente , Leucemia Linfocítica Crônica de Células B/tratamento farmacológico , Pirazóis/efeitos adversos , Pirimidinas/efeitos adversos , Adenina/análogos & derivados , Idoso , Alopurinol/uso terapêutico , Antimetabólitos/uso terapêutico , Antineoplásicos/administração & dosagem , Cromossomos Humanos Par 17 , Exantema/patologia , Humanos , Leucemia Linfocítica Crônica de Células B/patologia , Masculino , Piperidinas , Pirazóis/administração & dosagem , Pirimidinas/administração & dosagem , Síndrome de Smith-MagenisRESUMO
Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.
Assuntos
Tecido Adiposo Branco/imunologia , Tecido Adiposo Branco/metabolismo , Glicemia/metabolismo , Eosinófilos/fisiologia , Ativação de Macrófagos , Macrófagos/imunologia , Macrófagos/metabolismo , Tecido Adiposo , Tecido Adiposo Branco/citologia , Animais , Movimento Celular , Gorduras na Dieta/administração & dosagem , Eosinofilia/imunologia , Eosinófilos/imunologia , Intolerância à Glucose , Homeostase , Insulina/metabolismo , Resistência à Insulina , Interleucina-13/genética , Interleucina-13/metabolismo , Interleucina-4/genética , Interleucina-4/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Knockout , Nippostrongylus , Infecções por Strongylida/imunologia , Infecções por Strongylida/metabolismoRESUMO
Short-chain fatty acids (SCFAs) and dimethyl sulfoxide (DMSO) induce adult erythroid differentiation in murine erythroleukemia (MEL) cells, but only SCFAs concurrently up-regulate expression from the endogenous embryonic globin gene epsilony. The epsilony promoter, linked to a reporter gene and stably transfected into MEL cells, was tested during adult erythroid differentiation. Both the epsilony-CACCC site at -114 bp and enhancer sequences (hypersensitive site 2 [HS2]) from the beta-globin locus control region (LCR) were essential to maximal SCFA-mediated induction of expression from these constructs in MEL cells. Gel-shift analyses of binding activity from SCFA-induced MEL cell nuclear extracts showed in vitro binding by specificity proteins 1 and 3 (SP1, SP3) and basic or erythroid Krüppel-like factors (BKLF, EKLF) at the epsilony-CACCC site. In a functional analysis, transient cotransfections in nonerythroid NIH/3T3 cells of SP1, SP3, BKLF, or EKLF and HS2 epsilony promoter-luciferase constructs, with or without coactivators (p300, CREB-binding protein [CBP], or p300/CBP-associated factor [PCAF]) and SCFAs, were performed. SP1, SP3, and EKLF further increased expression from HS2 epsilony promoter constructs following exposure to SCFAs. This effect was variably augmented by coactivators and was diminished in EKLF mutants that were unable to undergo histone/factor-acetyl transferase (H/FAT)-mediated acetylation. In addition, acetylation of SP1 was detectable in NIH/3T3 cells following exposure to SCFAs. In sum, LCR sequence and an embryonic globin gene promoter CACCC site were essential to that promoter's up-regulation during SCFA-mediated induction of adult erythroid differentiation in vitro. Of factors that interact at the CACCC site, SCFA-mediated acetylation is implicated in SP1 and EKLF, and may be a mechanism through which SCFAs induce embryonic/fetal globin gene promoters during adult erythroid differentiation.