RESUMEN
BACKGROUND: Neonatal sepsis is characterized by an excessive inflammatory response induced by immune cells (monocytes). We investigated the initial stage of monocyte-pathogen interaction, i.e. bacterial ingestion and degradation at the single-cell level, by comparing a new flow cytometric procedure with culture methods. We also examined the hypothesis that, in terms of phagocytosis-induced cell death (PICD), phenotype, or cytokine production, cord blood monocytes (CBMO) differ from monocytes derived from adults (peripheral blood monocytes, PBMO). METHODS: Phagocytosis and intracellular degradation were assessed by means of flow cytometry and bacterial cultures of green fluorescent protein-labeled group B Streptococci (GBS) and Escherichia coli. The production of reactive oxygen species (ROS) was measured through luminol-enhanced chemiluminescence. Apoptosis, phenotype, and cytokine production were assessed through flow cytometry. RESULTS: Flow cytometry and bacterial cultures showed no difference between phagocytosis and degradation of GBS and E. coli by PBMO and CBMO. A high correlation between both methods was observed. No difference in ROS production was evident. In comparison with PBMO, CBMO apoptosis was lower after exposure to GBS and E. coli. Similarities were found between nonapoptotic monocytes and pro-inflammatory monocytes. CONCLUSIONS: PICD is lower in CBMO during the early stages of monocyte-pathogen interaction. Our results emphasize that monocyte apoptosis has a potential role in tailoring the immune response in neonatal sepsis.
Asunto(s)
Infecciones por Escherichia coli/inmunología , Sangre Fetal/inmunología , Monocitos/inmunología , Fagocitosis/inmunología , Fagocitosis/fisiología , Infecciones Estreptocócicas/inmunología , Adulto , Células Cultivadas , Ensayo de Unidades Formadoras de Colonias , Escherichia coli/genética , Escherichia coli/inmunología , Escherichia coli/metabolismo , Infecciones por Escherichia coli/genética , Infecciones por Escherichia coli/patología , Sangre Fetal/citología , Proteínas Fluorescentes Verdes/genética , Proteínas Fluorescentes Verdes/metabolismo , Humanos , Recién Nacido , Viabilidad Microbiana , Monocitos/patología , Especies Reactivas de Oxígeno/metabolismo , Coloración y Etiquetado/métodos , Infecciones Estreptocócicas/genética , Infecciones Estreptocócicas/patología , Streptococcus agalactiae/genética , Streptococcus agalactiae/inmunología , Streptococcus agalactiae/metabolismoRESUMEN
A 56-year-old man is reported who had suffered a frontal, frontobasal open craniocerebral injury four years ago. He presented for treatment with a glioblastoma of which the location and extent precisely corresponded to that of the prior brain injury. After surgical exposure of the tumor, we had the impression that the tumor initially showed granulating growth from the frontal injury site and had then given rise to more highly vascularized and also necrotizing tumor tissue spreading into the frontal medullary layer with typical glioblastoma characteristics. In view of the surgical site, it is logical to consider a tumorigenesis after cerebral trauma, which is also corroborated by the histological results, since more proliferative tumor growth was found near to the injury and more highly vascularized but also necrotizing (i.e. more typical of a glioblastoma) tumor growth far away from the injury. After the comparison of our observation with the corresponding cases in the literature, it is shown that there is at least in part a causal correlation between the trauma and tumorigenesis: in the previously healthy patient, the tumor developed precisely in the region of the injury (with detection of destroyed brain tissue) after a sufficiently long time interval. Near to the site of damage, it showed granulative growth with a low degree of vascularization, and then passed into the typical glioblastoma. Observations of genetic changes in glioblastoma patients is not inconsistent with this possible trauma genesis, but render it probable that trauma is the factor which can give rise to tumor growth in a corresponding susceptibility to tumorigenesis.
Asunto(s)
Neoplasias Encefálicas/diagnóstico por imagen , Lóbulo Frontal/lesiones , Glioblastoma/diagnóstico por imagen , Traumatismos Cerrados de la Cabeza/diagnóstico por imagen , Neoplasias Encefálicas/patología , Neoplasias Encefálicas/cirugía , Transformación Celular Neoplásica/patología , Angiografía Cerebral , Lóbulo Frontal/diagnóstico por imagen , Lóbulo Frontal/patología , Lóbulo Frontal/cirugía , Glioblastoma/patología , Glioblastoma/cirugía , Tejido de Granulación/patología , Traumatismos Cerrados de la Cabeza/patología , Traumatismos Cerrados de la Cabeza/cirugía , Humanos , Masculino , Persona de Mediana Edad , Tomografía Computarizada por Rayos XRESUMEN
A five-year-old boy with Crouzon Syndrome, short stature, and delayed bone age was found to have partial growth hormone deficiency. Accelerated growth was observed after human growth hormone replacement. Children with Crouzon Syndrome should be followed closely for all growth parameters, not just head circumference.