Airway inflammation, hyperreactivity, increased number of goblet cells, and mucus overproduction characterize asthma. Respiratory challenge with ovalbumin (OVA) of sensitized mice has been shown by several laboratories to cause pulmonary pathology similar to that observed in human allergic asthma. Recently, interleukin (IL)-13 has been shown to be a central mediator in this process. Because the airways of healthy mice have few, if any, mucus-producing cells, an increase in the number of these cells likely reflects induction of mucin-gene expression. The purpose of this study was to identify mucin genes induced as a result of airway goblet-cell metaplasia (GCM) in mice sensitized and challenged with OVA or in mice treated with IL-13 alone. BALB/c mice were sensitized by intraperitoneal injection (Days 0, 4, 7, 11, and 14) and intranasal instillation (Day 14) of 100 microg of OVA in saline, and then challenged by intranasal instillation (Days 25, 26, and 27) of the same. IL-13-treated mice received 5 microg of IL-13 by intranasal instillation on three consecutive days. Control mice were given saline alone. All mice were studied 24 h after the last challenge. Histologic analysis of the lungs revealed both a striking peribronchial and perivascular lymphocytic and eosinophilic inflammation and airway GCM in OVA-treated mice, and also airway GCM without inflammation in IL-13-treated mice. Northern blot analysis of lung RNA demonstrated (1) expression of Muc-5/5ac messenger RNA (mRNA) in OVA-treated and IL-13-treated mice, but not in control mice; (2) expression of Muc-1 mRNA at comparable levels in all mice regardless of treatment; and (3) no expression of Muc-2 or Muc-3 mRNA in control or treated mice. Western blot analysis demonstrated the expression of Muc-5/5ac protein (both apomucin and glycosylated mucin) in lung lysates of OVA-treated (but not control) mice, and also the expression of Muc-5/5ac mucins in the bronchoalveolar lavage fluid of OVA-treated and IL-13-treated mice. These findings demonstrate that airway GCM is associated with the induction of pulmonary expression of Muc-5/5ac mRNA and mucin in murine models of allergic asthma.
Pancreatoblastoma is typically a heterogeneous tumor with well-defined margins that may appear to arise from the pancreas or liver. It may behave aggressively, with localized vascular or bowel invasion or with widespread metastatic disease. Although it is rare, it should be considered in the differential diagnosis of an upper abdominal mass in a child.
We describe the clinical and pathological findings of the hemolytic uremic syndrome (HUS) in two children with human immunodeficiency virus (HIV) infection. Both patients presented with microangiopathic hemolytic anemia, thrombocytopenia, and subsequently developed renal failure. The diagnosis of HUS was confirmed by renal histopathology in both patients. None of these children presented with bloody diarrhea, evidence of circulating antibody response to Escherichia coli O157 lipopolysaccharide, or other known risk factors for HUS, except for the presence of HIV infection. Each patient was treated with intravenous plasma infusion and renal replacement therapy. Their clinical course was characterized by non-oliguria and lack of significant hypertension throughout the acute phase of the disease. Despite these favorable clinical parameters, both patients developed end-stage renal failure. The etiology of this atypical HUS characterized by poor renal survival remains unknown and the role of HIV infection in its pathogenesis, although possible, is unclear.
The early pathogenic events in cystic fibrosis (CF) include colonization of Pseudomonas in the lung, airway inflammation, and mucus hypersecretion with airway obstruction. The primary mechanisms leading to chronic infection and inflammation are not well understood. One possible explanation for this cascade of events is increased or altered expression of one or more mucin (MUC) genes by CF cells in the respiratory tract. We compared expression levels of three mucin genes, MUC1, MUC2, and MUC5/5AC, known to be expressed in the respiratory tract of CF, allergic rhinitis, and normal individuals. Mucin transcript levels in nasal epithelial cells free from inflammation were quantitated by an MUC mRNA slot-blot method. This study revealed three major findings: (1) MUC5/5AC mRNA was expressed at five- to tenfold greater levels than MUC2 or MUC1 for all subjects. (2) MUC2 mRNA levels were similar among all subject groups. (3) In CF subjects, there was a trend toward reduced MUC5/5AC expression. When normalized to the levels of MUC2 expression in individual specimens, MUC5/5AC expression was reduced significantly in CF cells compared with normal cells. These data suggest that mucin gene expression is altered in noninflamed CF nasal cells.
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