Increased seroprevalence of Enterovirus 71 IgE antibodies in asthmatic compared with non-asthmatic children.

BACKGROUND: Asthma is a common pediatric chronic inflammatory airway disease. Respiratory viral infections are frequent infectious triggers for exacerbations of asthma. OBJECTIVE: We sought to determine whether Enterovirus 71 (EV71), a ubiquitous virus that causes systemic inflammatory responses in children but is not a known respiratory pathogen, can also serve as an infectious trigger for asthma. METHODS: Specific EV71 IgE and IgM antibodies (Abs), total serum IgE, and IL-2 and IL-4 cytokine levels in serum of asthmatic and non-asthmatic children (N = 42, ages 5-19; N = 35, ages 1-20, respectively) were measured (ELISA). RESULTS: Asthmatic children had higher EV71 IgE Ab levels than non-asthmatic (P < 0.001). Non-asthmatic children had significantly higher EV71 IgM Ab levels than asthmatic (P < 0.001). Despite low serum IgE levels of non-asthmatic, compared with asthmatic (P < 0.001), the non-asthmatic children produced significantly more IL-2 and IL-4 than asthmatic (P < 0.001; P < 0.001). The ages of the asthmatics, but not the non-asthmatics had a significant effect on the levels of EV 71 IgE Abs (P = 0.02; P = 0.356). A test of difference between these two slopes was significant. However, the ages of the non-asthmatic, but not the asthmatic children had a significant effect on the levels of EV 71 IgM Abs; a test of difference between these two slopes was significant. CONCLUSIONS: Increased specific EV71 IgE Ab responses may indicate that EV71 infection may also be an infectious trigger in asthma. However, the role of specific EV71 IgM Abs, Th2 cytokines, and age in non-asthmatic children should be further studied.

CD8+CD60+ T cells, cells expressing epsilon specific mRNA and Th1/Th2 cytokines in cord blood and at 7 months of age.

IgE levels in cord blood have been investigated as predictors of atopy, but no definitive findings have been made. Other factors, including cells and/or cytokines may serve as predictors of this disease. Cord blood and peripheral blood was obtained at birth and at 7 months of age, respectively, from children (n = 2) with a family history of allergy. Cells in cord blood and peripheral blood were phenotyped and levels of serum immunoglobulins (IgM, IgG, IgA and IgE) were determined. In addition, placentas from these pregnancies were obtained and stained for IgE+ cells and CD8+CD60+ T cells. We found immunoglobulin levels were within normal ranges although IgE levels were negligible in cord blood and at 7 months of age. Similar numbers of CD8+ T cells and CD19+ B cells were detected in cord blood and at 7 months of age. However, CD4+ T cells increased (twofold) and CD16+/CD56+ natural killer precursor cells decreased (twofold) at 7 months of age. CD8+ T cells in their cord blood and at 7 months of age comprised of >50% CD8+CD60+ T cells. Cord blood cells expressed epsilon-specific mRNA and mRNA for interleukin-2 (IL-2), IL-4, IL-10 and interferon-gamma (IFN-gamma) but not IL-6. At 7 months of age, peripheral blood mononuclear cells expressed epsilon-specific mRNA and mRNA for all cytokines. In the placental membrane, we detected IgE+ cells, while CD8+CD60+ T cells were detected in the chorionic villi. CD8+CD60+ T cells, cells expressing epsilon-specific and IL-6-specific mRNA may contribute to the pathobiology and provide important prognostic indicators of atopy.

IgE anti-Borrelia burgdorferi components (p18, p31, p34, p41, p45, p60) and increased blood CD8+CD60+ T cells in children with Lyme disease.

Immunoglobulin (Ig) E may provide immunity against Borrelia burgdorferi infection (Lyme disease) in children which lasts throughout adulthood. We investigated the presence and persistence of IgE anti-B. burgdorferi antibodies (Abs) in paediatric patients infected with Lyme disease over time. Serum immunoglobulin levels, presence of IgG and IgE anti-B. burgdorferi components, and distributions of blood T, B and natural killer lymphocyte subsets were studied in B. burgdorferi-infected and -uninfected children (nephelometry, UniCAP Total IgE Fluoroenzymeimmunoassay, Western blot, flow cytometry). Total serum IgM, IgG, IgE and IgA levels, and distributions of blood lymphocytes (CD4(+), CD8(+), CD19(+)) of both groups, excluding CD8(+)CD60(+) T cells, were within normal ranges. However, infected, but not uninfected children made IgG anti-B. burgdorferi proteins p18, p31, p34, p41, p45, but not IgG anti-p60, and IgE anti-B. burgdorferi proteins p31, p34, p41, p45, p60, but not IgE anti-p18. These proteins were also detected in an infected child 1 year post-infection. Interestingly, CD8(+)CD60(+) T-cell numbers were significantly increased (fourfold) in infected, compared with uninfected, patients (P=0.001). These results demonstrate that specific IgE anti-B. burgdorferi Abs are generated and persist in children with Lyme disease and that CD8(+)CD60(+) T cells may play an important role in these responses.