Search

As part of the Partners in School Asthma Management Program, environmental data were collected from 385 rooms in 60 elementary schools in southeast Texas, using an Environmental Observation Checklist and a Q-TRAK Indoor Air Quality Monitor. Dust samples for allergen analysis were collected from floors, carpets, and area rugs in 80 classrooms in a subset of 20 schools. CO2 levels >1,000 ppm were found in 86% of rooms; 69% had indoor humidity above recommended levels. Der p I dust mite allergen levels >2,000 ng/g were present in 20% of rooms, but only 2.5% of rooms had Der f I mite allergen levels exceeding recommended tolerances. Detectable levels of cockroach allergen (Bla g II) were found in all schools (median 5.5 ng/g), with 10% of rooms over the recommended threshold. Almost two-thirds of classrooms had mold spore counts >10,000 col/g (median, 14,400 col/g; range, 2,000 – 52,000 col/g).

Background: Available information suggests that IgE levels are elevated in adults infected with human immunodeficiency virus (HIV), and that increased IgE levels correlate with allergic disease, with decreased CD4 counts, and with a poor prognosis. Data with respect to these factors in children are scant. Objective: We investigated whether serum IgE levels are elevated in children with HIV and, if so, whether the serum IgE level correlates with the degree of immunodeficiency and/or objective indicators of allergic disease. Methods: Serum IgE levels, CD4 counts, absolute eosinophil counts, and immediate hypersensitivity skin test (IHST) results were collected from 43 children with symptomatic HIV infection (mean age 7.2 years). Associations between serum IgE levels, CD4 counts, and eosinophil counts were investigated by multiple stepwise linear regression analysis. Data were stratified according to IHST positivity, and analysis of variance was used to compare mean values for age, CD4 counts, IgE levels, and eosinophil counts between the two groups. Results: Serum IgE values were elevated more than 2 SDs above control age-matched mean values in 17 of 43 patients (40%). IHST results were positive in 12 of 43 patients (28%). CD4 counts were less than 200/mm 3 in 17 of 43 patients (40%). Stepwise linear regression failed to demonstrate any correlation between serum IgE levels and either CD4 or eosinophil counts. With data divided into two groups according to IHST results (positive vs negative), analysis of variance failed to reveal significant differences between means for patient age, CD4 counts, IgE levels, or eosinophil counts. Conclusions: Our findings confirm that serum IgE levels are increased in children infected with HIV, just as in adults. However, an elevated serum IgE level did not correlate with allergic disease as measured by IHST results and eosinophil counts, nor with the degree of immune dysfunction as approximated by CD4 counts. The mechanism and significance of elevated serum IgE levels remain unclear in children with HIV, and warrant further investigation. (J Allergy Clin Immunol 1997;100:707-11.)

S de Kivit, E Saeland, AD Kraneveld. Allergy. 2012;67(3):343–352 To investigate whether galectin-9 has a role in the mechanism of suppression of allergic skin reactions and mast cell degranulation induced by dietary synbiotics. Three-week-old specific pathogen-free C3H/HeOuJ mice were studied in a cow’s milk allergy model with or without a probiotic or prebiotic. Ninety human infants with atopic dermatitis were studied in a double-blind, placebo-controlled multicenter trial in which they received a hydrolyzed formula with or without synbiotics. Mice were sensitized orally to whey …

LB van der Aa, WM van Aalderen, HS Heymans; Synbad Study Group. Allergy. 2011;66(2):170–177 Infants with atopic dermatitis (AD) are at high risk of developing asthma. These researchers sought to examine the effect of early intervention with synbiotics, a combination of probiotics and prebiotics, on the prevalence of asthma-like symptoms in infants with AD. Ninety term infants less than 7 months of age with AD were recruited from 2005 to 2007 in the Netherlands. Inclusion criteria included an AD score (Severity Scoring of Atopic Dermatitis [SCORAD]) of …

MT Salam, TM Bastain, EB Rappaport. Allergy. 2011;66(3):412–419 Elevated fractional exhaled nitric oxide (FeNO) has been shown to be a sensitive biomarker for airway inflammation in children with asthma. This study examined whether a relationship could be demonstrated between genetic variants in nitric-oxide synthase and arginase genes and FeNO in asthma. Subjects aged 5 to 7 years were recruited from 13 Southern California communities for a Children's …

BACKGROUND: Chronic granulomatous disease (CGD) of childhood is a rare congenital ahnormality of the phagocyte NADPH oxidase system. Affected neutrophils and macrophages have an ineffective respiratory burst and cannot destroy certain phagocytized bacteria and fungi. CGD patients usually present with recurrent pyogenic and fungal infections. Catalase-positive bacteria are frequently involved, since they metabolize the hydrogen peroxide they produce, making it unavailable for augmentation of microbicidal activity in CGD neutrophils. AI&ted patients also have a tendency to form granulomas, which can lead to obstruction of the gastrointestinal and genitourinary tracts. METHODS: Charts of 10 patients with CGD were reviewed for age at diagnosis, surgical procedures, complications of these procedures, and medical treatment. RESULTS: Eight of the 10 children were male. The average age at first presentation was 18 months (range 2 days to 9.8 years). Each child developed a mean of 9.9 infections and an average of 1.4 infections per year. All required surgical procedures, with an average of 2.9 procedures each. Five children had operative procedures for infections that preceded the diagnosis of CGD. The procedures performed most frequently were incision and drainage of soft-tissue abscesses (7) or perirectal abscess (3), thoracentesis (3), and bronchoscopy (3). Three children had poor wound healing following surgery. Two developed partial gastric outlet obstruction which resolved with antibiotic therapy. One developed granulomatous cystitis with obstruction which responded to antibiotics. CONCLUSIONS: Since patients with undiagnosed CGD may present with surgical problems, surgeons need to be familiar with this condition. The diagnosis should be suspected in children who have recurrent or unusual infections or unexplained problems with wound healing.

A patient wit angioimmunoblastic lymphadenopathy had low serum immunoglobulin values and no antibodies to injected immunogens. This occurred despite the proliferation of polyclonal B cells. T cells were deficient in number and in lymphoproliferative responses, but their helper and suppressor functions were maintained. Ia-antigen bearing leukocytes from the patient stimulated poorly in mixed leukocyte culture. In vitro immunoglobulin synthesis by mononuclear leukocytes form the patient was severely impaired. These leukocytes actively suppressed immunoglobulin synthesis by normal cells from healthy subjects in co-culture. The responsible cell had characteristics of a monocyte. The suppression was selective for humoral immunity and was manifest despite normal numbers of monocytes. It appears that heterogeneous immunoregulatory abnormalities can underlie the syndrome of angioimmunoblastic lymphadenopathy. Furthermore, monocyte suppressor abnormalities may be implicated in clinical disease phenomena.

We have investigated the cellular and antigenic requirements for incubation of secondary proliferative responses by human T lymphocytes. Two distinct properties of antigen-presenting peripheral blood mononuclear cells were studied: (a) the ability for appropriate cell surface constituents to construct an immunogenic moiety, and (b) the ability to present similar antigenic determinants when they are not covalently bound. Only Ia+ hapten-modified cells were effective stimulators. In contrast, both Ia+ and Ia- cell sonicates could stimulate secondary proliferative responses, but only in the presence of an accessory cell. This accessory cell was present in Ia+ macrophage, but not in Ia+ non-T lymphocyte, preparations. In contrast, macrophages or soluble factors produced by macrophages were not required for primed T cells to undergo hapten-specific proliferation in response to hapten-modified Ia+ stimulator cells. Thus, although all Ia+ cells tested can stimulate primed cells to proliferate, not all Ia+ cells can function as accessory cells for responses to sonicates. This may reflect the unique ability of a subpopulation(s) of Ia+ cells to bind or process sonicates or soluble antigens for appropriate recognition by primed T cells.

To investigate mechanisms by which antigen, macrophages, and interleukin 2 (IL2) participate in the induction of secondary T-cell proliferative responses, trinitrophenyl (TNP) was presented in three distinct modes: (i) TNP-modified peripheral blood mononuclear cells (TNP-PBMC), (ii) TNP-PBMC cell sonicates, and (iii) TNP-ovalbumin (TNP-OVA). Stimulators were depleted of Mac-120+ macrophages using Mac-120 monoclonal antibody plus complement. TNP-Mac-120 macrophages stimulated primed T cells nearly as well as TNP-unfractionated macrophages (which were about 40% Mac-120+). In contrast, although greater than 70% DR+, Mac-120- macrophages plus either TNP-OVA or TNP-PBMC sonicate elicited minimal responses compared to unfractionated macrophages plus antigen. After 21-28 days of in vitro priming, macrophage-depleted T cells were not stimulated to proliferate by either IL2 alone or sonicates alone. IL2 plus TNP-PBMC sonicates, however, stimulated significant proliferation. Furthermore, this response was considerably greater than that to IL2 plus either TNP-T cell sonicates or TNP-mouse spleen sonicates. Thus, the Mac-120+ macrophage population may have an important antigen-presenting and/or accessory function in the stimulation of primed T cells by soluble or particulate antigen, although it is unnecessary for responses to intact TNP-Ia+ PBMC. In addition, the data suggest that Ia+ sonicates alone may suffice for induction of IL2 responsiveness, but not for endogenous IL2 production and subsequent proliferation by primed T cells.

Clearer definition of the recognitive structures of human T lymphocytes for antigens will be required to elucidate the molecular basis of diseases and immunological responses induced or regulated by normal or abnormal T-cell function. For this purpose we have investigated the cellular requirements for immune responses in vitro to trinitrophenyl-conjugated peripheral blood mononuclear cells. The responding cell was characterized as a T cell on the basis of rosetting with sheep erythrocytes. T-cell recognition of hapten in proliferative responses depended upon presentation of antigen in an appropriate stimulator-cell context. Neither autologous hapten-modified erythrocytes nor T cells restimulated responses of in vitro-primed lymphocytes. Moreover, hapten-conjugated non-T cells were more effective than modified unfractionated cells in restimulating proliferative responses. Both macrophages and non-T lymphocytes effectively restimulated hapten-conjugate responses. Cell-mixing experiments indicated that the failure of haptenated T cells to stimulate proliferative responses was not because of a lack of fresh macrophages; these experiments suggested instead that T cells do not express appropriate structures necessary to present haptenic determinants in an immunogenic form. Hapten-modified T cells, however, were capable of inducing primed lymphocytes to become efficient cytotoxic effector cells, indicating that T-cell recognitive units for stimulation of proliferative and cytotoxic responses are different. These data support the concept that for induction of proliferative responses, human T cells recognize conventional antigens in association with HLA-D-region-encoded Ia-like molecules.