It was the aim of this study to investigate possible dysfunctions of the humoral immune system in asthmatic children with frequent respiratory infections. Forty-one severe asthmatics (7-15 years of age), classified according to the Second Brazilian Consensus in Asthma (1998), were divided into two groups: group I (n = 12) had recurrent respiratory infections; and group II (n = 29) were without recurrent respiratory infections. Immunoglobulin (Ig)G, IgA and IgM levels (nephelometry), and IgE (radioimmunoassay) and IgG subclasses (enzyme-linked immunosorbent assay), were evaluated using standard methods. Asthmatics with recurrent infections presented with worse clinical evolution, an increased number of hospital admissions, and a higher need of medication than the children without recurrent infections. There were no significant differences between the mean values of IgG, IgA or IgM levels, or IgE or IgG subclasses, in patients of both groups. A complete IgA deficiency was detected in two patients of group I (one was associated with IgG subclass deficiency). Deficiency of one or more IgG subclasses was verified in eight of 12 (66%) children from group I and in 16/29 (55%) from group II. The following deficiencies were found in both groups: IgG3 (10/41), IgG4 (three of 41), IgG2 (two of 41), IgG1 (one of 41), IgG3-IgG4 (four of 41), IgG1-IgG3 (two of 41), and IgG1-IgG3-IgG4 (one of 41). There were a higher proportion of children with low IgG4 levels in group I than in group II (p = 0.01). To conclude, IgA and IgG subclass deficiencies were detected in both severely asthmatic groups, with a predominance of IgG3 subclass deficiency. However, low IgG subclass levels appear not to be a suitable predictor of the development of infections in asthmatic children.
SUMMARYIn order to study B. henselae transmission among cats, five young cats were kept in confinement for two years, one of them being inoculated by SC route with B. henselae (10 5 UFC). Only occasional contact among cats occurred but the presence of fleas was observed in all animals throughout the period. Blood culture for isolation of bacteria, PCR-HSP and FTSZ (gender specific), and BH-PCR (species-specific), as well as indirect immunofluorescence method for anti-B. henselae antibodies were performed to confirm the infection of the inoculated cat as well as the other naive cats. Considering the inoculated animal, B. henselae was first isolated by blood culture two months after inoculation, bacteremia last for four months, the specific antibodies being detected by IFI during the entire period. All contacting animals presented with bacteremia 6 months after experimental inoculation but IFI did not detect seroconversion in these animals. All the isolates from these cats were characterized as Bartonella (HSP and FTSZ-PCR), henselae (BH-PCR). However, DNA of B. henselae could not be amplified directly from peripheral blood by the PCR protocols used. Isolation of bacteria by blood culture was the most efficient method to diagnose infection compared to PCR or IFI. The role of fleas in the epidemiology of B. henselae infection in cats is discussed.
Cellular immune responses are a significant defence mechanism in human paracoccidioidomycosis (PCM), an endemic mycosis in Latin America; however, little is known about the role of dendritic cells (DCs) in human PCM. We investigated monocyte‐derived DCs from patients with treated (TP) and active PCM (AP) compared with healthy non‐PCM donors (CO). DCs from the TP group showed higher expression of HLA‐DR, CD86 and DC‐SIGN compared with CO, whereas AP showed similar expression to CO. Production of IL‐10 was downregulated by TNF‐α in all groups and lower levels were observed in untreated DCs from AP compared with CO. Conversely, IL‐12p40 was significantly upregulated in the DCs of the TP group. TNF‐α‐activated DCs from the CO group produced significantly lower levels of IL‐12p40 when differentiated from magnetic‐sorted monocytes (MACS) compared with adhered monocyte‐derived DCs. This comparison in the TP group revealed similar levels of IL‐12p40, suggesting a T cell–independent increase in the production of IL‐12p40. Higher expression of surface molecules with increased IL‐12p40 may indicate a better activation of DCs after the treatment of PCM. Our findings suggest that DCs may be crucial in the protective response to Paracoccidioides brasiliensis and that in vitro‐generated DCs might be useful in enhancing antifungal immunity, especially during active PCM.
One hundred sixty-six cases of primary immunodeficiency diseases (PID) (95 males, 71 females), diagnosed according to WHO criteria, have been registered at the Children's Hospital, University of São Paulo, Brazil. The following frequencies were found: predominantly humoral defects, 60.8% (n = 101); T cell defects, 4.9% (n = 8); combined ID, 9.6% (n = 16); phagocyte disorders, 18.7% (n = 31); and complement deficiencies, 6% (n = 10). IgA deficiency was the most frequent disorder (n = 60), followed by transient hypogammaglobulinemia (n = 14), chronic granulomatous disease (n = 14), and X-linked agammaglobulinemia (n = 9). In comparison to other (national) reports, we observed higher relative frequencies of phagocyte and complement deficiencies. Recurrent infections were the cause of death in 12.7%. Allergic symptoms were observed in 41%, mainly in IgA-deficient, hypogammaglobulinemic, or hyper-IgE patients, and autoimmune disorders in 5%, predominantly in IgA and complement deficiencies. Five patients suffered from BCG dissemination; two of them died. This is the first Brazilian report on PID over an observation time of 15 years.
Paracoccidioidomycosis (PCM) is an important endemic, systemic disease in Latin America caused by
Paracoccidioides
spp. This mycosis has been associated with high morbidity and sequels, and its clinical manifestations depend on the virulence of the infecting strain, the degree and type of immune response, infected tissues, and intrinsic characteristics of the host. The T helper(Th)1 and Th17/Th22 cells are related to resistance and control of infection, and a Th2/Th9 response is associated with disease susceptibility. In this study, we focused on interleukin(IL)-12p35 (
IL12A
), IL-18 (
IL18
), and IFN-γ receptor 1 (
IFNGR1
) genetic polymorphisms because their respective roles have been described in human PCM. Real-time PCR was employed to analyze
IL12A
-504 G/T (rs2243115),
IL18
-607 C/A (rs1946518), and
IFNGR1
-611 A/G (rs1327474) single nucleotide polymorphisms (SNP). One hundred forty-nine patients with the acute form (AF), multifocal chronic (MC), or unifocal chronic (UC) forms of PCM and 110 non-PCM individuals as a control group were included. In the unconditional logistic regression analysis adjusted by ethnicity and sex, we observed a high risk of the
IL18
-607
A
-allele for both AF [
p
= 0.015; OR = 3.10 (95% CI: 1.24–7.77)] and MC groups [
p
= 0.023; OR = 2.61 (95% CI: 1.14–5.96)] when compared with UC. The
IL18
-607
A
-allele associated risk for the AF and MC groups as well as the protective role of the
C
-allele in UC are possibly linked to higher levels of IL-18 at different periods of the course of the disease. Therefore, a novel role of
IL18
-607 C/A SNP is shown in the present study, highlighting its importance in the outcome of PCM.
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