Ascaris lumbricoides-induced suppression of total and specific IgE responses in atopic subjects is interleukin 10-independent and associated with an increase of CD25(+) cells.
Ascaris presence in humans has been associated with high levels of blood eosinophils and serum IgE. This study was designed to address the influence of Ascaris infection on allergic and inflammatory parameters of atopic subjects. A cross-sectional design was used, and atopic individuals to be assessed were divided into 3 groups including Ascaris-infected, anti-Ascaris IgG-positive (seropositive), and control subjects. All subjects enrolled had positive skin test reactivity to at least 1 perennial or seasonal allergen; however, levels of C-reactive protein, C3, and C4 were within normal range values. Eosinophil percentage was not significantly different among the groups studied. Total IgE and specific anti-Ascaris IgE levels in the seropositive group were significantly higher than concentrations found in both control and infected groups. Interleukin (IL)-4 release in Ascaris-infected patients was significantly increased versus seropositives, who were able to produce more IL-4 than controls. The levels of IL-10 were lower in the seropositives as well as infected subjects in comparison with controls. CD25(+) lymphocyte populations were significantly increased in the infected group versus the seropositives as well as the controls. Lung function tests of some selected seropositive subjects were significantly impaired. The same parameters of a representative infected patient were not different from controls. Our data on T helper type 2 cells (Th2) and regulatory T cells (Treg) features, as well as CD25(+) lymphocyte increase, suggest an Ascaris-induced mechanism leading to parasite survival. Moreover, the stable control of both T helper type 1 cells (Th1) and Th2 immunity cascades, paralleled by the absence of overwhelming inflammatory systemic reactions and lack of allergic syndromes, may result in a favorable host condition.
Matera
Giovanni
G
Institute of Microbiology, University "Magna Graecia" of Catanzaro, 88100 Catanzaro, Italy. mmatera@unicz.it
Giancotti
Aida
A
Scalise
Sonia
S
Pulicari
Maria Concetta
MC
Maselli
Rosario
R
Piizzi
Chiara
C
Pelaia
Girolamo
G
Tancrè
Valentina
V
Muto
Valentina
V
Doldo
Patrizia
P
Cosco
Vincenzo
V
Cosimo
Paola
P
Capicotto
Renata
R
Quirino
Angela
A
Scalzo
Rosaria
R
Liberto
Maria Carla
MC
Parlato
Giuseppe
G
Focà
Alfredo
A
D000368:Aged; D000704:Analysis of Variance; D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D001196:Ascariasis / Q000276:immunology*; D017164:Ascaris lumbricoides / Q000276:immunology*; D003430:Cross-Sectional Studies; D004804:Eosinophils / Q000276:immunology; D005243:Feces / Q000469:parasitology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood* / Q000378:metabolism; D007371:Interferon-gamma / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis*; D007378:Interleukins / Q000097:blood; D008875:Middle Aged; D012129:Respiratory Function Tests; D012882:Skin Tests; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000913:Antibodies, Protozoan; D053645:Interleukin-2 Receptor alpha Subunit; D007378:Interleukins; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D007073:Immunoglobulin E; D007371:Interferon-gamma