Eosinophilic inflammation and airway hyper-responsiveness are profoundly inhibited by a helminth (Ascaris suum) extract in a murine model of asthma.
BACKGROUND
The increase of atopic disorders in developed countries has been associated with the decline of infectious diseases, including helminthic infections. We have already demonstrated that adult worm extracts from Ascaris suum (ASC) suppress the IgE antibody production against unrelated antigens.


OBJECTIVE
Here we investigated the influence of ASC on the development of pulmonary eosinophilic inflammation in a murine model of asthma.


METHODS
Heat-coagulated egg white alone (EWI) or mixed with ASC (EWI + ASC) was implanted subcutaneously in B10.A or C57BL/6 mice, and 14 days later they were challenged intratracheally with OVA or exposed to aerosolized OVA for 4 days.


RESULTS
The suppressive effect of ASC was demonstrated on the accumulation of cells into airways, with reduction of eosinophil numbers and of eosinophil peroxidase activity in EWI + ASC-immunized mice. This effect correlated with a marked reduction of IL-5 and IL-4 levels in the BAL from C57BL/6 and B10. A mice, respectively, and of eotaxin in BAL and lung tissue from both strains. OVA-specific IgG1 and IgE levels were also impaired in serum and BAL from these mice. Airway hyper-reactivity to methacholine was obtained in B10. A mice sensitized with EWI, but the respiratory mechanical parameters returned to normal levels in EWI + ASC-immunized mice.


CONCLUSIONS
These results indicate that ASC has a profound inhibitory effect on lung inflammation and hyper-responsiveness and that suppression of IL-5 or IL-4 and of eotaxin contributes to this effect.
Lima
C
C
Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Perini
A
A
Garcia
M L B
ML
Martins
M A
MA
Teixeira
M M
MM
Macedo
M S
MS
D000818:Animals; D000947:Antigens, Helminth / Q000008:administration & dosage*; D017165:Ascaris suum / Q000276:immunology*; D001249:Asthma / Q000276:immunology / Q000628:therapy*; D001980:Bronchi / Q000201:enzymology / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000628:therapy*; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D047209:Eosinophil Peroxidase; D004802:Eosinophilia / Q000628:therapy*; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007167:Immunotherapy / Q000379:methods*; D015847:Interleukin-4 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D023421:Models, Animal; D010544:Peroxidases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D000947:Antigens, Helminth; C515457:Ccl11 protein, mouse; C515458:Ccl11 protein, rat; D054413:Chemokine CCL11; D019742:Chemokines, CC; D007074:Immunoglobulin G; D015848:Interleukin-5; D015847:Interleukin-4; D007073:Immunoglobulin E; D047209:Eosinophil Peroxidase; D010544:Peroxidases