A Profilin from Toxoplasma gondii as adjuvant in an allergen-specific immunotherapy

MARCH F.; FENOY I.; SOTO A.; SANCHEZ V.; CASTERA F.; PICHIO M.; MARTIN V.; MORETTA R.; GOLDMAN A.

Los Cocos

Congreso; LXI Reunión Anual de la Sociedad Argentina de Inmunología; 2013

Sociedad Argentina de Inmunología

Asthma is a chronic airway inflammation orchestrated by Th2 cells. We have previously shown that Toxoplasma gondii infection prevents allergic lung inflammation. T. gondii profilin is a TLR protein ligand that induces a strong Th1 immune response, making profilin a good candidate to use as adjuvant for allergy treatment. Hence, we evaluated the capacity of a recombinant profilin (P) to treat lung allergy. Profilin was cloned from T. gondii RH strain tachyzoites, expressed and purified from E. coli cultures. BALB/c mice were sensitized with 2 ip OVA (allergen)/Alum and aerosol challenged with OVA 3%. Two days later, mice were treated 3 consecutive days by intranasal (IN) route with OVA plus P (O/OP). Control groups included non-sensitized mice IN treated with P alone (PBS/P) as negative control and sensitized mice treated IN with OVA alone (O/O) as positive control. One week later, mice were again aerosol challenged with OVA. O/OP mice showed a strong decrease in BAL eosinophilia, both in percentage (PBS/P: 0,0±0,0a; O/O: 29,05±4,4b; O/OP: 9,5±4,2c; %±SEM p<0,05 b vs c) and in total eosinophil number  (PBS/P: 0,0±0,0; O/O: 0,66±0,39; O/OP: 0,32±0,16, X±SEM x106), and an increase in macrophage percentage and absolute number (PBS/P: 75,33±0,33a; O/O: 41,57±6,91b; O/OPc: 65,52±6,89, %±SEM p<0,05 b vs c; PBS/P: 0,78±0,11; O/O: 1,05±0,25; O/OP:1,71±0,32, X±SEM x106). O/OP mice showed a decreased in OVA-specific IgE production (PBS/P: 0,04±0,003ª; O/O: 0,61±0,06b; O/OPc: 0,24±0,03; OD±SEM p<0,01 b vs c) and a trend to an increase in IgG2a levels (PBS/P: 0,07±0,2; O/O: 0,46±0,05; O/OP: 0,70±0,17; OD±SEM) in serum. Variation in IgG1 levels was not detected. Our results show an adjuvant capacity of r-profilin for atopic disorders treatment and suggest that this effect would be the result of Th2 to Th1 immune deviation.