Toxoplasma gondii and protection against allergic sensitization

BATALLA, E; MARTIN V; ROMERO Y; PIAZZON I, GOLDMAN A.

Córdoba, Argentina

Congreso; VII Congreso Latinoamericano de Inmunología; 2005

ALAI

Toxoplasma Gondii AND PROTECTION AGAINST ALLERGIC SENSITIZATION Batalla, E1; Martin V2; Romero Y1; Piazzon I3, Goldman A1. 1ECyT, UNSAM; 2INTECH, UNSAM; 3ILEX-CONICET-IIHEMA-Academia Nacional de Medicina; Bs As, Argentina The hygiene hypothesis postulates a link between decreased childhood infections and increased allergy in Western societies. Epidemiological studies showed that respiratory allergy is less frequent in people exposed to orofecal and foodborne microbes such as Toxoplasma gondii and hepatitis A virus (BMJ 2000, 320:412) but not to viruses transmitted through other routes. Infection with T. gondii leads to the induction of a strong cell mediated immunity characterized by a highly polarized Th1 response in early stages of infection (J.Immunol. 1994,153:2533). We sought to test the hypothesis that T. gondii infection will diminish the susceptibility to develop respiratory allergy. Adult BALB/c mice were subjected to a sensitization protocol (two i.p. injection of OVA, days 0 and 7) prior to aerosol challenge (days 14-16). One week before sensitization (day ?7), the experimental group was orally infected with T. gondii (15 oocysts). Allergic airway inflammation  (AI) (differential count in bronchoalveolar lavage (BAL) and lung histology), serum IgE and IgG1 OVA specific antibodies (Ab) and Th2 cytokines (IL-4) secreted by OVA stimulated thoracic lymph node cells were evaluated. Infection was confirmed by measuring toxoplasma specific Ab. Group IL-4 (pg/ml) BAL eos (%) IgE (ng/ml) IgG1 (mg/ml) toxo inf/OVA sens 18,2±0,3* 6,9±3,4 971,0±322,6* 50,6±12,2* sham inf/OVA sens 707,2±93,7 67,9±7,4 3244,1±390,6 298,3±25,9 toxo inf/sham sens <15,5 2,8±1,2 <78 <5,3x10-4 sham inf/sham sens ND 0 <78 <5,3x10-4 X±SEM. p<0,05 vs sham inf/OVA sens group. Histopathology showed a diminished allergic airway inflammation and goblet cell hyperplasia in OVA sensitized mice previously infected with T. gondii. Conclusions: Parasite infection substantially blocks development of AI in adult BALB/c mice. These results support the hygiene hypothesis.