Streptococcus Pneumoniae Augments Inflammatory Process In Asthma Model Without Changing Th2 Profile

Studies suggested that some aspects of asthma exacerbation by Spn infection remain unclear. Objective: to evaluate possible mechanism that worsen inflammation caused by Spn in an experimental model of chronic allergic inflammation. Methods: 30 BALB/c mice were divided in 4 groups: SAL (non-sensitized group), STREP (animals challenged with Spn), OVA (ovalbumin sensitized group), OVAST (OVA sensitized and challenged with Spn). OVA and OVAST groups received intraperitoneal injections of ovalbumin (OVA) solution (days 1 and 14). OVA challenges were performed on days 22, 24, 26, and 28. Afterwards, animals were challenged with pneumococcal strains M10 (11A)(50ul/bacteria in saline). After 12h, lung mechanics and bronchoalveolar lavage (BAL) were performed. Animals were euthanized, lungs removed for immunohistochemistry and morphometric analysis. Results: Challenge with Spn in OVA sensitized group induces an increase in of total cells (46.33±13.22x104cells/mL), neutrophils (23.70±14.39x104cells/mL), macrophages (7.70±2.03x104cells/mL) and eosinophils (14.52±13.88x104cells/mL) in BALF as well as increasing in polymorphonuclear cells (0.152±0.06mm2) and expression of IL-17 (12.12±2.67mm2) in peribronchovascular area in lung compared to OVA group (p<0.05). There were an increase in tissue damping (27.01±7.25cmH2O/mL/s(1-a)); expression of IL-5 (10.15±3.39mm2) and IL-13 (8.85±3.56mm2) in peribronchovascular area were observed in OVA groups compared to other groups (p<0.05). Conclusion: Challenge with Spn, in this model induces an increasing in lung inflammation by increasing IL-17 without changes in Th2 profile.Supported by FAPESP (19966-6), LIMHC-FMUSP, CNPq.