Heligmosomoides polygyrus infection down-regulates eotaxin concentration and CCR3 expression on lung eosinophils in murine allergic pulmonary inflammation.

There is growing evidence that helminth infections might suppress allergic responses by mechanisms potentially involving regulatory T lymphocytes, cytokines, helminth molecules and polyclonal IgE. Heligmosomoides polygyrus infection in mice is associated with reduced local and systemic immune responses, thus providing an excellent model to study the mechanisms of immune regulation. In this research, we examined the way that nematode infection modulates the influx of eosinophils into the airways of asthmatic mice. We observed a reduction in the total number and percentage of lung eosinophils that coincided with decreased levels of eotaxin in bronchoalveolar lavage fluid (BALF), lower expression of the CCR3 receptor on eosinophils and impaired chemotaxis of these cells toward eotaxin. We conclude that allergen-induced immune response was down-regulated as production of Th1 (IFN-gamma)-, Th2 (IL-4, IL-5)- and Treg (IL-10)-related cytokines as well as IL-6 and TNF-alpha was diminished upon nematode infection. We postulate that attenuation of allergic inflammation during H. polygyrus infection is a consequence of the dichotomy of the immune response in the face of concurrent antigenic challenge.