Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51834
immunologie@vetmed.fu-berlin.de
The immune mechanisms of resistance and susceptibility to Ascaris infection potentially causing overdispersion in infected humans and pigs are poorly understood. In an attempt, to comprehend the innate immune response which might provide resistance in natural hosts particularly during Ascaris larval hepato-tracheal migration, we used two mouse strains with contrasting susceptibilities to Ascaris infection. In mice the hepato-tracheal migration happens as in the natural hosts. In accordance with other studies, we could confirm the resistant phenotype of CBA mice and the susceptible phenotype presented by C57BL/6 mice. Significantly reduced Ascaris suum larvae in the liver were associated with decreased liver pathology in resistant CBA mice compared to susceptible C57BL/6 mice. This was accompanied with reduced eosinophilic infiltration at 4-day post-infection and intrinsically elevated frequencies of alternatively activated (M2) macrophages in the liver of the resistant CBA mouse strain in contrast to the susceptible strain. Moreover, increased frequencies of M2 alveolar macrophages were detectable in the lungs of resistant CBA mice at 4-day post-infection and associated with a reduced eosinophilic and neutrophilic inflammation as well as a decreased alveolar macrophage activation at 8-day post-infection. Thus, these results suggest not only an intrinsic M2 phenotype of liver macrophages but also infection-induced M2 alveolar macrophages to be involved in resistance against Ascaris suum larval migration and pathology