The enigmatic eosinophil: investigation of the biological role of eosinophils in parasitic helminth infection.
In many helminth infected hosts the number of eosinophils increases dramatically, often without any concurrent increases in the number of other leukocytes, so that eosinophils become the dominant cell type. Many experimental investigations have shown that the eosinophilia is induced by interleukin-5 (IL-5) but its functional significance remains unclear. Mice genetically deficient in IL-5 (IL-5-/-) have been used to evaluate the functional consequences of the IL-5 dependent eosinophilia in helminth infected hosts. Host pathology and level of infection were determined in IL-5-/- and wild type mice infected with a range of species representative of each major group of helminths. The effects of IL-5 deficiency were very heterogeneous. Of the six species of helminth examined, IL-5 dependent immune responses had no detectable effect in infections with three species, namely the cestodes Mesocestoides corti and Hymenolepis diminuta and the trematode Fasciola hepatica. In contrast, IL-5 dependent immune responses were functionally important in mice infected with three species, notably all nematodes. Damage to the lungs caused by migrating larvae of Toxocara canis was reduced in IL-5-/- mice. Infections of the intestine by adult stages of either Strongyloides ratti or Heligmosomoides polygyrus were more severe in IL-5-/- mice. Adult intestinal nematodes were clearly deleteriously affected by IL- 5 dependent processes since in its presence there were fewer worms which had reduced fecundity and longevity. The implications of these results for the viability of using inhibitors of IL-5 as a therapy for asthma are considered.
Ovington
K S
KS
Division of Biochemistry and Molecular Biology, Faculty of Science, Australian National University, Canberra, Australia. Karen.Ovington@anu.edu.au
Behm
C A
CA
D000818:Animals; D000835:Animals, Wild; D001249:Asthma / Q000188:drug therapy / Q000276:immunology; D004804:Eosinophils / Q000502:physiology*; D006373:Helminthiasis / Q000276:immunology*; D007109:Immunity / Q000502:physiology; D015848:Interleukin-5 / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout
D015848:Interleukin-5