C57BL/6 mice genetically deficient in interleukin-5 (IL-5(-/-)) and no
rmal C57BL/6 (IL-5(+/+)) mice were infected with larvae of a homogonic
strain of the nematode Strongyloides ratti. In primary infections bot
h male and female IL-5(-/-) mice released two to four times more eggs
and larvae than IL-5(+/+) mice. IL-5(-/-) mice harboured about 60% mor
e intestinal worms, which were more fecund, than IL5(+/+) mice. The du
ration of the infection was similar in normal and IL-5-deficient mice.
Both IL-5(-/-) and IL-5(+/+) mice resisted a secondary infection. IL5
(-/-) mice lost more weight during the infection than normal mice and
took longer to regain their initial weight after expelling the worms.
The number of eosinophils increased in the bone marrow, peritoneal cav
ity and small intestine of IL-5(+/+) mice, but not IL-5(-/-) mice, fol
lowing infection. No significant differences between infected IL-5(+/) and IL-5(-/-) mice in mast cells or other leucocytes were observed i
n the peritoneal cavity. Thus, IL-5 functions to protect the host in a
primary infection of S. ratti by limiting the number and fecundity of
worms establishing in the small intestine. This protection is correla
ted with elevated blood and tissue eosinophilia which occurs in normal
mice but not in IL-5(-/-) mice.