The role of T-cell memory in late-phase allergic lung inflammation is
not well defined. To evaluate the role of systemic T-cell memory in al
lergic late-phase lung inflammation, BALB/c mice were injected intrape
ritoneally with ovalbumin (OVA) or ragweed (RW) allergens (Test I and
Test II groups) or saline (control groups C I and C IV) and then chall
enged intratracheally with the allergen. Late-phase allergic lung infl
ammation was defined by: (i) recruitment of eosinophils to airways, (i
i) IL-5 mRNA upregulation in BAL fluid cells, and (iii) detection of a
Th2 cell cytokine profile in DAL fluids. The number of eosinophils re
cruited in allergic mice following intratracheal challenge with allerg
en was at least 300-fold higher P less than or equal to 0.01) in mice
with allergen-specific T-memory cells in BAL fluid (Test I and Test II
) than in control mice without allergen-specific T-memory cells (C I a
nd C nn. Further, the number of eosinophils recruited in Test I and II
correlated with the magnitude of in vitro T-cell memory responses (r
= 0.93, P less than or equal to 0.04). Moreover, IL-5 mRNA upregulatio
n in BAL cells and Th2 cytokine production in BAL fluids were observed
only in Test I and Test II, and not in any of the control groups. Fur
ther, results from pulmonary function tests performed on the same alle
rgic animals indicated that only animals from Test I and Test II group
s had impaired lung function after allergen challenge. Taken together,
these data strongly suggest that allergen-specific Th2-type T-cell. m
emory is required for the development of allergic asthma. That is, wit
hout T-cell memory responses, no eosinophil recruitment and release of
EPO (which is known to induce bronchoconstriction) occurred in the ai
rways, and no Th2 cytokine profile was detected in the BAL fluid. Furt
hermore, if the Th2 cytokine profile was absent, then pulmonary functi
ons remained normal. (C) 1996 Academic Press, Inc.