Abstract
Both human and murine neonates are characteristically highly susceptible to bacterial infections. However, we recently discovered that neonatal mice are surprisingly highly resistant to oral infection with
Yersinia enterocolitica
. This resistance was linked with activation of both innate and adaptive responses, involving innate phagocytes, CD4
+
cells, and B cells. We have now extended these studies and found that CD8
+
cells also contribute importantly to neonatal protection from
Y. enterocolitica
. Strikingly, neonatal CD8
+
cells in the mesenteric lymph nodes (MLN) are rapidly mobilized, increasing in proportion, number, and IFNγ production as early as 48 h post infection. This early activation appears to be critical for protection since B2m
−/−
neonates are significantly more susceptible than wt neonates to primary
Y. enterocolitica
infection. In the absence of CD8
+
cells,
Y. enterocolitica
rapidly disseminated to peripheral tissues. Within 48 h of infection, both the spleens and livers of B2m
−/−
, but not wt, neonates became heavily colonized, likely leading to their deaths from sepsis. In contrast to primary infection, CD8
+
cells were dispensable for the generation of immunological memory protective against secondary infection. These results indicate that CD8
+
cells in the neonatal MLN contribute importantly to protection against an extracellular bacterial enteropathogen but, notably, they appear to act during the early innate phase of the immune response.
