Exposure to environmental factors during fetal life and infancy is thought to play an important role in the early development of innate and adaptive immunity. The immunological relationship between mother and infant and the effect that environmental exposures have during pregnancy and early childhood have not been studied extensively. Here the production of
cytokines was measured in 146 pairs of mothers and their 2- month-old infants. The effect of place of residence, socio-economic variables,
parasitic infections as well as maternal and child characteristics on measured
cytokine production was determined. Mothers producing high levels of
IL-10, IFN-gamma and
IL-5 were more likely to have infants who also produced high levels of these
cytokines either spontaneously (OR 2.6(95%CI 1.2-5.4), OR 2.9(CI 1.3-6.6), OR 11.2(CI 4.6-27.2), respectively) or in response to PHA (IL-10: OR 3.0(CI 1.4-6.6), IFN-gamma: OR 2.0(CI 1.0-4.2), respectively) even after adjustment for potential confounding variables. This was not the case for
TNF-alpha. In response to LPS, place of residence was a strong determinant of infant
IL-10 (OR 0.2(CI 0.1-0.9)) and
TNF-alpha (OR 0.3(CI 0.1-0.9)) production. Maternal
protozoan infections was independently associated with reduced infant
IL10 in response to PHA and to LPS as well as reduced
TNF-alpha and IFN-gamma in response to PHA. These results indicate strong relationship between maternal and infant's cellular immune responses even after taking into account many environmental influences that could affect infant's response directly or indirectly through uterine microenvironment. However, place of residence and intestinal
infections may still directly affect the immune responses of the infant. Taken together, the study provides evidence for imprinted
cytokine responses of an infant which may have implications for their reaction to incoming
antigens, warranting further investigation into the role that genetics or epigenetics play in shaping the
cytokine response by an infant to self or external
antigens.