Abstract
The neonatal period represents a window of susceptibility for ruminants given the abundance of infectious challenges in their environment. Maternal transfer of immunity does not occur in utero but post-parturition, however this does not compensate for potential deficits in the cellular compartment. Here we present a cellular and transcriptomic study to investigate if there is an age-related difference in the monocyte response in cattle during intra-cellular protozoan infection. We utilized Neospora caninum, an obligate intracellular protozoan parasite that causes abortion and negative economic impacts in cattle worldwide, to study these responses. We found neonatal animals had a significant greater percentage of CD14+ monocytes with higher CD80 cell surface expression. Adult monocytes harbored more parasites compared to neonatal monocytes; additionally greater secretion of IL-1β was observed in neonates. Microarray analysis revealed neonates have 535 genes significantly upregulated compared to adult with 23 upregulated genes. Biological pathways involved in immune response were evaluated and both age groups showed changes in the upregulation of tyrosine phosphorylation of STAT protein and JAK-STAT cascade pathways. However, the extent to which these pathways were upregulated in neonates was much greater. Our findings suggest that neonates are more resistant to cellular invasion with protozoan parasites and that the magnitude of the responses is related to significant changes in the JAK-STAT network.
Highlights
Neonatal mortality amongst production livestock remains an endemic problem within developed and developing countries
We demonstrate that while neonatal monocytes contain lower numbers of N. caninum compared to adults following in vitro challenge they are more sensitive in terms of inflammatory reactions
To begin our investigation the monocyte pool was examined for differences between neonates and adults
Summary
Neonatal mortality amongst production livestock remains an endemic problem within developed and developing countries. These cells are no longer detectable by 36 h post transfer This paradigm for incrementally increasing adaptive clonal responses is well illustrated by the dynamics of nematode challenge—whereby hosts exposed on the first occasion develop large nematode worm burdens while adults with repeated exposures harbor lower nematode numbers [4, 5] due to the efficacy of the clonal populations in their adaptive compartments. This paradigm is challenged by the enhanced resistance of calves to Babesia bovis, whereby calves display lower parasitemia, clinical disease, and greater inflammatory reactions. Given the absence of a full antigen-experienced adaptive system during this early life period we sought to extend the findings above and sought to define a potential mechanism by which the neonatal immune system can compensate for the absence of fully functional adaptive response
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