Bovine neonate is deficient in innate immunity at birth.

With an objective to understand acquisition of innate immunity in bovine neonates, we analyzed perinatal expression of cytokine, adhesion molecule and complement component genes involved in innate and adaptive immune functions. Statistically robust transcriptomic analysis of 27 cytokines showed low IL1B, IL2 and IL7 but high IL23, TGFB1 and TGFB2 expression in bovine neonates post-birth. Unlike mice and humans, no TH 2 polarizing cytokine expression occurs in bovine neonates. Further, TH 17 and Treg differentiation in bovine neonates may differ from other species like mice and humans. Decreased IL7, IL23R, CXCR3 and increased TGFB1 and TGFB2 expression provides an immunosuppressive environment in the bovine neonate at birth. Transcriptomic analysis of 31 adhesion molecules showed rapid increase in ITGAL expression within a week post-birth in bovine neonates that permits acquisition of innate cytotoxic functions by granulocytes (antibody-mediated), cytotoxic T and NK cells. However, innate immune functions involving phagocytosis and platelet aggregation are deficient in bovine neonates at birth. Of twenty-seven, 18 complement component genes show no significant differential gene expression in neonates post-birth. But low expression of C1QA, C1QB, CQC, C1R and C2 compromises classical and lectin complement pathways mediated lytic function in bovine neonates. The complement-mediated cytotoxic functions, however, normalize between days 7 and 28 post-birth. To conclude, bovine neonate is immunosuppressed and deficient in innate immune competence at birth. Such differences with regard to global innate immune deficiency and lack of TH 2 polarization in bovine neonates have profound implications for designing vaccines to prevent neonatal infections. To conclude, species-specific unique characteristics of developing innate and adaptive immune system need to be taken into consideration while designing new immunization strategies to prevent neonatal mortality from infections.