The development of upper airway mucosal immune architecture depends on peri-natal bacterial colonisation.

摘要

Background. Mucosal immunity is incomplete at birth(1,2) and may depend early exposure to bacteria. Objectives. Determine how early neonatal exposure to bacteria alters leukocytes in mammalian upper airways. Method. Five sows were delivered by Caesarean section into a sterile tent. Group A (n = 9) was maintained germ-free. Others were colonised with Schaedler flora plus Staphylococcus (Group B, n = 6) or Bacillus (Group C, n = 5). In group A, two animals were killed at birth and two at 14 days. Remaining animals were killed at a median 24 days. CD4 (helper T-cells), MHC II (monocytic cells) and CD16 (monocyte activation) expression was measured in upper airway mucosa by quantitative immunofluorescence histology. Results. CD4+ cells were rare in Group A, but increased significantly in colonised animals (GpB P = 0.004, GpC P = 0.018). In Group A, MHC II and CD16 expression was low and unaltered by age. Group B exhibited a significant increase in both antigens compared to Group A (MHC II P = 0.002; CD16 P= 0.017). Although higher, levels in Group C were statistically similar to Group A (MHC II P = 0.76, cd16 P = 0.883). There was significantly less co-localisation of CD4+ cells with myeloid cells in Group A (P < 0.05). Conclusions. Normal development of upper airway mucosal immune architecture is dependent on the presence and content of its bacterial flora. Flora containing (aerobic) staphylococcus results in significantly greater acquisition of helper T-cells and myeloid cells than that containing (anaerobic) Bacillus. There is evidence that the bacteria also affect the functional interaction between T-cells and myeloid cells in the upper airway. References. 1 (2007) Vet. immunol. immunopathol. 119, 243-253 2 (2005) Dev. comp. immunol. 29, 977-987.