Immune dynamics of the digestive tract

The digestive system in chickens undergoes dramatic transformation during the immediate post-hatch period in terms of bacterial colonization and the demand to digest and absorb complex adult-type food stuffs. These changes call for rapid adaptations of several physiological systems, including digestive capacity, barrier formation and development of protective immunity. Notwithstanding the significant protection provided by maternal antibodies (present in both serum and gut yolk), the chick must rapidly consolidate the structure and function of its own enteral immune system. We have investigated the development and maturation of the intestinal immune system in chickens in terms of the conditions required for development of adequate protective immunity. We show a unique biphasic pattern of lymphocyte colonization of the intestine and gradual maturation of T cell functions by two weeks post hatch. The first maturation phase of the adaptive GALT occurs during the first week of life and is characterized by establishment of lymphocytic populations in the intestine. The second phase of maturation which takes place during the second week of life is characterized by functional maturation which is demonstrated by increase in chIL2, chIFNγ and the ability to mount humoral response to enteric administered proteins. We tested the development of the innate GALT in newly hatched chicks. Polymorphonuclear cells increased in number during the first two weeks post-hatch resulting from both migration and in-situ development in extra-medullar foci. Expression of proinflammatory cytokine genes was basal at hatch but increased rapidly thereafter, so that by day 2, levels were similar to those observed on day 7. Expression of the IgA transporter gene in epithelial cells occurred posthatch in correlation with development of adaptive immunity. The rapid increase in gene expression is related to the exposure to environmental microflora and demonstrates the capability of the enteric immune system to respond rapidly to inflammatory stimuli of external origin.