Thymic atrophy and impaired thymic hormone production as a key role in the pathogenesis of the Periweaning Failure-to-Thrive syndrome (PFTS) in piglets

Vollständiger Abstract

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Abstract Background Periweaning Failure-to-Thrive syndrome (PFTS) is an emerging syndrome characterized by progressive growth retardation, anorexia and debilitation in piglets during the 2–3 weeks post-weaning. Since its first description in 2008, the syndrome has been reported in several countries and represents an important concern for the swine industry due to its impact on productivity and mortality. A consistent pathological feature of affected animals is thymic atrophy, suggesting a possible role of thymic dysfunction and altered thymic hormone production in the pathogenesis of the syndrome. The present study aimed to evaluate histopathological and histomorphometric changes in the thymus of PFTS- affected piglets and to investigate their association with leukocyte counts, serum thymulin levels and endocrine thymus functionality. Results The histopathological study revealed that piglets with clinical signs compatible with PFTS showed different degrees of thymic atrophy ranging from mild to severe, whereas healthy animals displayed normal thymic morphology. On the other hand, the histomorphometric results revealed a significant reduction in the cortex/medulla ratio in affected piglets, and this reduction became more pronounced as the severity of the thymic atrophy increased, although the size of Hassall’s corpuscles did not differ significantly between healthy and affected animals. Hematological analysis revealed progressive decreases in several leukocyte populations, particularly total lymphocytes and large lymphocytes, associated with increasing severity of thymic atrophy. Serum thymulin concentrations were significantly lower in affected piglets and showed a negative correlation with the degree of thymic atrophy. When looking at gene expression, significant reductions in prothymosin alpha and thymopoietin in animals with severe thymic atrophy were seen, while most β-thymosins showed minimal variation. Overall, the correlation analyses supported a strong link between thymic atrophy, alterations in immune cell populations and reduced thymulin levels. Conclusions Our results support the hypothesis that thymic atrophy and reduced serum thymulin production are closely associated with the development of PFTS and may contribute to the immune alterations observed in affected piglets. Additionally, serum thymulin levels may provide a useful biomarker for the early detection of thymic dysfunction in pigs. Further research is needed to clarify the underlying mechanisms of this syndrome and to determine the role of other possible factors in its development.