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Livestock production systems are complex and evolve over time, affecting their adaptability to economic, political, and disease-related changes. In Europe, disease resilience is crucial due to threats like the African swine fever virus, which jeopardizes pork production stability. The European Union identifies farm production type as a key risk factor for disease spread, making it important to track changes in farm production types to assess disease risk. However, detailed production type data is often lacking in national databases. For Swiss pig farms, we used prediction and clustering algorithms to classify 9’687 − 11’247 trading farms between 2014 and 2019 by one of eleven production types. We then analyzed the pig trade network and stratified farm centrality measures (ICC and OCC) by production type. We found that 145 farms belonging to three production types have substantially higher ICC and OCC than other farms, suggesting that they could be the target of disease surveillance programs. Our predictions until 2025 show an increase both in overall pig trade network connectivity and in proportion of production types with high ICC and OCC, indicating that the structural changes in the Swiss pig production system may increase infectious disease exposure over time.

Inflammation and skeletal homeostasis are closely intertwined. Inflammatory diseases are associated with local and systemic bone loss, and post-menopausal osteoporosis is linked to low-level chronic inflammation. Phosphoinositide-3-kinase signalling is a pivotal pathway modulating immune responses and controlling skeletal health. Mice deficient in Src homology 2–containing inositol phosphatase 1 (SHIP1), a negative regulator of the phosphoinositide-3-kinase pathway, develop systemic inflammation associated with low body weight, reduced bone mass, and changes in bone microarchitecture. To elucidate the specific role of the immune system in skeletal development, a genetic approach was used to characterise the contribution of SHIP1-controlled systemic inflammation to SHIP1-dependent osteoclastogenesis. Lymphocyte deletion entirely rescued the skeletal phenotype in Rag2 −/− /Il2rg −/− /SHIP1 −/− mice. Rag2 −/− /Il2rg −/− /SHIP1 −/− osteoclasts, however, displayed an intermediate transcriptomic signature between control and Rag2 +/+ /Il2rg +/+ /SHIP1 −/− osteoclasts while exhibiting aberrant in vitro development and functions similar to Rag2 +/+ /Il2rg +/+ /SHIP1 −/− osteoclasts. These data establish a cell-intrinsic role for SHIP1 in osteoclasts, with inflammation as the key driver of the skeletal phenotype in SHIP1-deficient mice. Our findings demonstrate the central role of the immune system in steering physiological skeletal development.