Guillaume, J. | Search bioRxiv

bioRxiv2025

Pathway diversity: a resilience metric sensitive to agency applied to a lake eutrophication problem

Measuring resilience has been a longstanding challenge in social-ecological research. While there are established resilience metrics, they often do not account for agency, which is crucial in social-ecological systems. Pathway diversity is a recent approach to measuring resilience that integrates systems thinking with individual-based elements, such as agency. According to this approach, resilience is larger if actors have more decision pathways and can maintain them over time. Here we measure resilience using pathway diversity within a lake eutrophication model to analyse (a) the extent to which it is sensitive to changes in agency and (b) its compatibility with more established resilience metrics. Our findings reveal that pathway diversity is sensitive to regime shifts and can provide early warnings of them. Through five policy decision-making scenarios, we then show how pathway diversity can capture constraints on decision makers capability and agency that affect the systems resilience. We find that higher pathway diversity is associated with greater capability of decision-makers to influence the system. Pathway diversity addresses a critical gap by incorporating agency into a resilience metric while remaining compatible with established metrics. This work shows the potential of pathway diversity to identify resilience-based policy implications.

ecology↗

bioRxiv2021

Conditional deletion of HIF-1α provides new insight regarding the murine response to gastrointestinal infection with Salmonella Typhimurium

The hypoxia-inducible transcription factor 1 (HIF-1) has been shown to ameliorate different bacterial infections through enhancement of microbial killing. While the impact of HIF-1 on inflammatory diseases of the gut has been studied intensively, its function in bacterial infections of the intestine remains largely elusive. With the help of a publicly available gene expression data set, we could infer significant activation of the HIF-1 transcription factor after oral infection of mice with Salmonella Typhimurium. This prompted us to apply lineage-restricted deletion of the Hif1a locus in mice to examine cell type-specific functions of HIF-1 in this model. We show hypoxia-independent induction of HIF-1 activity upon Salmonella infection in the intestinal epithelium as well as in macrophages. Surprisingly, Hif1a deletion in intestinal epithelial cells impacted neither disease outcome nor inflammatory activity. The conditional knockout of Hif1a in myeloid cells enhanced the mRNA expression of the largely pro-inflammatory chemokine Cxcl2, revealing a potentially inflammatory effect of HIF-1 deficiency in myeloid cells in the gut in vivo. Again, the disease outcome was not affected. In vitro HIF-1-deficient macrophages showed an overall impaired transcription of pro-inflammatory factors, however, Salmonella bypassed direct intracellular, bactericidal HIF-1-dependent mechanisms in a Salmonella pathogenicity island (SPI)-2 independent manner. Taken together, our data suggest that HIF-1 in intestinal epithelial and myeloid cells is either dispensable or compensable in the immune defense against Salmonella Typhimurium.

microbiology↗