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Wauters, J.

Publications and source records attributed to Wauters, J..

2 recordsLinked to original sources

Compromised futures: gastrointestinal parasites reduce survival and recruitment but not reproductive performance in wild female spotted hyenas (Crocuta crocuta)

BackgroundGastrointestinal parasitic (GIP) infections can decrease the survival and reproductive performance of humans and livestock. Even so, the immediate and delayed fitness consequences of GIP in unmanaged wild mammal populations, particularly during the sensitive and energetically demanding early life stage, remain largely unknown. MethodsWe investigate non-invasively the effects of GIP during early life on the survival to adulthood, age at first reproduction and longevity of 68 individually known female spotted hyenas in the Serengeti National Park, Tanzania. We also test whether a high investment in gastrointestinal local immunity (i.e. faecal mucin and immunoglobulin A) and an elevated allostatic load (i.e. faecal glucocorticoid metabolites) decrease these measures of performance, when controlling for resource availability and maternal effects (i.e. maternal social rank) using logistic regression and Cox proportional hazards models. ResultsAncylostoma sp. infections and the level of immunoglobulin A both negatively associate with survival to adulthood, probably because of the damage caused by the parasite and resource allocation trade-off between immunity and maintenance. Conversely, maternal social rank has a positive influence on survival to adulthood and longevity. Immune responses, allostatic load and GIP do not affect the age at first reproduction, suggesting either no effect, a complex interaction between different life stages, or a more immediate time-dependent effect. ConclusionOur study highlights the critical role of GIP infections and maternal effects on early-life fitness and long-term outcomes in females of a wild carnivore, thereby contributing to our understanding of ecological dynamics in unmanaged ecosystems.

ecology↗

Targeting C5aR1 signaling reduced neutrophil extracellular traps and ameliorates COVID-19 pathology

Patients with severe COVID-19 develop acute respiratory distress syndrome (ARDS) that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that complement component 5a (C5a), through its cellular receptor C5aR1, has potent proinflammatory actions, and plays immunopathological roles in inflammatory diseases, we investigated whether C5a/C5aR1 pathway could be involved in COVID-19 pathophysiology. C5a/C5aR1 signaling increased locally in the lung, especially in neutrophils of critically ill COVID-19 patients compared to patients with influenza infection, as well as in the lung tissue of K18-hACE2 Tg mice (Tg mice) infected with SARS-CoV-2. Genetic and pharmacological inhibition of C5aR1 signaling ameliorated lung immunopathology in Tg-infected mice. Mechanistically, we found that C5aR1 signaling drives neutrophil extracellular trap (NET)s-dependent immunopathology. These data confirm the immunopathological role of C5a/C5aR1 signaling in COVID-19 and indicate that antagonist of C5aR1 could be useful for COVID-19 treatment.

immunology↗