Urbanization processes modulate the immunological challenges faced by animals.Urban habitat transformations reshape pathogen diversity and abundance,while high population density—common in urban exploiter species—pr...Urbanization processes modulate the immunological challenges faced by animals.Urban habitat transformations reshape pathogen diversity and abundance,while high population density—common in urban exploiter species—promotes disease transmission.Responses to urbanization may include adaptive adjustments of constitutive innate immune defenses(e.g.complement system and natural antibodies[NAbs]),which serve as first-line protection against infections.Here,we investigated associations of habitat urbanization and host population density with complement and NAbs in an urban bird,the feral pigeon Columba livia domestica.To do so,we employed the hemolysis-hemagglutination assay to analyze nearly 200 plasma samples collected across urbanization and pigeon population density gradients in five major cities in Poland.We found a negative association between urbanization score and hemagglutination(i.e.NAbs activity),but not hemolysis(i.e.complement activity),indicating either immunosuppression or adaptive downregulation of this immune defense in highly transformed urban landscape.Population density was not significantly related to either immune parameter,providing no evidence for densitydependent modulation of immune defenses.At the same time,there was a negative association of hemolysis with condition(scaled mass index),suggesting resource allocation trade-offs or contrasting effects of the urban environment on immune defenses and body condition.The results demonstrate that habitat structure can be an important factor shaping the immune defenses of the feral pigeon,although these associations were not mediated by variation in population density.Our study highlights the complexity of the links between immune defenses in wildlife and urbanization and reinforces the need for comprehensive ecoimmunological studies on urban animals.展开更多
During vertebrate development,the immune function is inefficient and is mainly controlled by innate defense.While there have been detailed studies of various aspects of innate immune function,the effects of this func&...During vertebrate development,the immune function is inefficient and is mainly controlled by innate defense.While there have been detailed studies of various aspects of innate immune function,the effects of this function in the growth of vertebrates is still not well known.Similarly,there is little information regarding how early endotoxin exposure would affect juvenile phenotypes,specifically in a non-model mammal like a precocial rodent.We evaluated the response to an antigen and its cost in offspring of the rodent Octodon degus.We inoculated pups at 4 different ages(8,15,22 and 30 days after birth)with an antigen to determine the ontogeny and costs of the response to an endotoxin.We assessed changes in body mass,body temperature,sickness behavior and the levels of a key mediator of the inflammatory response,the cytokine interleukin-1β.We also determined the effects of early endotoxin exposure on the resting metabolic rate of juvenile animals(i.e.90 days after birth).The cytokine levels,body mass and body temperature were unaffected by time of inoculation and treatment.However,pups subjected to inoculation at 22 days after birth with the antigen showed reduced locomotion.Juvenile resting metabolic rate was not affected by early endotoxin exposure.These results suggest that the magnitude of O.degus responses would not change with age.We discuss whether the lack of effect of the response on body mass or body condition is caused by environmental variables or by the precocial characteristics of O.degus.展开更多
基金financially supported by the research grant Preludium 16 of the National Science Centre in Poland(2018/31/N/NZ8/00832).
文摘Urbanization processes modulate the immunological challenges faced by animals.Urban habitat transformations reshape pathogen diversity and abundance,while high population density—common in urban exploiter species—promotes disease transmission.Responses to urbanization may include adaptive adjustments of constitutive innate immune defenses(e.g.complement system and natural antibodies[NAbs]),which serve as first-line protection against infections.Here,we investigated associations of habitat urbanization and host population density with complement and NAbs in an urban bird,the feral pigeon Columba livia domestica.To do so,we employed the hemolysis-hemagglutination assay to analyze nearly 200 plasma samples collected across urbanization and pigeon population density gradients in five major cities in Poland.We found a negative association between urbanization score and hemagglutination(i.e.NAbs activity),but not hemolysis(i.e.complement activity),indicating either immunosuppression or adaptive downregulation of this immune defense in highly transformed urban landscape.Population density was not significantly related to either immune parameter,providing no evidence for densitydependent modulation of immune defenses.At the same time,there was a negative association of hemolysis with condition(scaled mass index),suggesting resource allocation trade-offs or contrasting effects of the urban environment on immune defenses and body condition.The results demonstrate that habitat structure can be an important factor shaping the immune defenses of the feral pigeon,although these associations were not mediated by variation in population density.Our study highlights the complexity of the links between immune defenses in wildlife and urbanization and reinforces the need for comprehensive ecoimmunological studies on urban animals.
基金This study was funded by FONDECYT 3160133 to NRO and Millennium Institute of Immunology and Immunotherapy,Pontificia Universidad Católica de Chile。
文摘During vertebrate development,the immune function is inefficient and is mainly controlled by innate defense.While there have been detailed studies of various aspects of innate immune function,the effects of this function in the growth of vertebrates is still not well known.Similarly,there is little information regarding how early endotoxin exposure would affect juvenile phenotypes,specifically in a non-model mammal like a precocial rodent.We evaluated the response to an antigen and its cost in offspring of the rodent Octodon degus.We inoculated pups at 4 different ages(8,15,22 and 30 days after birth)with an antigen to determine the ontogeny and costs of the response to an endotoxin.We assessed changes in body mass,body temperature,sickness behavior and the levels of a key mediator of the inflammatory response,the cytokine interleukin-1β.We also determined the effects of early endotoxin exposure on the resting metabolic rate of juvenile animals(i.e.90 days after birth).The cytokine levels,body mass and body temperature were unaffected by time of inoculation and treatment.However,pups subjected to inoculation at 22 days after birth with the antigen showed reduced locomotion.Juvenile resting metabolic rate was not affected by early endotoxin exposure.These results suggest that the magnitude of O.degus responses would not change with age.We discuss whether the lack of effect of the response on body mass or body condition is caused by environmental variables or by the precocial characteristics of O.degus.
