Urban habitats can shape interactions between hosts and parasites by altering not only exposure rates but also within-host processes. Artificial light at night (ALAN) is common in urban environments, and chronic exposure can impair host immunity in ways that may increase infection. However, studies of causal links between this stressor, immunity, and infection dynamics are rare, particularly in migratory animals. Here, we experimentally tested how ALAN affects cellular immunity and haemosporidian parasite intensity across the annual cycle of migrant and resident subspecies of the dark-eyed junco ( Junco hyemalis ). We monitored an experimental group exposed to light at night and a control group under natural light/dark cycles as they passed through short days simulating early spring to longer days simulating the breeding season, followed by autumn migration. Using generalized additive mixed models, we show that ALAN increased inflammation, and leucocyte counts were greatest in early spring and autumn. At the start of the experiment, few birds had active infections based on microscopy, but PCR revealed many birds had chronic infections. ALAN increased parasitaemia across the annual cycle, with strong peaks in spring and autumn that were largely absent in control birds. As birds were kept in indoor aviaries to prevent vector exposure, this increased parasitaemia indicates relapse of chronic infection during costly life-history stages (i.e. reproduction). Although the immunological and parasitological time series were in phase for control birds, cross-correlation analyses also revealed ALAN desynchronized leucocyte profiles and parasitaemia, which could suggest a general exaggerated inflammatory response. Our study shows how a common anthropogenic influence can shape within-host processes to affect infection dynamics.
14Urban habitats can shape interactions between hosts and parasites by altering within-host 15 processes such as resistance. Artificial light at night is common in urban environments, and 16 chronic exposure can impair host immunity in ways that may increase infection. However, 17 studies of causal links between this stressor, immunity, and infection dynamics are rare, 18 particularly in migratory animals. Here, we experimentally tested how artificial light at night 19 affects cellular immunity and haemosporidian parasite intensity across the annual cycle of 20 migrant and resident subspecies of the dark-eyed junco (Junco hyemalis). We monitored an 21 experimental group exposed to light at night and a control group under nighttime darkness as 22 they passed through short days simulating early spring to longer days simulating the breeding 23 season, followed by fall migration. Using generalized additive models, we show that artificial 24 light at night increased inflammation, and leukocyte counts were greatest in early spring and fall. 25At the start of the experiment, few birds had active infections based on microscopy, but PCR 26 revealed many birds had chronic infections. Artificial light at night increased parasitemia across 27 the annual cycle, with strong peaks in spring and fall that were largely absent in control birds. As 28 birds were kept in indoor aviaries to prevent vector exposure, this increased parasitemia indicates 29 relapse of chronic infection during costly life history stages (i.e., reproduction). Although the 30 immunological and parasitological time series were in phase for control birds, cross-correlation 31 analyses also revealed artificial light at night desynchronized leukocyte profiles and parasitemia, 32 which could suggest a general exaggerated inflammatory response. Our study shows how a 33 common anthropogenic influence can shape within-host processes to affect infection dynamics. 34 35 As suburban and urban habitats expand globally, certain species are attracted to these 36 environments owing to a combination of altered microclimate, predation risk, and resource 37 availability [1,2]. Such changes in biotic and abiotic conditions can have cascading and complex 38 effects on wildlife [3,4]. When considering infectious disease, urban habitats can shape the 39 interactions between hosts and parasites by altering within-host processes such as resistance or 40 tolerance [5]. Understanding how urbanization affects these processes is especially important, as 41 it can facilitate novel cross-species transmission opportunities between various host species [6]. 42 One aspect of urban habitats that could have strong effects on these within-host processes 43 is artificial light at night (ALAN). By altering animal circadian rhythms, ALAN can cause a suite 44 of physiological changes relevant to infection [7]. In particular, chronic exposure to ALAN can 45 suppress various aspects of host immune function, including cellular response and microbial 46killing ability [8,9]. Prolonged ambient lig...
Substantial evidence suggests a role for immunotherapy in treating Alzheimer's disease (AD). Several monoclonal antibodies targeting aggregated forms of beta amyloid, have been shown to reduce amyloid plaques and in some cases, mitigate cognitive decline in early-stage AD patients. We sought to determine if genetically engineered macrophages could improve the targeting and degradation of amyloid plaques. Chimeric antigen receptor macrophages (CAR-Ms), which show promise as a cancer treatment, are an appealing strategy to enhance target recognition and phagocytosis of amyloid plaques in AD. We genetically engineered macrophages to express a CAR containing the anti-amyloid antibody aducanumab as the external domain and the Fc receptor signaling domain internally. CAR-Ms recognize and degrade beta amyloid; in vitro and on APP/PS1 brain slices ex vivo; however, when injected intrahippocampally, these first-generation CAR-Ms have limited persistence and fail to reduce plaque load. We overcame this limitation by creating CAR-Ms that secrete M-CSF and self-maintain without exogenous cytokines. These CAR-Ms have greater survival in the brain niche, and significantly reduce plaque load locally in vivo. These proof-of-principle studies demonstrate that CAR-Ms, previously only applied to cancer, may be utilized to target and degrade unwanted materials, such as amyloid plaques in the brains of AD mice.
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