Neutrophils and macrophages are critical to the innate immune response, but cooperative mechanisms used by these cells to combat extracellular pathogens are not well understood. This study reveals that S100A9-deficient neutrophils produce higher levels of mitochondrial superoxide in response to Staphylococcus aureus and, as a result, form neutrophil extracellular traps (suicidal NETosis). Increased suicidal NETosis does not improve neutrophil killing of S. aureus in isolation but augments macrophage killing. NET formation enhances antibacterial activity by increasing phagocytosis by macrophages and by transferring neutrophil-specific antimicrobial peptides to them. Similar results were observed in response to other phylogenetically distinct bacterial pathogens including Streptococcus pneumoniae and Pseudomonas aeruginosa, implicating this as an immune defense mechanism that broadly enhances antibacterial activity. These results demonstrate that achieving maximal bactericidal activity through NET formation requires macrophages and that accelerated and more robust suicidal NETosis makes neutrophils adept at increasing antibacterial activity, especially when A9 deficient.
Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow ( Passer domesticus ), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.
Light pollution is a growing problem, but its impacts on infectious disease risk have not been considered. Previous research has revealed that dim light at night (dLAN) dysregulates 25 various immune functions and biorhythms, which hints that dLAN could change the risk of disease epidemics. Here, we demonstrate that dLAN enhances infectiousness of the house sparrow (Passer domesticus), an urban-dwelling avian host of West Nile virus (WNV).Sparrows exposed to dLAN maintained viral titers above the transmission threshold to a biting vector (10 5 plaque-forming units) for two days longer than controls but did not die at higher 30 2 rates. A mathematical model revealed that such effects could increase WNV outbreak potential by ~41%. dLAN likely affects other host and vector traits relevant to transmission, so additional research is needed to advise management of zoonotic diseases in light polluted areas.Main Text: Among the many anthropogenic changes that impact humans and wildlife, one of 35 the most pervasive but least understood is light pollution (1). Light pollution takes many forms (i.e. sky glow, light clutter, glare; 2), but dim light at night (dLAN) is exceptionally common and important in both urban centers and non-urban areas including farms, airports, warehouses, and wherever lighting is necessary for human activities at night (Fig. 1). Indeed, greenspaces near roadways experience extensive dLAN exposure from billboards, street lamps, residential 40 lighting, and headlights emanating from passing vehicles (3).Although dLAN is widespread, its effects on human and wildlife health have been under-studied.Early research on human health found that individuals working throughout the night routinely suffer higher rates of Type II diabetes, heart conditions and other non-infectious maladies 45 compared to day-working staff (4). The recent switch to energy efficient night-lighting, which has converted incandescent bulbs to short wavelength cool white LEDs, may increase health risk further. In domesticated rodents, such short wavelength light has been linked to metabolic dysregulation, immunosuppression, and the development of some cancers (4). Levels of blue light as low as 0.2 lux can suppress melatonin secretion in humans (5,6), and in wildlife, 50 comparable forms of dLAN alter many behavioral, life history, and physiological traits (7,8).Despite the diverse and strong effects of dLAN, no study has yet investigated whether and to what degree it might affect infectious disease risk. This is surprising given the pervasiveness of
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