Inflammation is a pervasive phenomenon that operates during severe perturbations of homeostasis, such as infection, injury, and exposure to contaminants, and is triggered by innate immune receptors that recognize pathogens and damaged cells. Among vertebrates, the inflammatory cascade is a complex network of immunological, physiological, and behavioral events that are coordinated by cytokines, immune signaling molecules. Although the molecular basis of inflammation is well studied, its role in mediating the outcome of host-parasite interactions has received minimal attention by ecologists. This review provides a synopsis of vertebrate inflammation, its life-history modulation, and its effects upon host-pathogen dynamics as well as host-commensal microbiota interactions in the gut. What emerges is evidence for phenotypic plasticity of inflammatory responses despite the apparently invariant and redundant nature of the immunoregulatory networks that regulate them.

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Sleep deprivation induces acute inflammation and increased glucocorticosteroids in vertebrates, but effects from fragmented, or intermittent, sleep are poorly understood. Considering the latter is more representative of sleep apnea in humans, we investigated changes in proinflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokine gene expression in the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) of a murine model exposed to varying intensities of sleep fragmentation (SF). Additionally, serum corticosterone was assessed. Sleep was disrupted in male C57BL/6J mice using an automated sleep fragmentation chamber that moves a sweeping bar at specified intervals (Lafayette Industries). Mice were exposed to bar sweeps every 20 s (high sleep fragmentation, HSF), 120 s (low sleep fragmentation, LSF), or the bar remained stationary (control). Trunk blood and tissue samples were collected after 24 h of SF. We predicted that HSF mice would exhibit increased proinflammatory expression, decreased anti-inflammatory expression, and elevated stress hormones in relation to LSF and controls. SF significantly elevated IL-1β gene expression in adipose tissue, heart (HSF only), and hypothalamus (LSF only) relative to controls. SF did not increase TNF-α expression in any of the tissues measured. HSF increased TGF-β1 expression in the hypothalamus and hippocampus relative to other groups. Serum corticosterone concentration was significantly different among groups, with HSF mice exhibiting the highest, LSF intermediate, and controls with the lowest concentration. This indicates that 24 h of SF is a potent inducer of inflammation and stress hormones in the periphery, but leads to upregulation of anti-inflammatory cytokines in the brain.

Polar environments are characterized by discrete periods of continuous light or darkness during the summer and winter months, respectively. Because the light/dark cycle serves as the primary Zeitgeber to synchronize rhythms of most organisms, its seasonal absence in polar regions poses challenges to the circadian organization of organisms that reside in these environments. Although some species become arrhythmic, others, such as migratory songbirds, are able to maintain an intact diurnal rhythm during polar summer. This suggests that birds may switch to alternative environmental cues, such as daily changes in light intensity and ambient temperature, which may have the potential to reset the biological clock. However, identifying the low-amplitude Zeitgeber that synchronizes rhythms in free-living polar-dwelling animals has been difficult to demonstrate. In this study, we measured behavioral and melatonin profiles of free-living Lapland longspurs (Calcarius lapponicus) near Barrow, Alaska (71°N) during the continuous daylight of summer in the Arctic. Diel cycles in activity and male singing were apparent throughout the polar day with a quiescence period of 4-5 hr starting around 24:00 Alaska Daylight Time. This inactivity corresponded with elevated melatonin profiles. In contrast, territorial aggression of males in response to a conspecific intruder was not dependent upon time-of-day. Diel changes in light intensity and ambient temperature were negatively associated with daily melatonin profiles after taking into account time-of-day effects. These results suggest that photic and thermal cues may act either as alternative Zeitgeber cues, or possibly masking agents. Distinguishing between these two possibilities will require further study.

Multidirectional interactions among the immune, endocrine, and nervous systems have been demonstrated in humans and non-human animal models for many decades by the biomedical community, but ecological and evolutionary perspectives are lacking. Neuroendocrine-immune interactions can be conceptualized using a series of feedback loops, which culminate into distinct neuroendocrine-immune phenotypes. Behavior can exert profound influences on these phenotypes, which can in turn reciprocally modulate behavior. For example, the behavioral aspects of reproduction, including courtship, aggression, mate selection and parental behaviors can impinge upon neuroendocrine-immune interactions. One classic example is the immunocompetence handicap hypothesis (ICHH), which proposes that steroid hormones act as mediators of traits important for female choice while suppressing the immune system. Reciprocally, neuroendocrine-immune pathways can promote the development of altered behavioral states, such as sickness behavior. Understanding the energetic signals that mediate neuroendocrine-immune crosstalk is an active area of research. Although the field of psychoneuroimmunology (PNI) has begun to explore this crosstalk from a biomedical standpoint, the neuroendocrine-immune-behavior nexus has been relatively underappreciated in comparative species. The field of ecoimmunology, while traditionally emphasizing the study of non-model systems from an ecological evolutionary perspective, often under natural conditions, has focused less on the physiological mechanisms underlying behavioral responses. This review summarizes neuroendocrine-immune interactions using a comparative framework to understand the ecological and evolutionary forces that shape these complex physiological interactions.