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Introduction: Parents of preterm infants face a stressful life event which might have long term impact on the parent-child relation as well as on the infant's cognitive and socio-emotional development. Both music therapy (MT) and physical contact (PC) are stress-reducing interventions for parents and preterm infants on the neonatal intensive care unit (NICU). Meanwhile, especially close PC is considered as standard care (SC) in most NICUs. However, the effect of live performed MT with PC on parental perceived stress and cortisol levels has barely been investigated. We hypothesized that MT with PC leads to reduced stress levels and lower salivary cortisol concentrations compared to SC in parents of preterm infants during the first 4 weeks after birth. Methods: Randomized-controlled trial enrolling the parents of 99 preterm infants (MT n = 50, SC n = 49 infants). The infants received either MT with PC or SC only. Perceived stress was measured with the perceived stress questionnaire 20 (PSQ-20) after birth and 4 weeks later. Salivary cortisol levels were obtained and measured weekly after birth for 4 weeks. Results: Forty-two mothers and eight fathers of the intervention group (MT with PC) as well as n = 43 mothers and n = 6 fathers of the control group (SC) were enrolled. For the intervention group, salivary cortisol was reduced 4 weeks after birth [mothers 5.5 nmol/l (confidence interval (CI) 3.6-7.5); fathers 8.3 (CI 7.2-9.4)] compared to the control group [mothers 10.3 nmol/l (CI 5.4-15.3); fathers 14.8 (CI 8.9-20.7)]. Overall perceived stress scores decreased in the intervention group (mothers -17.6; fathers -12.6) and increased in the control group (mothers +6.1; fathers +21.4) over 4 weeks. Discussion: Live-performed MT with PC in preterm infants might be an effective, non-invasive intervention to reduce parental stress and cortisol levels. Future studies should investigate the long-term effects of this intervention on the parent-infant relation as well as on the infants' cognitive and socio-emotional development. [ABSTRACT FROM AUTHOR]

Tissues often experience hypoxia at sites of inflammation due to malperfusion, massive immune cell recruitment, and increased oxygen consumption. Organisms adapt to these hypoxic conditions through the transcriptional activation of various genes. In fact, there is significant crosstalk between the transcriptional responses to hypoxia and inflammatory processes. This interaction, named inflammatory hypoxia, plays a crucial role in various diseases including malignancies, chronic inflammatory lung diseases, and sepsis. To further elucidate the crosstalk between hypoxia and inflammation in vivo and assess its potential for innovative therapies, our study aimed at investigating the impact of acute hypoxic conditions on inflammation-induced immune responses. To this end, we exposed healthy human subjects to hypoxia either before (hypoxia priming) or after a single intravenous (i.v.) injection of 0.4 ng/kg LPS. Our data show that hypoxia exposure prior to LPS injection (hypoxia priming) amplified the proinflammatory response. This was reflected by an increase in body temperature, plasma noradrenaline levels, and the production of proinflammatory cytokines (i.e., IL-6 and TNF-α), compared with LPS control conditions. These effects were not observed when participants were exposed to hypoxia after LPS administration, demonstrating that the interaction between hypoxia and inflammation highly depends on the timing of both stimuli. Our findings suggest that acute hypoxia (i.e., hypoxia priming) modulates transient inflammation, leading to an enhanced proinflammatory response in healthy human subjects. This highlights the need for further investigations to understand the pathology of various hypoxia-inducible factor (HIF)-associated inflammatory diseases and to develop suitable, innovative therapies. NEW & NOTEWORTHY: To our knowledge, this is the first in vivo study investigating the effects of hypoxia preceding (hypoxia priming) or following LPS administration on the endotoxin-induced inflammatory response in healthy human subjects. The data show that hypoxia priming amplified the proinflammatory response, reflected by an increased body temperature, increased plasma noradrenaline levels, and higher production of proinflammatory cytokines (i.e., IL-6 and TNF-α) compared with LPS control conditions. [ABSTRACT FROM AUTHOR]

The brain and immune system communicate through complex bidirectional pathways, but the specificity by which the brain perceives or even remembers alterations in immune homeostasis is still poorly understood. Recent data revealed that immune-related information under peripheral inflammatory conditions, termed as "immunengram", were represented in specific neuronal ensembles in the insular cortex (IC). Chemogenetic reactivation of these neuronal ensembles was sufficient to retrieve the inflammatory stages, indicating that the brain can store and retrieve specific immune responses. Against this background, the current approach was designed to investigate the ability of the IC to process states of immunosuppression pharmacologically induced by the mechanistic target of rapamycin (mTOR) inhibitor rapamycin. We here show that the IC perceives the initial state of immunosuppression, reflected by increased deep-brain electroencephalography (EEG) activity during acute immunosuppressive drug treatment. Following an experienced period of immunosuppression, though, diminished splenic cytokine production as formerly induced by rapamycin could not be reinstated by nonspecific chemogenetic activation or inhibition of the IC. These findings suggest that the information of a past, or experienced status of pharmacologically induced immunosuppression is not represented in the IC. Together, the present work extends the view of immune-to-brain communication during the states of peripheral immunosuppression and foster the prominent role of the IC for interoception. [ABSTRACT FROM AUTHOR]