Bridging science and spirituality: the intersection of religion and public health in the COVID-19 pandemic.

Background: The COVID-19 pandemic has had global impacts on social interactions and religious activities, leading to a complex relationship between religion and public health policies. This article reviews impact of the COVID-19 pandemic on religious activities and beliefs in relation to the spread of the virus, as well as the potential of religious leaders and faith communities in mitigating the impact of the pandemic through public health measures and community engagement. Methods: A literature review was conducted using PubMed and Google Scholar, with search terms including "religion," "COVID-19," "pandemic," "coronavirus," and "spirituality." We included English articles published between January 2020 and September 2022, focusing on intersection of religion and COVID-19. Results: We identified two main themes emerging, with the selected 32 studies divided in 15 studies focused on the relationship between religious practices, beliefs, and the spread of COVID-19, while 17 studies explored the role of religious leaders and faith communities in coping with and mitigating the impact of COVID-19. Religious activities were found to correlate with virus spread, particularly in early days of the pandemic. The relationship between religiosity and adherence to government guidelines was mixed, with some studies suggesting increased religiosity contributed to misconceptions about the virus and resistance to restrictions. Religious beliefs were also associated with vaccine hesitancy, particularly conservative religious beliefs. On the other hand, religious leaders and communities played a crucial role in adapting to COVID-19 measures, maintaining a sense of belonging, fostering emotional resilience, and upholding compliance with public health measures. The importance of collaboration between religious leaders, institutions, and public health officials in addressing the pandemic was emphasized. Conclusions: This review highlights the essential role of religious leaders, faith-based organizations, and faith communities in promoting education, preparedness, and response efforts during the COVID-19 pandemic. Engaging with religious leaders and communities can improve pandemic control and prevention efforts. Collaboration between religious leaders, governments, and healthcare professionals is necessary to combat vaccine hesitancy and ensure successful COVID-19 vaccination campaigns. The insights from this review can guide future research, policy development, and public health interventions to minimize the impact of the pandemic and improve outcomes for individuals and communities affected.

Involvement of Cxcl12a/Cxcr4b Chemokine System in Mediating the Stimulatory Effect of Embryonic Ethanol Exposure on Neuronal Density in Zebrafish Hypothalamus.

BACKGROUND: Embryonic exposure to ethanol (EtOH) produces marked disturbances in neuronal development and alcohol-related behaviors, with low-moderate EtOH doses stimulating neurogenesis without producing apoptosis and high doses having major cytotoxic effects while causing gross morphological abnormalities. With the pro-inflammatory chemokine system, Cxcl12, and its main receptor Cxcr4, known to promote processes of neurogenesis, we examined here this neuroimmune system in the embryonic hypothalamus to test directly if it mediates the stimulatory effects low-moderate EtOH doses have on neuronal development. METHODS: We used the zebrafish (Danio rerio) model, which develops externally and allows one to investigate the developing brain in vivo with precise control of dose and timing of EtOH delivery in the absence of maternal influence. Zebrafish were exposed to low-moderate EtOH doses (0.1, 0.25, 0.5% v/v), specifically during a period of peak hypothalamic development from 22 to 24 hours postfertilization, and in some tests were pretreated from 2 to 22 hpf with the Cxcr4 receptor antagonist, AMD3100. Measurements in the hypothalamus at 26 hpf were taken of cxcl12a and cxcr4b transcription, signaling, and neuronal density using qRT-PCR, RNAscope, and live imaging of transgenic zebrafish. RESULTS: Embryonic EtOH exposure, particularly at the 0.5% dose, significantly increased levels of cxcl12a and cxcr4b mRNA in whole embryos, number of cxcl12a and cxcr4b transcripts in developing hypothalamus, and internalization of Cxcr4b receptors in hypothalamic cells. Embryonic EtOH also caused an increase in the number of hypothalamic neurons and coexpression of cxcl12a and cxcr4b transcripts within these neurons. Each of these stimulatory effects of EtOH in the embryo was blocked by pretreatment with the Cxcr4 antagonist AMD3100. CONCLUSIONS: These results provide clear evidence that EtOH's stimulatory effects at low-moderate doses on the number of hypothalamic neurons early in development are mediated, in part, by increased transcription and intracellular activation of this chemokine system, likely due to autocrine signaling of Cxcl12a at its Cxcr4b receptor within the neurons.

Role of melanin-concentrating hormone in drug use disorders.

Melanin-concentrating hormone (MCH) is a neuropeptide primarily transcribed in the lateral hypothalamus (LH), with vast projections to many areas throughout the central nervous system that play an important role in motivated behaviors and drug use. Anatomical, pharmacological and genetic studies implicate MCH in mediating the intake and reinforcement of commonly abused substances, acting by influencing several systems including the mesolimbic dopaminergic system, glutamatergic as well as GABAergic signaling and being modulated by inflammatory neuroimmune pathways. Further support for the role of MCH in controlling behavior related to drug use will be discussed as it relates to cerebral ventricular volume transmission and intracellular molecules including cocaine- and amphetamine-regulated transcript peptide, dopamine- and cAMP-regulated phosphoprotein 32 kDa. The primary goal of this review is to introduce and summarize current literature surrounding the role of MCH in mediating the intake and reinforcement of commonly abused drugs, such as alcohol, cocaine, amphetamine, nicotine and opiates.

Moderate Prenatal Ethanol Exposure Stimulates CXCL12/CXCR4 Chemokine System in Radial Glia Progenitor Cells in Hypothalamic Neuroepithelium and Peptide Neurons in Lateral Hypothalamus of the Embryo and Postnatal Offspring.

BACKGROUND: Prenatal exposure to ethanol (EtOH) has lasting effects on neuropeptide and neuroimmune systems in the brain alongside detrimental alcohol-related behaviors. At low-to-moderate doses, prenatal EtOH stimulates neurogenesis in lateral hypothalamus (LH) and increases neurons that express the orexigenic peptides hypocretin/orexin (Hcrt/OX) and melanin-concentrating hormone (MCH), and the proinflammatory chemokine CCL2, which through its receptor CCR2 stimulates cell differentiation and movement. Our recent studies demonstrated that CCL2 and CCR2 colocalize with MCH neurons and are involved in EtOH's stimulatory effect on their development but show no relation to Hcrt/OX. Here, we investigated another chemokine, CXCL12, and its receptor, CXCR4, which promote neurogenesis and neuroprogenitor cell proliferation, to determine if they also exhibit peptide specificity in their response to EtOH exposure. METHODS: Pregnant rats were intraorally administered a moderate dose of EtOH (2 g/kg/d) from embryonic day 10 (E10) to E15. Their embryos and postnatal offspring were examined using real-time quantitative PCR and immunofluorescence histochemistry, to determine if EtOH affects CXCL12 and CXCR4 and the colocalization of CXCR4 with Hcrt/OX and MCH neurons in the LH and with radial glia neuroprogenitor cells in the hypothalamic neuroepithelium (NEP). RESULTS: Prenatal EtOH strongly stimulated CXCL12 and CXCR4 in LH neurons of embryos and postnatal offspring. This stimulation was significantly stronger in Hcrt/OX than MCH neurons in LH and also occurred in radial glia neuroprogenitor cells dense in the NEP. These effects were sexually dimorphic, consistently stronger in females than males. CONCLUSIONS: While showing prenatal EtOH exposure to have a sexually dimorphic, stimulatory effect on CXCL12 and CXCR4 in LH similar to CCL2 and its receptor, these results reveal their distinct relationship to the peptide neurons, with the former closely related to Hcrt/OX and the latter to MCH, and they link EtOH's actions in LH to a stimulatory effect on neuroprogenitor cells in the NEP.