The association of race and ethnicity on obstetric patients' COVID-19 outcomes: A summary of current literature.

Amidst the ongoing coronavirus disease 2019 (COVID-19) pandemic, evidence suggests racial and ethnic disparities in COVID-19-related outcomes. Given these disparities, it is important to understand how such patterns may translate to high-risk cohorts, including obstetric patients. A PubMed search was performed to identify studies assessing pregnancy, neonatal, and other health-related complications by race or ethnicity in obstetric patients with COVID-19 infection. Forty articles were included in our analysis based on novelty, relevance, and redundancy. These articles revealed that Black and Hispanic obstetric patients present an increased risk for SARS-CoV-2 infection and maternal mortality; racial and ethnic minority patients, particularly those of Black and Asian backgrounds, are at increased risk for hospitalization and ICU admission; racial and ethnic minority groups, in particular Black patients, have an increased risk for mechanical ventilation; Black and Hispanic patients are more likely to experience dyspnea; Hispanic patients showed higher rates of pneumonia; and Black patients present an increased risk of acute respiratory distress syndrome (ARDS). There is conflicting literature on the relationship between race and ethnicity and various pregnancy and neonatal outcomes. Several factors may underly the racial and ethnic disparities observed in the obstetric population, including biological mechanisms and social determinants of health.

Distinct Th17 effector cytokines differentially promote microglial and blood-brain barrier inflammatory responses during post-infectious encephalitis.

Group A Streptococcus (GAS) infections can cause neuropsychiatric sequelae in children due to post-infectious encephalitis. Multiple GAS infections induce migration of Th17 lymphocytes from the nose into the brain, which are critical for microglial activation, blood-brain barrier (BBB) and neural circuit impairment in a mouse disease model. How endothelial cells (ECs) and microglia respond to GAS infections, and which Th17-derived cytokines are essential for these responses are unknown. Using single-cell RNA sequencing and spatial transcriptomics, we found that ECs downregulate BBB genes and microglia upregulate interferon-response, chemokine and antigen-presentation genes after GAS infections. Several microglial-derived chemokines were elevated in patient sera. Administration of a neutralizing antibody against interleukin-17A (IL-17A), but not ablation of granulocyte-macrophage colony-stimulating factor (GM-CSF) in T cells, partially rescued BBB dysfunction and microglial expression of chemokine genes. Thus, IL-17A is critical for neuropsychiatric sequelae of GAS infections and may be targeted to treat these disorders.