Serological response after COVID-19 mRNA-1273 booster dose in immunocompromised patients, Taiwan, July to August 2021.

BACKGROUND: Whether immunocompromising conditions affect the immunogenicity of COVID-19 booster vaccination remains a concern, which impedes the vaccination campaign in people most vulnerable to COVID-19-associated morbidity and mortality. We aimed to evaluate the effect of immune dysfunction on immunogenicity of homologous and heterologous prime-boost COVID-19 vaccination. METHODS: Between July and August, 2021, 399 participants were randomized to receive ChAdOx1/ChAdOx1 8 weeks apart, ChAdOx1/mRNA-1273 8 weeks apart, ChAdOx1/mRNA-1273 4 weeks apart, and mRNA-1273/mRNA-1273 4 weeks apart. The anti-SARS-CoV-2 spike IgG antibody titers on the day before booster vaccination and 4 weeks after booster vaccination were compared between participants with and without immunocompromising conditions. RESULTS: Among ChAdOx1-primed participants, a trend of lower anti-SARS-CoV-2 spike IgG titers before booster vaccination were found in participants with autoimmune diseases (geometric means, 34.76 vs. 84.25 binding antibody units [BAU]/mL, P = 0.173), compared to those without. Participants receiving immunosuppressants and/or immunomodulators had significant lower anti-SARS-CoV-2 spike IgG titers before booster vaccination than those without (geometric means, 36.39 vs. 83.84 BAU/mL; P = 0.001). Among mRNA-1273-boosted participants, anti-SARS-CoV-2 spike IgG titers 4 weeks after booster vaccination were similar across all the strata. Participants with autoimmune diseases and receiving immunosuppressants and/or immunomodulators, had numerically lower anti-SARS-CoV-2 spike IgG titers 4 weeks after booster vaccination compared to those without (geometric means, 1474.34 vs. 1923.23 and 1590.61 vs. 1918.38 BAU/mL; P > 0.05). CONCLUSION: The immunogenicity of prime vaccination with ChAdOx1 decreased by immune dysfunction, but enhanced after receiving boost vaccination with mRNA-1273. Our study results support the efficacy of mRNA-1273 booster dose among immunocompromised hosts.

Antidepressant Effects of NSAIDs in Rodent Models of Depression-A Systematic Review.

In recent years much focus has been on neuroimmune mechanisms of depression. As a consequence, many preclinical and clinical trials have been performed examining potential antidepressant effects of several anti-inflammatory drugs. The results of such trials have been varied. With the current manuscript we wished to elucidate the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on depressive-like behaviour in rodent models of depression by performing a systematic review of the available literature. We performed a systematic literature search in PubMed for rodent models of depression where NSAIDs were administered and a validated measure of depressive-like behaviour was applied. 858 studies were initially identified and screened using Covidence systematic review software. Of these 36 met the inclusion criteria and were included. The extracted articles contained data from both rat and mouse studies but primarily male animals were used. Several depression models were applied and 17 different NSAIDs were tested for antidepressant effects. Our results suggest that stress models are the best choice when examining antidepressant effects of NSAIDs. Furthermore, we found that rat models provide a more homogenous response than mouse models. Intriguingly, the use of female animals was only reported in three studies and these failed to find antidepressant effects of NSAIDs. This should be explored further. When comparing the different classes of NSAIDs, selective COX-2 inhibitors were shown to provide the most stable antidepressant effect compared to non-selective COX-inhibitors. Suggested mechanisms behind the antidepressant effects were attenuation of neuroinflammation, HPA-axis dysregulation and altered monoamine expression.