Search

The risk of severe outcomes following respiratory tract infections is significantly increased in individuals over 60 years, especially in those with chronic medical conditions, i.e., hypertension, diabetes, cardiovascular disease, dementia, chronic respiratory disease, and cancer. Down Syndrome (DS), the most prevalent intellectual disability, is caused by trisomy-21 in similar to 1:750 live births worldwide. Over the past few decades, a substantial body of evidence has accumulated, pointing at the occurrence of alterations, impairments, and subsequently dysfunction of the various components of the immune system in individuals with DS. This associates with increased vulnerability to respiratory tract infections in this population, such as the influenza virus, respiratory syncytial virus, SARS-CoV-2 (COVID-19), and bacterial pneumonias. To emphasize this link, here we comprehensively review the immunobiology of DS and its contribution to higher susceptibility to severe illness and mortality from respiratory tract infections.

A correction to this paper has been published: https://doi.org/10.1007/s12017-021-08657-z

Chicken gizzard telokin was purified to apparent homogeneity by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. This preparation yielded upon mass spectrometry analysis seven mass peaks spanning from 15 858 to 17 100 Da. Anion exchange-high performance liquid chromatography of the purified telokin revealed a high diversity of telokin molecules. By combining protein chemistry to chromatography and mass spectrometry, the telokin heterogeneity was analyzed. Three acetylated N-termini were found, AMI, MIS, and SGR. Cyanogen bromide cleavage of telokin yielded six different C-terminal peptides corresponding to the removal of one to six C-terminal glutamyl residues from the protein sequence deduced from the cDNA. Phosphorylation of telokin was detected, thus increasing the heterogeneity of the telokin preparation. In addition, peptide sequencing has shown that telokin contained either an aspartyl or a glutamyl residue at position 27, probably resulting from chicken polymorphism.

Neuroanatomical data show that olfactory mucosa (OM) is a possible place for interactions between nutrition and smell. A combination of differential display mRNA analysis together with a macroarray screening was developed to identify transcripts that are differentially expressed in rat OM following food deprivation. Using this method, backed on a stringent statistical analysis, we identified molecules that fell into several Gene Ontology terms including cellular and physiological process, signal transduction, and binding. Among the 15 most differentially expressed molecules, only one was upregulated, but 14 were downregulated in the fasted state among which was, unexpectedly, odorant-binding protein 1F (OBP-1F). Because of its potential relevance to olfactory physiology, we focused our further analysis on OBP-1F using in situ hybridization, quantitative polymerase chain reaction, and western blot analysis. OBP-1F was highlighted in the lateral nasal glands, but its expression (mRNA and protein) did not change following food deprivation. Only the minor fraction of OBP-1F mRNA expressed by the OM itself was downregulated following 48 h fasting. Altogether, our results suggest that the fine transcriptional control of OBP-1F in the OM following food deprivation could be efficient only at the local level, close to its site of secretion to participate in the perireceptor events of the olfactory signal reception.