Abstract
Nasal mucosa and olfactory bulb are separated by the cribriform plate which is perforated by olfactory nerves. We have previously demonstrated that the cribriform plate is permissive for T cells and monocytes and that viruses can enter the bulb upon intranasal injection by axonal transportation. Therefore, we hypothesized that nasal mucosa and olfactory bulb are equipped to deal with constant infectious threats. To detect genes involved in this process, we compared gene expression in nasal mucosa and bulb of mice kept under specific pathogen free (SPF) conditions to gene expression of mice kept on non-SPF conditions using RNA deep sequencing. We found massive alterations in the expression of immune-related genes of the nasal mucosa, while the bulb did not respond immunologically. The absence of induction of immune-related genes in the olfactory bulb suggests effective defence mechanisms hindering entrance of environmental pathogens beyond the outer arachnoid layer. The genes detected in this study may include candidates conferring susceptibility to meningitis.
Highlights
The nasal mucosa is a location of many facultative pathogenic germs, such as Haemophilus, Staphylococcus and Neisseria, which are potential causes of meningitis [1]
We worked with 60 samples from 30 seven weeks old animals consisting of 30 nasal mucosae (Fig 1) and 30 olfactory bulbs, 15 from specific pathogen free (SPF) and 15 non-SPF animals, respectively
It should be noted that changes in mRNA levels can be either caused by regulation of gene expression or changes in cell composition which both would be indicative of an immune response
Summary
The nasal mucosa is a location of many facultative pathogenic germs, such as Haemophilus, Staphylococcus and Neisseria, which are potential causes of meningitis [1]. Meningitis is an often lethal infectious disease which can affect children and adolescents without known immune defect. Neisseria meningitidis is a commensal resident of the human pharyngeal mucosa [2] where binding of neisserial colony opacity-associated protein adhesins (Opa) to carcinoembryonic antigen-related cell adhesion molecule CEACAM 1 induces an inflammatory response [3]. It has been calculated that less than 1 in 25,000 natural infections in humans lead to invasive meningococcal disease during endemic periods [4] rendering likely genetic variants driving invasive disease as it has been shown for deficiencies in the complement system [5]. The nasal mucosa is likely to be a site of permanent interaction with infectious.
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