Olfactory function in children with cystic fibrosis.
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Adolescent↗
Biomedical subjects
Christian A Mueller
Publications and source records attributed to Christian A Mueller.
A self-administered odor identification test procedure using the "Sniffin' Sticks".
Assessment of smell function in clinical routine is often limited due to a lack of time and/or costs of the personnel administering the test. The aim of the present study was to validate a procedure allowing for self-administered olfactory testing in a clinical setting. Seventy-four healthy subjects (13 male, 61 female) from 18 to 30 years of age (mean 20.3 years) were tested on 2 days (interval 7-21 days, mean 8.7 days) with 16 odors of the "Sniffin' Sticks" identification test kit. On one occasion, the test was administered by an examiner. On another occasion, subjects administered the test to themselves, with the odors being identified after they had been "painted" on a sheet of paper. No significant differences were obtained between the results from both test procedures. With a maximum score of 16, assisted testing yielded a mean score of 13.7 [standard deviation (SD) 1.3] while the self-administered procedure yielded an average score of 13.8 (SD = 1.5) (P = 0.72). The mean difference between the assisted and the self-administered smell test procedures was 0.05 (SD = 1.28). The 95% confidence interval of differences ranged from -2.51 to 2.61. These results suggest that odor identification with the Sniffin' Sticks can also be administered by the subjects themselves.
Adolescent↗
Spinal cord injury-induced expression of the immune-regulatory chemokine interleukin-16 caused by activated microglia/macrophages and CD8+ cells.
OBJECT: Spinal cord injury (SCI) elicits a strong inflammatory response that readily participates in lipid oxygenation, edema formation, apoptotic cell death, and tissue remodeling. Because cytokines determine the postinjury inflammatory milieu, the authors analyzed the expression of the immunomodulatory chemokine interleukin- 16 (IL- 16) after SCI. METHODS: The authors detected a highly significant, persistent, lesional accumulation of parenchymal IL-16+ microglia/macrophages, which reached a maximal level 3 days postinjury compared with control rats. The majority of cells that demonstrated positive labeling for IL-16 also had positive labeling for ED1 (> 70%) and OX-8/CD8; these cells exhibited the morphological hallmarks of activated microglia/macrophages and pronounced MHC Class II expression. In contrast to IL-16+ED1+ cells, IL-16+ microglia/macrophages that coexpressed OX-8 were exclusively seen in the pannecrotic lesion core. In addition, clustering of IL-16+ cells was observed in perivascular Virchow-Robin-like spaces in areas of the primary injury (lesion core) and in immediately adjacent areas of secondary injury. Furthermore, on Day 3 postinjury, IL-16+ microglia/macrophages were frequently observed in a perineuronal position. CONCLUSIONS: The early lesional accumulation of IL-16+ microglia/macrophages suggests a role for IL-16 in the early postinjury immune response such as recruitment and activation of immune cells, leading to microvessel clustering and secondary damage progression.
Animals↗
Expression of interleukin-16 by microglial cells in inflammatory, autoimmune, and degenerative lesions of the rat brain.
Here we report a comparative analysis of interleukin-16 (IL-16) expression by microglial cells of the normal rat brain in trimethyltin (TMT) neurotoxicity, experimental autoimmune uveitis (EAU), encephalomyelitis (EAE), and viral infection (Borna disease, Borna disease virus) by immunohistochemistry. Striking differences were observed. In contrast to the human brain, IL-16 was not expressed constitutively in the rat brain. Remote activation of microglial cells of the optic tract in EAU did not result into IL-16 expression. TMT intoxication induced expression in microglial cells of the hippocampus. In EAE and BDV, massive IL-16(+) microglial cells could be seen. Thus, IL-16 is a descriptor of microglial cell activation that discriminates between different disease models, and might be a valuable marker for the detection of microglia activation in human and rat central nervous system (CNS) diseases.
Animals↗
Accumulation of the proinflammatory cytokine endothelial-monocyte-activating polypeptide II in ramified microglial cells in brains of Borna virus infected Lewis rats.
Borna disease virus (BDV) infection of adult Lewis rats induces a severe and often fatal neurologic disease characterized by a massive mononuclear meningo-encephalitis, and activation of microglial cells. Therefore, we analyzed expression of endothelial monocyte activating polypeptide II (EMAP II) by immunohistology as a marker for activation of microglial cells in BDV infected rat brains. EMAP II is a chemotactic peptide, inducing activation of macrophages and endothelial cells, and is considered a proinflammatory mediator of the innate immune system. An up to 30-fold increase in numbers of EMAP II+ microglial cells and a massive expression by infiltrating macrophages at perivascular inflammatory foci was observed in infected brains, with a maximum on day 25 after infection. These results provide evidence that EMAP II contributes to immune responses in inflammatory processes caused by viral infections.
Animals↗