The aim of this study was to clarify the association between tongue pressure and factors related to sarcopenia such as aging, activities of daily living, nutritional state, and dysphagia. One-hundred-and-four patients without a history of treatment of stroke and without a diagnosis of neurodegenerative disease (36 men and 68 women), with a mean age of 84.1 ± 5.6 years, hospitalized from May 2013 to June 2013 were included in this study. Maximum voluntary tongue pressure against the palate (MTP) was measured by a device consisting of a disposable oral balloon probe. Nutritional and anthropometric parameters such as serum albumin concentration, Mini-Nutritional Assessment short form (MNA-SF), body mass index, arm muscle area (AMA), and others and presence of sarcopenia and dysphagia were analyzed to evaluate their relationships. Correlation analysis and univariate or multivariate analysis were performed. Simple correlation analysis showed that MTP correlated with Barthel index (BI), MNA-SF, serum albumin concentration, body mass index, and AMA. Univariate and multivariate analysis showed that sarcopenia, BI, MNA-SF, and age were the independent explanatory factors for decreased MTP, and the propensity score for dysphagia, including causes of primary or secondary sarcopenia, and the presence of sarcopenia were significantly associated with the presence of dysphagia. Decreased MTP and dysphagia were related to sarcopenia or the causes of sarcopenia in the studied population. Furthermore, the clinical condition of sarcopenic dysphagia may be partially interpreted as the presence of sarcopenia and causal factors for sarcopenia.

Sarcopenia was an independent risk factor for dysphagia among older individuals. However, further studies are required to define causality.

This study provides evidence for sarcopenic dysphagia and its risk factors. Preventive and therapeutic interventions require further study.

Secondary lymphoid tissue chemokine (SLC) is a CC chemokine expressed mainly in lymph nodes, appendix and spleen, and specifically chemotactic for lymphocytes (Nagira et al., J. Biol. Chem. 1997. 272: 19518-19524). Here, we carried out transendothelial migration assays to determine the classes and subsets of lymphocytes migrating toward SLC. SLC attracted freshly isolated B cells with high efficiency and T cells modestly. Thus, SLC is the first CC chemokine with a strong chemotactic activity on fresh B cells. Among T cell types and subsets, SLC broadly attracted CD4+ and CD8+ cells, CD45RO- (naive) and CD45RO+ (memory) cells, and CD26high (activated) and CD26low- (resting) cells. SLC also attracted both L-selectin+ and L-selectin- subpopulations of various T cell subsets and B cells. Furthermore, mitogenic stimulation strongly enhanced migratory responses of T cells and B cells toward SLC. By in situ hybridization, SLC mRNA was detected in the cortical parafollicular regions (the T cell areas) of a lymph node and an appendix. Collectively, SLC may be a basic chemokine supporting homeostatic migration of a broad spectrum of lymphocytes into the secondary lymphoid tissues. SLC may also be involved in immune responses by inducing highly efficient migration of T and B cells following antigenic stimulation.

EBI1-ligand chemokine (ELC) is a CC chemokine constitutively expressed in various lymphoid tissues and a high-affinity functional ligand for EBI1/CCR7, a seven transmembrane G-protein-coupled receptor originally identified as an Epstein-Barr virus (EBV)-inducible gene. Here we examined chemotactic activity of ELC on peripheral blood leukocytes. ELC attracted both CD4+ and CD8+ T cells, particularly efficiently after activation with IL-2 or with phytohemagglutinin (PHA) plus IL-2, as well as CD19+ B cells, but not CD16+ NK cells, CD14+ monocytes or neutrophils. Among CD3+ T cells, ELC attracted both CD45RO- naive and CD45RO+ memory subsets. ELC also induced vigorous calcium mobilization in T cells stimulated with IL-2 with an ED50 of 3 nM. ELC fused with the secreted form of alkaline phosphatase (ELC-SEAP) specifically bound to lymphocytes and this binding was blocked only by ELC among 10 CC chemokines so far tested. Notably, lymphocytes stimulated with IL-2 or T cells expanded by PHA plus IL-2 showed much higher levels of binding than fresh lymphocytes. Consistently, CCR7 mRNA was detected in CD4+ and CD8+ T cells as well as B cells, but not in NK cells, monocytes or neutrophils, and was dramatically increased in T cells upon treatment with IL-2 or with PHA plus IL-2. Like ELC mRNA, CCR7 mRNA was expressed in various lymphoid tissues. By in situ hybridization, ELC and CCR7 mRNA were detected in the parafollicular and inner cortical regions of a lymph node, and in the parafollicular regions of an appendix. Collectively, ELC and CCR7 may be involved in the trafficking of a broad spectrum of lymphocytes, especially activated T cells, into and within various lymphoid tissues.