PubMed Health⌕ Search

Biomedical subjects

Yoh Ishiguro

Publications and source records attributed to Yoh Ishiguro.

9 recordsLinked to original sources
PubMed2006

Resistance to experimental colitis depends on cytoprotective heat shock proteins in macrophage migration inhibitory factor null mice.

Macrophage migration inhibitory factor plays an important role in inflammatory diseases. We investigated the role of macrophage migration inhibitory factor (MIF) in the development of dextran sulfate sodium (DSS)-induced colitis using MIF null ((-/-)) mice. MIF(-/-) mice given 3% DSS showed no clinical and histological feature of colitis in contrast to wild-type (WT) mice. Lack of MIF suppressed the up-regulation of TNF-alpha and IFN-gamma as Th1-derived cytokines, and increased the level of IL-4 as Th2-derived cytokine in the colon tissues. Moreover, we found that the expressions of heat shock protein (HSP)40 and HSP70 were markedly up-regulated in the colon of MIF(-/-) mice in response to DSS compared with WT mice. Additionally, quercetin, an inhibitor of HSP synthesis, inhibited the up-regulation of HSP40 and 70 expressions and developed DSS-induced colitis in MIF(-/-) mice. Our findings in this study provide more information in the role of MIF in colitis.

Animals↗
PubMed2006

The role of macrophage migration inhibitory factor in lethal Listeria monocytogenes infection in mice.

Macrophage migration inhibitory factor (MIF) has been characterized as a proinflammatory cytokine. Previous studies have indicated that MIF may play a beneficial role or a detrimental role in microbial infections, depending on pathogens. In this study, we investigated the role of MIF in Listeria monocytogenes infection. The MIF titers increased 6h after lethal L. monocytogenes infection but not in the sublethal infection. The elimination of bacteria from the spleens and livers was not affected by anti-MIF antibody (Ab) injection in the sublethal infection, whereas anti-MIF Ab treatment rescued mice from the lethal infection, suggesting that MIF plays a deteriorating role in lethal L. monocytogenes infection. Anti-MIF Ab treatment significantly augmented interleukin (IL)-10 production in the spleens and livers 24h after infection, suggesting that MIF might down-regulate IL-10 production. Although the administration of anti-IL-10 monoclonal Ab showed no significant effect on the bacterial growth in the organs, the bacterial infection was deteriorated by the combined administration of Abs against MIF and IL-10. On the other hand, anti-MIF Ab treatment also increased in the serum cortisol titer 6h after infection compared with the control immunoglobulin G-injected group. Depletion of endogenous IL-10 decreased serum cortisol titers. These results suggested that IL-10 and cortisol might be involved in the deteriorating effect of MIF on lethal L. monocytogenes infection.

Animals↗
PubMed2006

Macrophage migration inhibitory factor has a proinflammatory activity via the p38 pathway in glucocorticoid-resistant ulcerative colitis.

Macrophage migration inhibitory factor (MIF) is a cytokine that has potent anti-steroid effects and might be implicated in the pathogenesis of Ulecrative colitis (UC). We defined the functional role of MIF in the glucocorticoid (GC)-resistant inflammatory response in UC. Twenty-four colonic samples were obtained from GC responsive cases, GC refractory cases, Crohn's disease and controls. LPMC were isolated from surgical specimens. MIF was strongly expressed at mRNA levels in refractory cases rather than responsive cases with UC and controls. IL-8 production from LPMC was significantly reduced by GC addition in responsive cases but not in refractory cases. In refractory cases, anti-MIF Ab ameliorated GC-resistant IL-8 production and p38-MAPK activity of LPMC. In addition, p38-MAPK antagonist SB230580 also ameliorated GC-resistant IL-8 production. These results suggest that MIF has an additional proinflammatory activity through the p38-MAPK pathway in GC-resistant UC.

Adolescent↗
PubMed2004

The presentation of haptenated proteins and activation of T cells in the mesenteric lymph nodes by dendritic cells in the TNBS colitis rat.

We described the role of dendritic cells (DCs) in aspects of T cell activation at the mesenteric lymph nodes (MLN) in trinitrobenzene sulfonic acid (TNBS)-induced colitis. An antigenic-immune response is induced at the MLN, and dendritic cells are the affected cell type. Cross-linking and GRO/CINC-1 have synergistic effects for DC maturation.

Animals↗
PubMed2004

Transforming growth factor-{beta} regulates susceptibility of epithelial apoptosis in murine model of colitis.

Transforming growth factor (TGF)-beta has a key role in intestinal homeostasis. Our present data suggest that TGF-beta, which was constitutively expressed by lamina propria mononuclear cells and epithelium, affected epithelial cells. Abnormal suppression of TGF-beta could enhance the sensitivity of epithelial cells to apoptosis associated with interferon-gamma in DSS-induced colitis.

Animals↗