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Dive into the research topics where Toshinobu Kuroishi is active.

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Featured researches published by Toshinobu Kuroishi.


Clinical & Experimental Allergy | 2007

Lipopolysaccharide promotes and augments metal allergies in mice, dependent on innate immunity and histidine decarboxylase.

Naoki Sato; Masayuki Kinbara; Toshinobu Kuroishi; Keiko B. Kimura; Yoichiro Iwakura; Hiroshi Ohtsu; Shunji Sugawara; Yasuo Endo

Background Few adequate murine models exist for metal allergies, it being especially difficult to induce Ni allergy in mice.


Molecular Genetics and Metabolism | 2011

Biotinylation is a natural, albeit rare, modification of human histones

Toshinobu Kuroishi; Luisa Rios-Avila; Valerie Pestinger; Subhashinee S.K. Wijeratne; Janos Zempleni

Previous studies suggest that histones H3 and H4 are posttranslationally modified by binding of the vitamin biotin, catalyzed by holocarboxylase synthetase (HCS). Albeit a rare epigenetic mark, biotinylated histones were repeatedly shown to be enriched in repeat regions and repressed loci, participating in the maintenance of genome stability and gene regulation. Recently, a team of investigators failed to detect biotinylated histones and proposed that biotinylation is not a natural modification of histones, but rather an assay artifact. Here, we describe the results of experiments, including the comparison of various analytical protocols, antibodies, cell lines, classes of histones, and radiotracers. These studies provide unambiguous evidence that biotinylation is a natural, albeit rare, histone modification. Less than 0.001% of human histones H3 and H4 are biotinylated, raising concerns that the abundance might too low to elicit biological effects in vivo. We integrated information from this study, previous studies, and ongoing research efforts to present a new working model in which biological effects are caused by a role of HCS in multiprotein complexes in chromatin. In this model, docking of HCS in chromatin causes the occasional binding of biotin to histones as a tracer for HCS binding sites.


Microbiology and Immunology | 2002

Lactoferrin stimulates A Staphylococcus aureus killing activity of bovine phagocytes in the mammary gland.

Kenzo Kai; Ken-ichi Komine; Yumiko Komine; Toshinobu Kuroishi; Tomoyuki Kozutsumi; Jin Kobayashi; Minoru Ohta; Hajime Kitamura; Katsuo Kumagai

Lactoferrin (Lf) may play a key role in the clearance of microorganisms from a host. To study in vitro the bactericidal mechanisms of Lf during nonlactating periods, we investigated whether the effects of Lf were influenced by bovine mammary gland secretory cells (MGSC) and fresh normal bovine serum (NBS) as a source of complement. Phagocytic killing tests demonstrated that a phagocytic mixture of unopsonized Staphylococcus aureus (S. aureus) and MGSC in the presence of Lf reduced bacterial growth, compared with that of unopsonized S. aureus and MGSC without Lf. The opsonization with Lf and fresh NBS together resulted in more than a 95% reduction in CFU. The activation of complement induced by Lf also resulted in increased deposition of C3 on S. aureus, and the phagocytic activity of MGSC was augmented by opsonization with Lf and fresh NBS. Inhibition of C3 deposition by Lf was not induced in the presence of Mg‐EGTA, but was induced by the addition of bovine Lf antiserum. These results strongly suggest that Lf induces the activation of complement in fresh NBS mainly through an alternative pathway. The results demonstrated a Lf‐dependent, antibody‐independent and complement‐mediated phagocytic killing of S. aureus, and implied that Lf was synergistically capable of activating both the alternative pathway of the bovine complement cascade and phagocytosis by phagocytes.


European Journal of Pharmacology | 2013

Analgesic effects of the non-nitrogen-containing bisphosphonates etidronate and clodronate, independent of anti-resorptive effects on bone.

Siyoung Kim; Masahiro Seiryu; Satoru Okada; Toshinobu Kuroishi; Teruko Takano-Yamamoto; Shunji Sugawara; Yasuo Endo

Nitrogen-containing bisphosphonates (NBPs) have greater anti-bone-resorptive effects than non-nitrogen-containing bisphosphonates (non-NBPs). Hence, NBPs are the current first-choice drug for osteoporosis. However, NBPs carry a risk of osteonecrosis of jaws. Some animal and human studies suggest that non-NBPs may have anti-bone-resorptive effect-independent analgesic effects, but there has been no detailed comparison between NBPs and non-NBPs. Here, we compared the analgesic effects of several non-NBPs and NBPs, using (a) writhing responses induced in mice by intraperitoneal injection of 1% acetic acid, (b) acetic acid-induced neuronal expression of c-Fos, (c) acetic acid-induced elevation of blood corticosterone, and (d) hindpaw-licking/biting responses induced by intraplantar injection of capsaicin. Among the NBPs and non-NBPs tested, only etidronate and clodronate displayed clear analgesic effects, with various routes of administration (including the oral one) being effective. However, they were ineffective when intraperitoneally injected simultaneously with acetic acid. Intracerebroventricular administration of etidronate or clodronate, but not of minodronate (an NBP), was also effective. The effective doses of etidronate and clodronate were much lower in writhing-high-responder strains of mice. Etidronate and clodronate reduced acetic acid-induced c-Fos expression in the brain and spinal cord, and also the acetic acid-induced corticosterone increase in the blood. Etidronate and clodronate each displayed an analgesic effect in the capsaicin test. Etidronate and clodronate displayed their analgesic effects at doses lower than those inducing anti-bone-resorptive effects. These results suggest that etidronate and clodronate exert potent, anti-bone-resorptive effect-independent analgesic effects, possibly via an interaction with neurons, and that they warrant reappraisal as safe drugs for osteoporosis.


Clinical and Vaccine Immunology | 2004

Induction of Nitric Oxide Production Mediated by Tumor Necrosis Factor Alpha on Staphylococcal Enterotoxin C-Stimulated Bovine Mammary Gland Cells

Ken-ichi Komine; Toshinobu Kuroishi; Yumiko Komine; Kouichi Watanabe; Jin Kobayashi; Takahiro Yamaguchi; Shin-ichi Kamata; Katsuo Kumagai

ABSTRACT Mammary gland (MG) secretions (MGS) derived from secretory cows infected with coagulase-negative staphylococci (CoNS) showed somatic cell counts and lactoferrin similar to levels found in the MGS of secretory cows infected with Staphylococcus aureus. However, nitrite and nitrate (NOx) and staphylococcal enterotoxin C (SEC) were found in MGS infected with S. aureus at much higher levels than in cows infected with CoNS. These results suggested that NOx could be intimately correlated with the production of SEC in secretory cows infected with S. aureus. Therefore, we examined the production of NOx and the expression of proinflammatory cytokines and microsomal cytochrome P450 (CYP450) after injection of SEC into the MGS of secretory cows. We were able to detect NOx and the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) on MG cells of SEC-injected MGS. It was also found that CYP450 in the MG cells from SEC-injected MGS was down-regulated by approximately one-third in comparison with the cells from phosphate-buffered saline-injected MGS. This in vitro system also showed that NOx could be induced in the culture of bovine macrophage-lined cells (FBM-17) with the supernatants of SEC-stimulated bovine peripheral blood lymphocytes (BoPBLs) but not in the culture of peripheral mononuclear cells with SEC-stimulated BoPBLs. The expression of the mRNA for both inducible nitric oxide synthase and TNF-α in FBM-17 was enhanced by culturing with the supernatant of SEC-stimulated BoPBLs, although CYP450 was down-regulated. These results indicate that the down-regulation of CYP450 was caused by the production of TNF-α in SEC-stimulating MG cells containing macrophages and via NOx production. Therefore, we suggest that NOx released from activated MG cells via the superantigenic activity of SEC caused oxidative damage to the MG in S. aureus-induced mastitis.


Journal of Oral and Maxillofacial Surgery | 2010

Inhibition of necrotic actions of nitrogen-containing bisphosphonates (NBPs) and their elimination from bone by etidronate (a non-NBP): a proposal for possible utilization of etidronate as a substitution drug for NBPs.

Takefumi Oizumi; Hiromi Funayama; Kouji Yamaguchi; Masayoshi Yokoyama; Harue Takahashi; Miou Yamamoto; Toshinobu Kuroishi; Hiroyuki Kumamoto; Keiichi Sasaki; Hiroshi Kawamura; Shunji Sugawara; Yasuo Endo

PURPOSE Nitrogen-containing bisphosphonates (NBPs) have powerful anti-bone-resorptive effects (ABREs). However, recent clinical applications have disclosed an unexpected side effect, osteonecrosis of the jaw. We previously found in mice that etidronate (a non-NBP), when coadministered with alendronate (an NBP), inhibited the latters inflammatory effects. However, etidronate also reduced the ABRE of alendronate. The present study examined in mice the modulating effects of etidronate on the inflammatory and necrotic actions of zoledronate (the NBP with the strongest anti-bone-resorptive activity and the highest incidence of osteonecrosis of the jaw) and on ABREs of various NBPs including zoledronate. MATERIALS AND METHODS NBPs were subcutaneously injected into ear pinnas of mice and ensuing inflammation and necrosis at the site of the injection were evaluated. ABREs of NBPs were evaluated by analyzing sclerotic bands induced in mouse tibias. RESULTS Coinjection of etidronate reduced inflammatory and necrotic reactions induced by zoledronate, and also reduced the amount of zoledronate retained within the ear tissue. When both agents were intraperitoneally injected, etidronate reduced the ABRE of zoledronate and those of other NBPs. Notably, etidronate reduced the ABRE of zoledronate even when this non-NBP was injected 16 hours after the injection of zoledronate. Bone scintigram indicated that etidronate reduced the amount of zoledronate that had already bound to bone. CONCLUSIONS These results suggest that etidronate may 1) inhibit the entry of NBPs into cells related to inflammation and/or necrosis, 2) inhibit the binding of NBPs to bone hydroxyapatite, 3) at least partly eliminate (or substitute for) NBPs that have already accumulated within bones, and thus 4) if used as a substitution drug for NBPs, be effective at treating or preventing NBP-associated osteonecrosis of the jaw.


Journal of Leukocyte Biology | 2005

Involvement of neutrophil recruitment and protease-activated receptor 2 activation in the induction of IL-18 in mice

Keiji Ikawa; Takashi Nishioka; Zhiqian Yu; Yumiko Sugawara; Junichi Kawagoe; Toshiaki Takizawa; Valeria Primo; Boris Nikolic; Toshinobu Kuroishi; Takashi Sasano; Hidetoshi Shimauchi; Haruhiko Takada; Yasuo Endo; Shunji Sugawara

Activated neutrophils produce serine proteases, which activate cells through protease‐activated receptor 2 (PAR2). As proteinase 3 (PR3) induces the secretion of interleukin (IL)‐18 from epithelial cells in combination with lipopolysaccharide (LPS) in vitro, we examined whether neutrophils, serine proteases, and PAR2 are involved in the induction of serum IL‐18 and IL‐18‐dependent liver injury in mice treated with heat‐killed Propionibacterium acnes and LPS. LPS‐induced serum IL‐18 levels in P. acnes‐primed mice were reduced significantly by anti‐Gr‐1 injection (depletion of neutrophils and macrophages) but not by a macrophage “suicide” technique, using liposomes encapsulating clodronate. The IL‐18 induction was decreased significantly by coadministration of a serine protease inhibitor [Nafamostat mesilate (FUT‐175)] with LPS. Serum levels of tumor necrosis factor α and liver enzymes induced by P. acnes and LPS were abolished by anti‐Gr‐1 treatment, and concomitantly, liver injury (necrotic change and granuloma formation) and Gr‐1+ cell infiltration into the liver were prevented by the treatment. A deficiency of PAR2 in mice significantly impaired IL‐18 induction by treatment with P. acnes and LPS, and only slight pathological changes in hepatic tissues occurred in the PAR2‐deficient mice treated with P. acnes and LPS. Furthermore, coadministration of exogenous murine PR3 or a synthetic PAR2 agonist (ASKH95) with LPS in the anti‐Gr‐1‐treated mice restored the serum IL‐18 levels to those in control mice treated with P. acnes and LPS. These results indicate that neutrophil recruitment and PAR2 activation by neutrophil serine proteases are critically involved in the induction of IL‐18 and IL‐18‐dependent liver injury in vivo.


Basic & Clinical Pharmacology & Toxicology | 2009

Necrotic actions of nitrogen-containing bisphosphonates and their inhibition by clodronate, a non-nitrogen-containing bisphosphonate in mice: potential for utilization of clodronate as a combination drug with a nitrogen-containing bisphosphonate.

Takefumi Oizumi; Kouji Yamaguchi; Hiromi Funayama; Toshinobu Kuroishi; Hiroshi Kawamura; Shunji Sugawara; Yasuo Endo

Nitrogen-containing bisphosphonates (NBPs) exhibit powerful anti-bone-resorptive effects (ABREs) via inhibition of farnesyl pyrophosphate synthase during cholesterol biosynthesis. Clinical applications have disclosed an unexpected side effect, namely osteonecrosis of jaw bones, and although thousands of cases have been documented in the last few years the mechanism remains unclear. Since NBPs accumulate in bone-hydroxyapatite, more jaw bone osteonecrosis cases may come to light if NBPs continue to be used as they are being used now. We have previously reported that in mice, systemic (intraperitoneal) injection of clodronate (a non-NBP) prevents the inflammatory effects of NBPs. Here, we examined in mice the local necrotic actions of various NBPs and the anti-necrotic effects of clodronate. A single subcutaneous injection of an NBP into the ear pinna induced necrosis at the injection site (relative potencies of necrotic actions of NBPs: zoledronate >> pamidronate > or = alendronate > risedronate), while non-NBPs lacked this effect. Clodronate, when injected together with an NBP, reduced or prevented the necrosis induced by that NBP, but not its ABRE. Clodronate reduced the amount of each NBP retained within tissues. These results, together with those of previous studies, suggest that (i) clodronate inhibits the inflammatory and necrotic actions of NBPs by inhibiting their incorporation into cells related to inflammation and/or necrosis, (ii) clodronate could be useful as a combination drug with NBPs for preventing their necrotic actions while retaining their ABREs and (iii) clodronate could also be useful as a substitution drug for NBPs in patients at risk of osteonecrosis of jaw bones.


Innate Immunity | 2011

Muramyldipeptide augments the actions of lipopolysaccharide in mice by stimulating macrophages to produce pro-IL-1β and by down-regulation of the suppressor of cytokine signaling 1 (SOCS1).

Yosuke Shikama; Toshinobu Kuroishi; Yasuhiro Nagai; Yoichiro Iwakura; Hidetoshi Shimauchi; Haruhiko Takada; Shunji Sugawara; Yasuo Endo

Muramyldipeptide (MDP), the minimum essential structure responsible for the immuno-adjuvant activity of peptidoglycan, is recognized by intracellular nuclear-binding oligomerization domain 2 (NOD2). Muramyldipeptide enhances the activities of lipopolysaccharide (LPS), but the mechanism underlying this effect is unclear. Here, we obtained evidence that intravenously injected MDP augments LPS-induced hypothermia in wild-type mice, but not in mice deficient in interleukin (IL)-1α/β and/or tumor-necrosis factor (TNF)-α. Muramyldipeptide also: (i) increased pro-IL-1β in tissues, but did not increase IL-1β in serum (since caspase-1 was not activated by MDP); (ii) downregulated the expression of suppressor of cytokine signaling 1 (SOCS1; a negative-feedback regulator of LPS-induced signaling); and (iii) augmented the LPS-induced production of TNF-α, IL-12 p40, and interferon (IFN)-γ. Moreover, by performing in vivo and in vitro experiments, we obtained evidence that macrophages were involved in these effects of MDP. These results suggest that two different mechanisms may underlie the augmenting effect of MDP: namely, stimulation of pro-IL-1β production by, and down-regulation of SOCS1 in, macrophages. We consider that this work may help to elucidate the pathogenesis of mixed bacterial infections, including septic shock and multiple organ dysfunction syndrome (MODS).


British Journal of Dermatology | 2011

Allergy‐inducing nickel concentration is lowered by lipopolysaccharide at both the sensitization and elicitation steps in a murine model

Masayuki Kinbara; Naoki Sato; Toshinobu Kuroishi; Teruko Takano-Yamamoto; Shunji Sugawara; Yasuo Endo

Background  Nickel (Ni) is the major cause of contact allergy. We previously found that lipopolysaccharide (LPS, a cell‐surface component of Gram‐negative bacteria) markedly promotes Ni allergy in a murine model. Establishing the minimum concentration or amount of Ni needed to induce allergic responses may help us to prevent or reduce such responses.

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