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Ikuta, K.

Publications and source records attributed to Ikuta, K..

5 recordsLinked to original sources

Identification of a pharmacokinetic interaction between teicoplanin and sulfo-butyl ether-β-cyclodextrin, an excipient in the intravenous posaconazole formulation

Patients undergoing hematopoietic stem cell transplantation (HSCT) often receive multiple antibiotics and antifungals concurrently, making it crucial to understand their potential pharmacokinetic interactions of these agents. We report here an interaction between the glycopeptide antibiotic teicoplanin (TEIC) and sulfo-butyl ether-{beta}-cyclodextrin (SBECD), a solubilizing excipient in the intravenous formulation of posaconazole (PSCZ). We performed a single-center retrospective analysis of patients who underwent HSCT and received oral and intravenous PSCZ during TEIC therapy. The associations between PSCZ administration and TEIC concentration-to-dose (C/D) ratios were evaluated using linear mixed-effects models. We also examined the effects of intravenous PSCZ and SBECD on TEIC pharmacokinetics in rats by assessing the area under the concentration-time curve (AUC) and urinary excretion of total TEIC and its components. In addition, molecular docking and in vitro protein-binding assays were conducted to investigate the interaction between TEIC and SBECD. In patients who underwent HSCT, TEIC C/D ratio was significantly lower following intravenous PSCZ administration than without administration. In contrast, the effect of oral PSCZ administration relative to non-administration was not statistically significant. In rats, intravenous PSCZ and SBECD decreased the AUC of TEIC and increased urinary excretion, particularly in the A2 group. Docking simulations indicated that the hydrophobic side chain of TEIC A2-2 fit within the SBECD cavity, and in vitro assays confirmed SBECD concentration-dependent increases in TEIC unbound fractions. The co-administration of intravenous PSCZ containing SBECD may reduce TEIC protein binding, thereby enhancing renal excretion.

pharmacology and toxicology↗

Generation and therapeutic efficacy of the novel Fc-modified cross-neutralizing human monoclonal antibodies against dengue virus

Background: Dengue disease is a mosquito-borne infection caused by four dengue virus serotypes (DENV1-4). Secondary infections can produce flavivirus cross-reactive antibodies at sub-neutralizing levels. This phenomenon can significantly increase the severity of secondary infections via antibody-dependent enhancement (ADE). ADE activity is associated with a high risk of viral infection in immune effector cells, triggering cytokine cascade and activating the complement system, which lead to severe symptoms. Despite extensive studies, therapeutic antibodies, particularly fully human monoclonal antibodies, which can be an option for immune passive therapy, have not yet been discovered. Methodology/Principal Findings: This study generated LALA-mutated human monoclonal antibody clone B3B9 (LALA-B3B9 HuMAb) that can neutralize all four DENV serotypes without enhancing viral activity. The number of infected cells obtained with the ADE assay was compared among wild-type antibody (B3B9), and modified Fc, LALA-B3B9 HuMAb, and N297Q (N297Q-B3B9), with or without complement proteins. Moreover, the therapeutic efficacy of these HuMAbs against ADE infection by competing with natural antibodies in patients with acute dengue was determined using the in vitro suppression-of-enhancement assay in K562 cells. The novel Fc-modified antibody LALA-B3B9 (Leu234Ala/Leu235Ala mutations) could have a therapeutic effect. Further, it exhibited neutralization properties against all dengue virus serotypes without triggering ADE activity at any antibody concentration. This outcome was similar to that of the previous Fc-modified N297Q-B3B9 antibody (N297Q mutation). Moreover, the effect of complement protein on enhancing and neutralizing activities was evaluated to assess unwanted inflammatory responses to these therapeutic antibodies. Results showed that the elimination of complement activity could reduce the severity of dengue. The activities of LALA-B3B9 and N297Q-B3B9 HuMAbs were complement-independent in all dengue virus serotypes. Conclusions: LALA-B3B9 and N297Q-B3B9 HuMAbs can prevent the suppression-of-enhancement activity in K562 cells caused by human DENV2. Hence, they are promising candidates for dengue treatment. Author SummaryDengue is among the most important mosquito-borne infections that cause serious health issues in tropical and subtropical countries. There are no approved effective antiviral therapies available. The significant challenges for developing efficient therapeutic drugs include the presence of multiple serotypes and antibody-dependent enhancement. To overcome these issues, the LALA-mutated human monoclonal antibody clone B3B9 (LALA-B3B9) was generated. This antibody potently neutralizes all dengue virus serotypes and eliminates viral enhancement activity. Moreover, compared with the previous Fc-modified antibody clone N297Q-B3B9, LALA-B3B9 and N297Q-B3B9 HuMAbs do not activate the complement response, which is advantageous in reducing complement-mediated vascular leakage in vivo. In addition, they can compete with natural antibodies causing antibody-dependent enhancement in patients with acute dengue. Hence, LALA-B3B9 and N297Q-B3B9 HuMAbs have promising effects against dengue and can be further developed as a therapeutic drug in the future.

immunology↗

Liver type 1 innate lymphoid cells lacking IL-7 receptor are a native killer cell subset fostered by parenchymal niches

Group 1 innate lymphoid cells (G1-ILCs), including circulating natural killer (NK) cells and tissue-resident type 1 ILCs (ILC1s), are innate immune sentinels critical for responses against infection and cancer. In contrast to relatively uniform NK cells through the body, diverse ILC1 subsets have been characterized across and within tissues in mice, but their developmental and functional heterogeneity remain unsolved. Here, using multimodal in vivo approaches including fate-mapping and targeting of the interleukin 15 (IL-15)-producing microenvironment, we demonstrate that liver parenchymal niches support the development of a cytotoxic ILC1 subset lacking IL-7 receptor (7R- ILC1s). During ontogeny, fetal liver (FL) G1-ILCs arise perivascularly and then differentiate into 7R- ILC1s within sinusoids. Hepatocyte-derived IL-15 supports parenchymal development of FL G1-ILCs to maintain adult pool of 7R- ILC1s. IL-7R+ (7R+) ILC1s in the liver, candidate precursors for 7R- ILC1s, are not essential for 7R- ILC1 development in physiological conditions. Functionally, 7R- ILC1s exhibit killing activity at steady state through granzyme B expression, which is underpinned by constitutive mTOR activity, unlike NK cells with exogenous stimulation-dependent cytotoxicity. Our study reveals the unique ontogeny and functions of liver-specific ILC1s, providing a detailed interpretation of ILC1 heterogeneity.

immunology↗

IRF4 deficiency vulnerates B cell progeny for leukemogenesis via somatically acquired Jak3 mutations conferring IL-7 hypersensitivity

The processes leading from disturbed B cell development to adult B cell progenitor acute lymphoblastic leukemia (BCP-ALL) are poorly understood. Here, we describe Irf4-/- mice as prone to developing BCP-ALL with age. Irf4-/- preB-I cells exhibited impaired differentiation but enhanced proliferation in response to IL-7, along with reduced retention in the IL-7 providing bone marrow niche due to decreased CXCL12 responsiveness. Thus selected, preB-I cells acquired Jak3 mutations, probably following irregular AID activity, resulting in malignant transformation. We demonstrate heightened IL-7 sensitivity due to Jak3 mutants, devise a model to explain it and describe structural and functional similarities to Jak2 mutations often occurring in human Ph-like ALL. Finally, targeting JAK signaling with Ruxolitinib in vivo prolonged survival of mice bearing established Irf4-/- leukemia. Intriguingly, organ infiltration including leukemic meningeosis was selectively reduced without affecting blood blast counts. In this work, we present spontaneous leukemogenesis following IRF4 deficiency with potential implications for high-risk BCP-ALL in adult humans.

cancer biology↗

Fully Human Monoclonal Antibodies Effectively Neutralizing Botulinum Neurotoxin Serotype B

Botulinum neurotoxin (BoNT) is the most potent natural toxin known. Of the seven BoNT serotypes (A to G), types A, B, E, and F cause human botulism. Treatment of human botulism requires the development of effective toxin-neutralizing antibodies without side effects such as serum sickness and anaphylaxis. In this study, we generated fully human monoclonal antibodies (HuMAbs) against serotype B BoNT (BoNT/B1) using a murine-human chimera fusion partner cell line named SPYMEG. Of these HuMAbs, M2, which specifically binds to the light chain of BoNT/B1, showed neutralization activity in a mouse bioassay (approximately [≥] 100 i.p. LD50/mg of antibody), and M4, which binds to the C-terminal of heavy chain, showed partial protection. The combination of M2 and M4 was able to completely neutralize BoNT/B1 with a potency greater than 10,000 i.p. LD50/mg of antibodies, and was effective both prophylactically and therapeutically in the mouse model of botulism. Moreover, this combination showed broad neutralization activity against three type B subtypes, namely BoNT/B1, BoNT/B2, and BoNT/B6. These data demonstrate that the combination of M2 and M4 is promising in terms of a foundation for new human therapeutics for BoNT/B intoxication. IMPORTANCEBotulinum neurotoxins (BoNTs) produced by Clostridium botulinum and related species cause human botulism. Immunotherapy is the most effective treatment for botulism and equine immune serum formulations are used in cases of human botulism. However, these antisera may cause serum sickness or anaphylaxis. Additionally, the production of immune sera involves complicated and time-consuming manufacturing processes and quality management. Therefore, the development of safe, effective, and higher productive antibodies is required. Here we generated fully human monoclonal antibodies against serotype B BoNT (BoNT/B). We found that the combination of these antibodies (M2+M4) had potent and broad neutralization activity against BoNT/B, and showed therapeutic and preventive effects against botulism in mouse models. These data indicate that M2+M4 are promising candidates for the development of human therapeutics and prophylactics for BoNT/B intoxication.

microbiology↗