Faculty Profiles - MATSUKAWA Akihiro

Papers - MATSUKAWA Akihiro

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Neutrophil infiltration as a crucial step for monocyte chemoattractant protein (MCP)-1 to attract monocytes in lipopolysaccharide-induced arthritis in rabbits Reviewed

S Miyazaki, A Matsukawa, S Ohkawara, K Takagi, M Yoshinaga

INFLAMMATION RESEARCH 49 ( 12 ) 673 - 678 2000.12

Language：English Publishing type：Research paper (scientific journal) Publisher：BIRKHAUSER VERLAG AG

Objective and Design: To evaluate the mechanism whereby monocyte chemoattractant protein (MCP)-1 attracts monocytes in vivo.
Subjects: New Zealand white rabbits (175 rabbits) were used.
Treatment: LPS, MCP-1 or IL-8 was injected into knee joints. Antibodies against various cytokines or IL-1 receptor antagonist were injected to neutralize cytokine activities.
Methods: The numbers of leukocyte populations, levels of cytokines in joints were estimated.
Results: Partial inhibition of neutrophil influx with anti-IL-8 IgG (10 mug) suppressed LPS-induced macrophage influx by 43 +/- 8.5% (p<0.05) without affecting the MCP-I level. Intraarticular injection of MCP-1 (1-30 <mu>g) induced macrophage influx. The event was accompanied by a small number of neutrophils in an early phase. Go-injection of IL-8 (1.0 mug) enhanced the MCP-1-induced macrophage infiltration (p<0.01). In neutrophil-depleted rabbits, LPS failed to induce macrophage influx even though the MCP-1 level was maintained, and macrophage influx following exogenously administered MCP-1 was also dramatically inhibited.
Conclusions: Early events associated with neutrophil infiltration appear to be important for MCP-1 to induce a later macrophage influx in LPS-arthritis.

DOI： 10.1007/s000110050645

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Chemokine C10 promotes disease resolution and survival in an experimental model of bacterial sepsis Reviewed

ML Steinhauser, CM Hogaboam, A Matsukawa, NW Lukacs, RM Strieter, SL Kunkel

INFECTION AND IMMUNITY 68 ( 11 ) 6108 - 6114 2000.11

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER SOC MICROBIOLOGY

Previous studies have suggested that the C-C chemokine C10 is involved in the chronic stages of host defense reactions. The present study addressed the role of C10 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Unlike other C-C chemokines, C10 levels in the peritoneal wash were increased approximately 30-fold above baseline levels at 48 h after CLP surgery. Immunoneutralization of peritoneal C10 Levels with polyclonal anti-C10 antiserum during CLP-induced peritonitis negatively impacted mouse survival over 4 days. In contrast,,when 500 ng of recombinant murine C10 was administered immediately after CLP surgery, the ii-day survival rate increased from 20% to over 60%. The C10 therapy appeared to facilitate a rapid and significant enhancement of the Levels of tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-I) and a later increase in interleukin-13 (IL-13) levels in the peritoneal cavity. In vitro studies showed that the combination of IL-1 beta and C10 markedly augmented TNF-alpha synthesis by peritoneal macrophages and that C10 synthesis was induced in these cells following their exposure to IL-13, At 24 h after CLP surgery, only 25% of C10-treated mice were bacteremic versus 85% of the control group that exhibited dissemination of bacteria into the circulation, The Lack of bacteremia in C10-treated mice appeared to be related, in part, to in vitro evidence that C10 significantly enhanced the bacterial phagocytic activity of peritoneal macrophages. In addition, in vivo evidence suggested that C10 therapy significantly reduced the amount of material that leaked from the damaged gut. Taken together, the results of this study demonstrate that the C10 chemokine rapidly promotes disease resolution in the CLP model through its direct effects on the cellular events critically involved in host defense during septic peritonitis.

DOI： 10.1128/IAI.68.11.6108-6114.2000

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Acute effects of smoke exposure on the cellular and cytokine profile in isolated perfused lungs Reviewed

M Kyi, Y Miyazaki, T Inoue, S Miyake, A Matsukawa, Y Yoshizawa

RESPIRATION PHYSIOLOGY 123 ( 1-2 ) 143 - 151 2000.10

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

The aim of this study was to assess the acute effects of cigarette smoke exposure on cellular and cytokine profile in BAL fluids in an isolated perfused rabbit assay. The experimental animals were categorized into four groups: (1) unexposed controls and (2) cigarette smoke-exposed animals perfused with autologous whole blood; (3) unexposed controls and cigarette smoke-exposed; (4) cigarette smoke-exposed animals perfused with Krebs' Ringer solution containing 5% bovine serum albumin and glucose. Cigarette smoke induced an increase in total cell numbers (mainly alveolar macrophages in BAL fluids) and an increase in the permeability index of BAL. Levels of interleukin 8 were also significantly decreased in BAL fluids due to acute effects of cigarette smoke exposure. The most likely explanation for cigarette smoke-induced increase of inflammatory cells in BAL in lungs is because of the release of pre-existing cells from reservoirs within the lungs. The acute effects of cigarette smoke-induced increase of pulmonary epithelial permeability may also play an important role in the cellular recruitment into airspaces from the lung reservoirs. (C) 2000 Elsevier Science B.V. All rights reserved.

DOI： 10.1016/S0034-5687(00)00147-X

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Pivotal role of the CC chemokine, macrophage-derived chemokine, in the innate immune response Reviewed

A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, HL Evanoff, SL Kunkel

JOURNAL OF IMMUNOLOGY 164 ( 10 ) 5362 - 5368 2000.5

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：AMER ASSOC IMMUNOLOGISTS

Macrophage-derived chemokine (MDC), a recently identified CC chemokine, has been regarded to be involved in chronic inflammation and dendritic cell and lymphocyte homing, In this study, we demonstrate a pivotal role for MDC during experimental sepsis induced by cecal ligation and puncture (CLP), Intraperitoneal administration of MDC (1 mu g/mouse) protected mice from CLP-induced lethality. The survival was accompanied by increased number of peritoneal macrophages and decreased recovery of viable bacteria from the peritoneum and peripheral blood. In addition, mice treated with an i.p. injection of MDC cleared bacteria more effectively than those in the control when 3 x 10(8) CFU live Escherichia coli was i.p. inoculated. Endogenous MDC was detected in the peritoneum after CLP, and neutralization of the MDC with anti-MDC Abs decreased CLP-induced recruitment of peritoneal macrophages and increased the recovery of viable bacteria from the peritoneum and peripheral blood. MDC blockade was deleterious in the survival of mice after CLP. In vitro, MDC enhanced the phagocytic and killing activities of peritoneal macrophages to E, coli and induced both a respiratory burst and the release of lysozomal enzyme from macrophages, Furthermore, MDC dramatically ameliorated CLP-induced systemic tissue inflammation as well as tissue dysfunction, which were associated in part with decreased levels of TNF-alpha, macrophage inflammatory proteins-1 alpha and -2, and KC in specific tissues. Collectively, these results indicate novel regulatory activities of MDC in innate immunity during sepsis and suggest that MDC may aid in an adjunct therapy in sepsis.

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Therapeutic use of chemokines Reviewed

CM Hogaboam, C Bone-Larson, A Matsukawa, ML Steinhauser, K Blease, NW Lukacs, SL Kunkel

CURRENT PHARMACEUTICAL DESIGN 6 ( 6 ) 651 - 663 2000.4

Language：English Publisher：BENTHAM SCIENCE PUBL BV

Chemokines are involved in a number of pathological processes, and therefore represent important targets. However, it has also become apparent that chemokines have exciting therapeutic applications in inflammatory, infectious and cancer-related diseases. The following review will highlight the application of novel therapies including viral-encoded, recombinant, and genetically engineered chemokines to a number of diseases or disorders. Advances in the application of novel chemokine delivery procedures both at the research bench and the clinical bedside will also be discussed. Overall, the utilization of chemokines to prevent and treat disease has tremendous potential.

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Exaggerated hepatic injury due to acetaminophen challenge in mice lacking C-C chemokine receptor 2 Reviewed

CM Hogaboam, CL Bone-Larson, ML Steinhauser, A Matsukawa, J Gosling, L Boring, IF Charo, KJ Simpson, NW Lukacs, SL Kunkel

AMERICAN JOURNAL OF PATHOLOGY 156 ( 4 ) 1245 - 1252 2000.4

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER SOC INVESTIGATIVE PATHOLOGY, INC

Monocyte chemoattractant protein-1 is one of the major C-C chemokines that has been implicated in liver injury. The C-C chemokine receptor, CCR2, has been identified as the primary receptor that mediates monocyte chemoattractant protein-1 (MCP-1) responses in the mouse. Accordingly, the present study addressed the role of CCR2 in mice acutely challenged with acetaminophen (APAP). Mice genetically deficient in CCR2 (CCR2(-/-)) and their wild-type counterparts (CCR2(+/+)) were fasted for 10 hours before receiving an intraperitoneal injection of APAP (300 mg/kg), Liver and serum samples were removed from both groups of mice before and at 24 and 48 hours post APAP, Significantly elevated levels of MCP-1 were detected in liver samples from CCR2(+/+) and CCR2(-/-) mice at 24 hours post-APAP. Although CCR2(+/+) mice exhibited no liver injury at any time after receiving APAP, CCR2(-/-) mice exhibited marked evidence of necrotic and TUNEL-positive cells in the liver, particularly at 24 hours post-APAP, Enzyme-linked immunosorbent assay analysis of liver homogenates from both groups of mice at the 24 hours time point revealed that liver tissue from CCR2(-/-) mice contained significantly greater amounts of immunoreactive IFN-gamma and TNF-alpha. The in vivo immunoneutralization of IFN-gamma or TNF-alpha significantly attenuated APAP-induced liver injury in CCR2(-/-) mice and increased hepatic IL-13 levels. Taken together, these findings demonstrate that CCR2 expression in the liver provides a hepatoprotective effect through its regulation of cytokine generation during APAP challenge.

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Endogenous MCP-1 influences systemic cytokine balance in a murine model of acute septic peritonitis Reviewed

A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, RM Strieter, SL Kunkel

EXPERIMENTAL AND MOLECULAR PATHOLOGY 68 ( 2 ) 77 - 84 2000.4

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS INC

Sepsis and septic syndrome represent an intense systemic response with multiple physiologic and immunologic abnormalities, leading to multiple organ failure. Recent investigations suggest that the critical conditions are balanced by endogenous cytokines. In the present study, we examined the involvement of endogenous monocyte chemoattractant protein (MCP)-1 in the regulation of cytokine production in tissue/organs in a murine model of acute septic peritonitis induced by cecal ligation and puncture (CLP). Initial studies showed that CLP induced elevated levels of MCP-1 in tissues, such as liver, lung, and kidney. To neutralize endogenous MCP-1, either anti-MCP-1 antibodies or control antibodies were intraperitoneally administered 2 h prior to CLP. Administration of anti-MCP-1 antibodies resulted in a decrease in the level of interleukin (IL)-13 in tissues, while increasing the level of tumor necrosis factor-alpha, compared to control. In addition, anti-MCP-1 treatment decreased the level of IL-12 and, in contrast, increased the level of IL-10 in specific tissues. These findings suggest that endogenous MCP-1 influences the cytokine balance in tissues in favor of antiinflammatory and immune-enhancing cytokines, probably protecting the host from tissue/organ damage during sepsis. (C) 2000 Academic Press.

DOI： 10.1006/exmp.1999.2296

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Lazaroid reduces production of IL-8 and IL-1 receptor antagonist in ischemic spinal cord injury Reviewed

T Kunihara, S Sasaki, N Shiiya, H Ishikura, Y Kawarada, A Matsukawa, K Yasuda

ANNALS OF THORACIC SURGERY 69 ( 3 ) 792 - 798 2000.3

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE INC

Background. 21-aminosteroids (lazaroids) have demonstrated the protective effect against cerebral ischemic injury through the inhibition of lipid peroxidation. We examined whether lazaroids affected the production of proinflammatory and antiinflammatory cytokines in ischemic spinal cord injury model.
Materials. Anesthetized New Zealand white rabbits underwent a 20-minute infrarenal aortic cross-clamping (AXC) with pretreatment of either an intravenous 3 mg/kg lazaroid U74389G (group L; n = 10) or the same volume saline (group P; n = 10), Sham operation group (group S; n = 6) underwent only exposure of the aorta. Plasma concentrations of interleukin (IL)-8, -1 beta, -1 receptor antagonist (IL-1ra) and tumor necrosis factor (TNF)-alpha were measured at four time points. Functional assessment with Tarlov score at 24 and 48 hours after pretreatment, pathologic assessment of the spinal cord, and measurements of cytokine levels in the spinal cord were performed.
Results, The maximum elevation of plasma IL-8 and -1ra levels occurred at 1 hour after declamping in four measurement points, Plasma IL-8 and -1ra levels in group L were significantly lower than those in group P (*p < 0.05), Plasma TNF alpha peaked at 5 minutes after declamping, but decreased afterwards. Plasma TNF alpha levels were not different among three groups, Spinal IL-8 levels in group L (0.98 +/- 0.34 ng/g tissue) were lower than those in group P (7.26 +/- 2.26 ng/g tissue) (*p < 0.05), Spinal IL-1ra and TNF alpha were not significantly different Tarlov scare and pathologic assessment were better in group L,
Conclusions. Lazaroid U-74389G reduced the production of systemic IL-8 and -1ra and spinal IL-8 when AXC. caused spinal cord injury. These results indicate that lazaroids may attenuate ischemic endothelial cell injury or activation of leukocytes,
(C) 2000 by The Society of Thoracic Surgeons.

DOI： 10.1016/S0003-4975(99)01413-7

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Expression and contribution of endogenous IL-13 in an experimental model of sepsis Reviewed

A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, HL Evanoff, RM Strieter, SL Kunkel

JOURNAL OF IMMUNOLOGY 164 ( 5 ) 2738 - 2744 2000.3

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：AMER ASSOC IMMUNOLOGISTS

IL-13 has been shown to exert potent anti-inflammatory properties. In this study, we elucidated the functional role of endogenous IL-13 in a murine model of septic peritonitis induced by cecal ligation and puncture (CLP). Initial studies demonstrated that the level of IL-13 increased in tissues including liver, lung, and kidney, whereas no considerable increase was found int either peritoneal fluid or serum after CLP, Immunohistochemically, IL-13-positive cells were Kupffer cells in liver, alveolar macrophages in lung, and epithelial cells of urinary tubules in kidney. IL-13 blockade with anti-IL-13 Abs significantly decreased the survival rate of mice after CLP from 53% to 14% on day 7 compared with control, To determine the potential mechanisms whereby IL-13 exerted a protective role in this model, the effects of anti-IL-13 Abs on both local and systemic inflammation were investigated, Administration of anti-IL-13 Abs did not alter the leukocyte infiltration and bacterial load in the peritoneum after CLP hut dramatically increased the neutrophil influx in tissues after CLP, an effect that was accompanied by significant increases in the serum levels of aspartate transaminase, alanine transaminase, blood urea nitrogen, and creatinine, Tissue injury caused by IL-13 blockade was associated with increases in mRNA and the protein levels of CXC chemokines macrophage inflammatory protein-2 and KC as web as the CC chemokine macrophage inflammatory protein-1 alpha and the proinflammatory cytokine TNF-alpha. Collectively, these results suggest that endogenous IL-13 protected mice from CLP-induced lethality by modulating inflammatory responses via suppression of overzealous production of inflammatory cytokines/chemokines in tissues.

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CXC chemokine GRO is essential for neutrophil infiltration in LPS-induced uveitis in rabbits Reviewed

JS Mo, A Matsukawa, S Ohkawara, M Yoshinaga

EXPERIMENTAL EYE RESEARCH 70 ( 2 ) 221 - 226 2000.2

Language：English Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS LTD

The purpose of this study was to investigate the role and regulation of the CXC chemokine GRO and the interaction between GRO and IL-8 in LPS-induced uveitis in rabbits. Uveitis was induced by intravitreal injection of 100 ng of LPS in rabbits. After the LPS injection, GRO was produced in aqueous humor and peaked at 24 hr. Immunohistochemistry showed that ciliary epithelial cells were responsible for production of GRO. Blocking the activity of GRO by anti-GRO serum reduced LPS-induced aqueous neutrophil counts by 80%, but did not reduce the mononuclear cell counts or protein levels or IL-8 levels. Regulation of GRO production by TNF alpha, IL-1 and IL-8 was studied. Anti-TNF alpha mAb alone did not inhibit the 24 hr LPS induced GRO levels, whereas rrIL-1Ra inhibited the GRO production by 58%. The combination of anti-TNF alpha mAb and rrIL-1Ra inhibited 93 % of GRO production. Although treatment with anti-IL-8 IgG inhibited the neutrophil infiltration by 66%, treatment with this antibody did not inhibit GRO production.
Taken together, our results suggest that GRO is an essential mediator for neutrophil infiltration in LPS-induced uveitis in rabbits. Most of GRO production is mediated by TNF alpha and IL-1. GRO and IL-8 act in concert to mediate neutrophil infiltration. (C) 2000 Academic Press.

DOI： 10.1006/exer.1999.0778

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Adenoviral-mediated overexpression of monocyte chemoattractant protein-1 differentially alters the development of Th1 and Th2 type responses in vivo Reviewed

A Matsukawa, NW Lukacs, TJ Standiford, SW Chensue, SL Kunkel

JOURNAL OF IMMUNOLOGY 164 ( 4 ) 1699 - 1704 2000.2

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：AMER ASSOC IMMUNOLOGISTS

The expression of chemokines during an immune response may participate in determining the intensity and type of the developing immune response. In the present study, we have examined the effect of overexpressing monocyte chemoattractant protein (MCP)-1 at the site of immunization during different stages of Th1- and Th2-type granulomatous responses. The overexpression of MCP-1 by MCP-1 adenovirus during the sensitization phase of the purified protein derivative Th1-type model significantly reduced the elicitation of the granulomatous response. In contrast, the overexpression of MCP-1 during the sensitization phase of the schistosome egg Ag Th2 response led to an enhanced granulomatous reaction. When cytokines were examined upon restimulation of splenocytes ex vivo, an altered cytokine profile was observed, as compared with control mice. IFN-gamma and IL-12 were significantly reduced in the purified protein derivative Th1-type response, whereas IL-10 and IL-13 were up-regulated in the schistosome egg Ag Th2-type response. The regulation of the immune response was further examined by using the MCP-1 adenovirus at later time points during the elicitation phase. When MCP-1 was overexpressed during the elicitation phase of the responses, neither the Th1-type nor the Th2-type granuloma was altered. Likewise, the cytokine profiles after restimulation of splenocytes ex vivo were unchanged, Thus, the function of MCP-1 may depend on the stage and type of immune response.

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緑膿菌誘発家兎慢性細気管支炎モデルにおけるエリスロマイシンの効果-アポトーシスに対する作用

高橋利弘, 菅守隆, 佐藤圭創, 岡本龍哉, 一安秀範, 松川昭博, 大河原進, 吉永秀, 安藤正幸

Jpn. J. Antibiot 2000

若年性多発性硝子化線維腫症の1症例

本田由美, 大河原進, 猪山賢一, 松川昭博, 吉永秀

診断病理 17 ( 2 ) 190 - 192 2000

Chemokines and innate immunity Invited Reviewed

Matsukawa A, Hogaboam CM, Lukacs NW, Kunkel SL

Rev. Immunogenetics 2: 339-358 2000

大腿骨後顆に高度なosteolysisをきたしたTKAの1例

桑原公倫, 白石稔, 水田博志, 中村英一, 高木克公, 吉田正一, 松川昭博

整形外科と災害外科 48 ( 2 ) 383 - 390 1999.3

Language：Japanese Publisher：西日本整形・災害外科学会

66歳女,変形性膝関節症にてMg-II,セメントレス人工膝関節置換術を施行し,4年後より膝関節腫脹と疼痛を来し,X線像で大腿骨後顆にosteolysisを認めた.再置換術を施行した際,大腿骨内側顆後方と外側顆後方に各30×20×15mm,15×15×10mm大の骨欠損と,滑膜増生,metallosis,膝蓋骨面のHDP及びtibia surfaceの磨耗を認めた

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Functional roles of MCP-1 in Propionibacterium acnes-induced, T cell-mediated pulmonary granulomatosis in rabbits Reviewed

ICHIYASU H

J Leukoc Biol 65 ( 4 ) 482 - 91 1999

Galectin-9 expands immunosuppressive macrophages to ameliorate T-cell-mediated lung inflammation. Reviewed International journal

Tomohiro Arikawa, Naoki Saita, Souichi Oomizu, Masaki Ueno, Akihiro Matsukawa, Shigeki Katoh, Keisuke Kojima, Keiko Nagahara, Minoru Miyake, Akira Yamauchi, Hirotsugu Kohrogi, Mitsuomi Hirashima

European journal of immunology 40 ( 2 ) 548 - 558 1999

Language：English Publishing type：Research paper (scientific journal)

Galectin-9 (Gal-9) plays pivotal roles in the modulation of innate and adaptive immunity to suppress T-cell-mediated autoimmune models. However, it remains unclear if Gal-9 plays a suppressive role for T-cell function in non-autoimmune disease models. We assessed the effects of Gal-9 on experimental hypersensitivity pneumonitis induced by Trichosporon asahii. When Gal-9 was given subcutaneously to C57BL/6 mice at the time of challenge with T. asahii, it significantly suppressed T. asahii-induced lung inflammation, as the levels of IL-1, IL-6, IFN-gamma, and IL-17 were significantly reduced in the BALF of Gal-9-treated mice. Moreover, co-culture of anti-CD3-stimulated CD4 T cells with BALF cells harvested from Gal-9-treated mice on day 1 resulted in diminished CD4 T-cell proliferation and decreased levels of IFN-gamma and IL-17. CD11b(+)Ly-6C(high)F4/80(+) BALF Mphi expanded by Gal-9 were responsible for the suppression. We further found in vitro that Gal-9, only in the presence of T. asahii, expands CD11b(+)Ly-6C(high)F4/80(+) cells from BM cells, and the cells suppress T-cell proliferation and IFN-gamma and IL-17 production. The present results indicate that Gal-9 expands immunosuppressive CD11b(+)Ly-6C(high) Mphi to ameliorate Th1/Th17 cell-mediated hypersensitivity pneumonitis.

DOI： 10.1002/eji.200939886

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Crucial role of group IIA phospholipase A2 in oleic acid-induced acute lung injury in rabbits. Reviewed

Furue S, Kuwabara K, Mikawa K, Nishina K, Shiga M, Maekawa N, Ueno M, Chikazawa Y, Ono T, Hori Y, Matsukawa A, Yoshinaga M, Obara H

Am. J. Respir. Crit. Care Med 160 1292 - 1302 1999

Role and regulation of IL-8 and MCP-1 in LPS-induced uveitis in rabbits. Reviewed

Mo JS, Matsukawa A, Ohkawara S, Yoshinaga M

Exp. Eye Res. 68 333 - 340 1999

Endogenous monocyte chemoattractant protein-1 (MCP-1) protects mice in a model of acute septic peritonitis: cross-talk between MCP-1 and leukotriene B4. Reviewed

Matsukawa A, Hogaboam CM, Lukacs NW, Lincoln PM, Strieter RM, Kunkel SL

J. Immunol. 163 6148 - 6154 1999

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Papers - MATSUKAWA Akihiro