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Featured researches published by Taichin Koh.


Journal of Trauma-injury Infection and Critical Care | 2001

Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis.

Hiroshi Ogura; Tomio Kawasaki; Hiroshi Tanaka; Taichin Koh; Reiichirou Tanaka; Yasushi Ozeki; Hideo Hosotsubo; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Activated platelets have been recently reported to produce platelet microparticles and to enhance platelet-leukocyte interaction. The precise role of platelets in systemic inflammatory response syndrome (SIRS) has not been clarified. The objective of this study was to evaluate microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis. METHODS Twenty-six patients with severe SIRS (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 12 healthy volunteers were studied. The severe SIRS was caused by trauma in 12 patients and sepsis in 14. Microparticle formation, P-selectin expression on platelets, platelet-monocyte binding, and platelet-polymorphonuclear leukocyte (PMNL) binding were measured by flow cytometry in the presence or absence of ionomycin, N-formyl-methionyl-leucyl-phenylalanine, or anti-CD62p monoclonal antibody. Soluble P-selectin, thrombomodulin, neopterin, and PMNL elastase in blood were also measured. RESULTS Microparticle formation, P-selectin expression on platelets, platelet-monocyte binding with or without ionomycin, and platelet-PMNL binding with ionomycin significantly increased in patients with severe SIRS in comparison with values in normal volunteers. The increased platelet-leukocyte binding in severe SIRS patients was markedly inhibited by P-selectin blockade and was not enhanced by N-formyl-methionyl-leucyl-phenylalanine. Soluble P-selectin, thrombomodulin, neopterin, and PMNL elastase in blood also increased in these patients. CONCLUSION Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis. Enhanced platelet-leukocyte interaction is dependent on P-selectin expression and may be involved in the systemic inflammatory response after severe inflammatory insult.


Journal of Trauma-injury Infection and Critical Care | 1998

Priming, second-hit priming, and apoptosis in leukocytes from trauma patients

Hiroshi Ogura; Hiroshi Tanaka; Taichin Koh; Naoyuki Hashiguchi; Yasuyuki Kuwagata; Hideo Hosotsubo; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Polymorphonuclear leukocytes (PMNL) play important roles in both host defenses and systemic inflammatory responses after insults. The objectives of this study are to examine the serial changes in PMNL priming and apoptosis in severely injured patients and to evaluate the impact of second hits on primed PMNL function and systemic vascular endothelial damage. METHODS Twenty-four severely injured patients (mean Injury Severity Score, 31.1 +/- 9.7) were included. Infections were seen as second hits after trauma in seven patients. Oxidative activity, phagocytosis, and apoptosis of PMNL from serial blood samples were measured by flow cytometry. Oxidative activity with no stimulus and with formylmethionyl-leucyl-phenylalanine (FMLP) were analyzed as the priming index and FMLP response, respectively. Interleukin (IL)-6, IL-10, PMNL elastase, and thrombomodulin concentrations in blood were also measured before and after the second hit. RESULTS The PMNL priming index was elevated from days 2 to 13, especially days 2 to 5 after injury. FMLP response was enhanced from days 2 to 21 after injury. Apoptosis of PMNL was inhibited for as long as 3 weeks after injury. Infections as second hits after trauma enhanced both the priming index and the FMLP response within 24 hours after diagnosis of infection and increased serum IL-6 concentrations. However, serum thrombomodulin levels were not affected by second hits. All patients with second hits survived. CONCLUSION Severe trauma stimulated acute-phase priming in PMNL and inhibited apoptosis. Infections after trauma induced second-hit priming in PMNL, but the unchanged serum levels of thrombomodulin suggest that priming per se may not cause systemic vascular endothelial damage.


Journal of Trauma-injury Infection and Critical Care | 2001

Enhanced expression of heat shock proteins in activated polymorphonuclear leukocytes in patients with sepsis.

Naoyuki Hashiguchi; Hiroshi Ogura; Hiroshi Tanaka; Taichin Koh; Yasushi Nakamori; Mitsuhiro Noborio; Tadahiko Shiozaki; Masato Nishino; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Heat shock proteins (HSPs) in cells, as molecular chaperons, have been reported to regulate cell functions. The objective of this study was to investigate the HSP expression in polymorphonuclear leukocytes (PMNLs) from severe septic patients and the relation between the expression of HSPs and PMNL function. METHODS In blood samples from 21 patients with sepsis and serum C-reactive protein levels more than 10 mg/dL, we used flow cytometry to measure expressions of HSP27, HSP60, HSP70, and HSP90; oxidative activity; and levels of apoptosis in PMNLs during sepsis. In in vitro studies, we used cells from 14 healthy volunteers to examine the relation between the expression of HSP70 and PMNL function. Quercetin (30 microM), a suppressor of HSP, and sodium arsenite (100 microM), an inducer of HSP, were used to regulate the expression of HSP70 in PMNLs, and oxidative activity and apoptosis in these cells were measured. RESULTS In patients with sepsis, the expressions of HSP27, HSP60, HSP70, and HSP90 and oxidative activity in PMNLs were significantly increased. Apoptosis of these PMNLs was markedly inhibited. In the in vitro studies, administration of sodium arsenite enhanced the expression of HSP70, significantly increased oxidative activity, and inhibited apoptosis. Administration of quercetin before sodium arsenite prevented the expression of HSP70, the increase in oxidative activity, and the inhibition of apoptosis. CONCLUSION Sepsis causes the enhanced expression of HSPs in activated PMNLs. In PMNLs with enhanced expression of HSP70, oxidative activity is increased and apoptosis is inhibited. The enhanced expression of HSPs may play a role in regulating PMNL function in patients with sepsis.


Shock | 2004

Early activation of γδ T lymphocytes in patients with severe systemic inflammatory response syndrome

Hiroshi Ogura; Kieko Fujita; Taichin Koh; Hiroshi Tanaka; Yuka Sumi; Kazuhisa Yoshiya; Hideo Hosotsubo; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

Innate immunity plays an important role in host defense after severe insult. γδ T lymphocytes are recognized as the first line of defense against microbial invasion. In this study, we evaluated γδ T lymphocytes in the peripheral blood of patients with severe systemic inflammatory response syndrome (SIRS), and examined on role of these cells. Thirty-seven patients with severe SIRS (SIRS criteria and serum C-reactive protein ≥ 10 mg/dL) and 27 healthy volunteers were studied. Severe SIRS was caused by trauma in 14 patients (Injury Severity Score of 30.1 ± 10.8) and by sepsis in 23 patients. The counts of γδ and αβ T lymphocytes were determined by flow cytometry of cells stained with monoclonal antibodies to γδ and αβ T lymphocyte receptors. The activation of these cells was evaluated by flow cytometry of cells stained with monoclonal antibodies to CD69 and HLA-DR. Serial counts and activation of γδ and αβ T lymphocytes were also determined in eight trauma patients (Injury Severity Score of 31.0 ± 13.5) during a 2-week observation period. The count of γδ T lymphocytes in the peripheral blood of SIRS patients (30.1 ± 6.0/μL) was significantly lower (P < 0.05) than that of the healthy volunteers (104.3 ± 10.9/μL). The expression of CD69, an index of early activation of T lymphocytes, was significantly greater on γδ T lymphocytes from SIRS patients (patients 23.9% ± 3.4%, healthy controls 4.8% ± 0.6%, P < 0.05). In trauma patients, the expression of CD69 on γδ T lymphocytes increased rapidly within 48 h after injuries. In conclusion, γδ T lymphocytes are activated and decreased in the peripheral blood of severe SIRS patients. In trauma patients, the activation of γδ T lymphocytes occurs in the fairly acute phase after injuries. These results suggest a significant role for γδ T lymphocytes as early responders after severe insult.


Journal of Trauma-injury Infection and Critical Care | 2002

Activated polymorphonuclear leukocytes enhance production of leukocyte microparticles with increased adhesion molecules in patients with sepsis

Satoshi Fujimi; Hiroshi Ogura; Hiroshi Tanaka; Taichin Koh; Hideo Hosotsubo; Yasushi Nakamori; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Leukocyte microparticles (MPs) derived from polymorphonuclear leukocytes (PMNLs) have been recently found to be activators of vascular endothelium in vitro. The precise role of leukocyte MPs has not been clarified in patients suffering severe insult. The objective of this study was to evaluate production of leukocyte MPs and expression of adhesion molecules on the MP surface in patients with sepsis. METHODS Twenty-one patients with severe infection (fulfilling the criteria of sepsis with serum C-reactive protein > 10 mg/dL) and 21 healthy volunteers were included as study subjects. Production of leukocyte MPs, expression of CD11b on the MPs, and oxidative activity of PMNLs were measured by flow cytometry in the presence and absence of formyl-methionyl-leucyl-phenylalanine. CD11b expression was evaluated according to the MP size (more than, equal to, or less than 1.0 microm). Soluble E-selectin, thrombomodulin, and PMNL elastase were also measured in blood. RESULTS Production of leukocyte MPs and superoxide production in PMNLs with and without formyl-methionyl-leucyl-phenylalanine increased significantly in patients with sepsis in comparison with production in normal volunteers. In patients with sepsis, expression of CD11b was also markedly enhanced on MPs less than 1.0 microm in diameter in comparison with expression in control subjects. Levels of soluble E-selectin, thrombomodulin, and PMNL elastase in blood were significantly increased in patients with sepsis. We succeeded in detecting leukocyte MPs visually by fluorescence microscopy. CONCLUSION Activated PMNLs enhance production of leukocyte MPs with increased adhesion molecules in patients with sepsis. Activated leukocyte MPs may play a role in the pathogenesis of endothelial activation and leukocyte-endothelium interaction in the presence of sepsis.


Journal of Trauma-injury Infection and Critical Care | 2003

Mild hypothermia reduces expression of heat shock protein 60 in leukocytes from severely head-injured patients

Naoyuki Hashiguchi; Tadahiko Shiozaki; Hiroshi Ogura; Hiroshi Tanaka; Taichin Koh; Mitsuhiro Noborio; Keiko Fugita; Pavel Akimau; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Infectious complications are among the most serious problems that occur in severely head-injured patients treated with mild hypothermia. The mechanism underlying the susceptibility to infection has not been clarified. Heat shock protein (HSP) 60 has been reported to play an essential role in innate immunity. Thus, we conducted a study to clarify the impact of mild hypothermia on the expression of HSPs in polymorphonuclear leukocytes (PMNLs) in severely head-injured patients. METHODS Between September 1997 and November 1999, 17 severely head-injured patients with a Glasgow Coma Scale score of 8 or less at admission in whom intracranial pressure could be maintained below 20 mm Hg by conventional therapy were randomly assigned to two treatment groups: a mild hypothermia group (HT group, nine patients) and a normothermia group (NT group, eight patients). The HT group was subjected to mild hypothermia (intracranial temperature, 34 degrees C) for 48 hours followed by rewarming at a rate of 1 degrees C per day for 3 days, whereas the NT group was subjected to normothermia (intracranial temperature, 37 degrees C) for 5 days. Blood samples were serially obtained at three time points; days 0 to 1, days 2 to 5, and days 6 to 14 after head injury. We measured the expression of HSP27, HSP60, HSP70, and HSP90 by flow cytometry. RESULTS The two groups were similar with respect to prognostic factors, and there was no difference in clinical outcome. The expression of PMNL HSP60 in the HT group was significantly lower in all three time periods compared with that in the NT group (p < 0.05), whereas expression of the other HSPs did not differ significantly between the groups. The incidence of infectious complications was significantly increased in the HT group over that in the NT group (p < 0.05). In in vitro studies, PMNLs from 10 healthy volunteers were incubated at 37 degrees C, 34 degrees C, or 26 degrees C for 1 hour with sodium arsenite (100 micromol/L), an HSP inducer. The expression of HSP60 at 26 degrees C and 34 degrees C was significantly lower than that at 37 degrees C (p < 0.05), whereas expression of the other HSPs did not differ significantly at 26 degrees C, 34 degrees C, or 37 degrees C. CONCLUSION Mild hypothermia reduces the expression of HSP60 in PMNLs from severely head-injured patients. Thus, mild hypothermia may suppress innate immunity.


Journal of Burn Care & Rehabilitation | 2002

Long-term enhanced expression of heat shock proteins and decelerated apoptosis in polymorphonuclear leukocytes from major burn patients.

Hiroshi Ogura; Naoyuki Hashiguchi; Hiroshi Tanaka; Taichin Koh; Mitsuhiro Noborio; Yasushi Nakamori; Masato Nishino; Yasuyuki Kuwagata; Takeshi Shimazu; Hisashi Sugimoto

Heat shock proteins (HSPs), as molecular chaperones, have been reported to protect cells against a variety of environmental stresses. The objective of this study was to clarify the serial changes in expression of HSPs, oxidative activity, and apoptosis in polymorphonuclear leukocytes (PMNLs) from burn patients. Eight patients with severe burns (mean burn index 24.0 +/- 6.1) were included. Blood samples were serially obtained at five time points: days 0 to 1, days 2 to 7, days 8 to 14, days 15 to 21, and days 22 to 28. We measured expressions of HSP27, HSP60, HSP70, and HSP90 in permeabilized PMNLs by flow cytometry with the use of a monoclonal antibody against each HSP. The oxidative activity and apoptosis in PMNLs were also measured by flow cytometry. During all five time periods, expressions of HSP27, HSP60, and HSP70 in PMNLs from burn patients were significantly greater than those in PMNLs from healthy volunteers. The expression of HSP90 in PMNLs of burn patients increased between days 2 and 21. Oxidative activity in their PMNLs was significantly enhanced between days 2 and 28, and PMNL apoptosis was markedly inhibited for as long as 4 weeks after thermal injury. In conclusion, major burn causes long-term, enhanced expression of HSPs in PMNLs along with increased oxidative activity and decelerated apoptosis. The enhanced expression of HSPs may regulate the oxidative stress response and life-span of PMNLs in burn patients.


Journal of Trauma-injury Infection and Critical Care | 2013

Platelet mitochondrial membrane potential correlates with severity in patients with systemic inflammatory response syndrome.

Kazuma Yamakawa; Hiroshi Ogura; Taichin Koh; Yoshihito Ogawa; Naoya Matsumoto; Yasuyuki Kuwagata; Takeshi Shimazu

BACKGROUND The role of mitochondrial dysfunction has not been thoroughly clarified in the pathogenesis of critically ill patients. The objective of this study was to investigate mitochondrial membrane potential (&Dgr;&PSgr;m) and apoptosis in circulating platelets in patients with systemic inflammatory response syndrome (SIRS). METHODS This prospective observational study was conducted from May 2011 to February 2012. Criteria for inclusion were adult patients with SIRS. We used mitochondrial indicator JC-1 in conjunction with flow cytometry to measure &Dgr;&PSgr;m and annexin V to evaluate apoptosis in peripheral blood platelets. &Dgr;&PSgr;m was expressed as the percentage of platelets with altered &Dgr;&PSgr;m. Severity of illness was assessed by SIRS score, Acute Physiology and Chronic Health Evaluation II score, and Sequential Organ Failure Assessment score. RESULTS This study was composed of 36 patients who met the inclusion criteria and 12 healthy controls. Causes of SIRS were sepsis in 13, trauma in 13, and others in 10 patients. Platelet &Dgr;&PSgr;m depolarization was significantly enhanced in patients with SIRS versus that in controls (median [interquartile range], 10.6% [8.1–12.6%] vs. 7.1% [6.1–8.0%]; p < 0.001). The percentage of apoptotic platelets was significantly higher in patients with SIRS than in controls (8.7% [5.5–13.5%] vs. 5.4% [3.9–7.0%]; p = 0.006). Interestingly, &Dgr;&PSgr;m depolarization increased significantly with the increase in SIRS scores (p < 0.001). There was a significant correlation between &Dgr;&PSgr;m depolarization and severity of illness, as indicated by Acute Physiology and Chronic Health Evaluation II score, Sequential Organ Failure Assessment score, and serum lactate levels (all, p < 0.05). CONCLUSION We demonstrated that &Dgr;&PSgr;m depolarization and apoptosis were enhanced in circulating platelets in patients with SIRS. Our findings suggest that &Dgr;&PSgr;m depolarization may be associated with the progression of SIRS. LEVEL OF EVIDENCE Diagnostic study, level III.


Journal of Trauma-injury Infection and Critical Care | 2001

Enhanced expression of heat shock proteins in leukocytes from trauma patients.

Naoyuki Hashiguchi; Hiroshi Ogura; Hiroshi Tanaka; Taichin Koh; Masayuki Aoki; Tadahiko Shiozaki; Tetsuya Matsuoka; Takeshi Shimazu; Hisashi Sugimoto

BACKGROUND Heat shock proteins (HSPs) play essential roles as molecular chaperones in cells to assist in the repair of degenerated proteins. The expression of HSPs in polymorphonuclear leukocytes (PMNLs) following insult has not been delineated. The objective of this study was to clarify the serial changes in HSP expression in PMNLs from trauma patients. METHODS Fifty severely injured patients (mean Injury Severity Score of 31.8 +/- 10.8) and 17 healthy volunteers were included as study subjects. Blood samples were serially obtained at three time points: days 0 to 1, days 2 to 5, and days 6 to 14 after the trauma event. We measured expressions of HSP27, HSP60, HSP70, and HSP90 in permeabilized PMNLs by flow cytometry using a monoclonal antibody generated against each HSP and fluorescein isothiocyanate-conjugated antimouse immunoglobulins as secondary reagents. We also evaluated the expression of HSP70 mRNA in PMNLs by Northern blot hybridization and the expression of HSP70 in PMNLs by fluorescence microscopy. RESULTS Expressions of HSP27, HSP70, and HSP90 in PMNLs from trauma patients were significantly greater than in PMNLs from healthy volunteers in all three periods (days 0-1, days 2-5, and days 6-14). The expression of HSP60 in PMNLs from trauma patients was significantly greater than normal expression on days 2 to 5 and days 6 to 14. The values for HSP27, HSP60, and HSP70 on days 2 to 5 were significantly higher than those on days 0 to 1. The expression of HSP70 mRNA in PMNLs was significantly enhanced for as long as 2 weeks after trauma compared with that in normal volunteers. CONCLUSION Severe trauma causes demonstrated enhanced expression of HSPs in PMNLs during the acute phase. This enhanced expression of HSPs may regulate PMNL functions.


Shock | 2015

Enhanced Expression of Cell-Specific Surface Antigens on Endothelial Microparticles in Sepsis-Induced Disseminated Intravascular Coagulation

Hisatake Matsumoto; Kazuma Yamakawa; Hiroshi Ogura; Taichin Koh; Naoya Matsumoto; Takeshi Shimazu

ABSTRACT Sepsis-induced disseminated intravascular coagulation (DIC) is a major cause of death in patients admitted to intensive care units. Endothelial injury with microparticle production is reported in the pathogenesis of sepsis. Endothelial microparticles (EMPs) present several cell-specific surface antigens with different bioactivities, for example, tissue factor (TF), thrombomodulin (TM), and endothelial protein C receptor (EPCR). We investigated associations between these three different surface antigen–positive EMPs and sepsis-induced DIC. This cross-sectional study composed of 24 patients with sepsis and 23 healthy controls was conducted from November 2012 to September 2013. Blood samples were collected from patients within 24 h of diagnosis of severe sepsis and from healthy controls. Numbers of TF-positive EMPs (TF+ EMPs), TM-positive EMPs (TM+ EMPs), and EPCR-positive EMPs (EPCR+ EMPs) were measured by flow cytometry immediately thereafter. Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were assessed in the severe sepsis patients at enrollment. We assessed DIC with the International Society of Thrombosis and Haemostasis (ISTH) overt DIC diagnostic criteria algorithm. Numbers of antigen-positive EMPs were increased significantly in both severe sepsis patients and controls and with the increase in ISTH DIC score. Numbers of TF+ EMPs and EPCR+ EMPs correlated significantly with Sequential Organ Failure Assessment score, and numbers of EPCR+ EMPs correlated significantly with Acute Physiology and Chronic Health Evaluation II score. Numbers of the three antigen-positive EMPs were increased significantly in severe sepsis patients versus those in healthy controls and with the increase of ISTH DIC score, suggesting that the specific bioactivity of each antigen-positive EMP may play a role in the progression of sepsis-induced DIC.

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