Abstract: The present invention provides a neutrophil activation regulator comprising a histidine-rich glycoprotein (HRG) for the treatment of systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation in a subject in need thereof. Further, the present invention provides methods for predicting the severity of systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation in a subject in need thereof, and methods for predicting the survival of a subject with systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation, that comprise determining the blood level of histidine-rich glycoprotein in the subject.

Abstract: The present invention provides a therapeutic agent, a treatment method and an inspection method for diseases caused by activation of neutrophils. More specifically, the invention relates to a neutrophil activation regulator which comprising a histidine-rich glycoprotein (HRG) as an active ingredient, and provides a therapeutic agent for diseases caused by neutrophil activation comprising the neutrophil activation regulator, a treatment method for diseases caused by neutrophil activation, and further an inspection method for diseases caused by neutrophil activation. The present invention is based on the neutrophil activation regulator including the HRG as an active ingredient. The present invention extends to the depressant agent for neutrophil-vascular endothelial cell interaction including the HRG of the present invention as an active ingredient, the treatment method for diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation.

Abstract: The present invention provides a neutrophil activation regulator comprising a histidine-rich glycoprotein (HRG) for the treatment of systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation in a subject in need thereof. Further, the present invention provides methods for predicting the severity of systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation in a subject in need thereof, and methods for predicting the survival of a subject with systemic inflammatory response syndrome (SIRS), diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation, that comprise determining the blood level of histidine-rich glycoprotein in the subject.

Abstract: The present invention provides a therapeutic agent, a treatment method and an inspection method for diseases caused by activation of neutrophils. More specifically, the invention relates to a neutrophil activation regulator which comprising a histidine-rich glycoprotein (HRG) as an active ingredient, and provides a therapeutic agent for diseases caused by neutrophil activation comprising the neutrophil activation regulator, a treatment method for diseases caused by neutrophil activation, and further an inspection method for diseases caused by neutrophil activation. The present invention is based on the neutrophil activation regulator including the HRG as an active ingredient. The present invention extends to the depressant agent for neutrophil-vascular endothelial cell interaction including the HRG of the present invention as an active ingredient, the treatment method for diseases caused by neutrophil activation and/or inflammatory diseases accompanied by neutrophil activation.

Abstract: The objective of the present invention is to provide an agent which is useful for suppressing actual atherosclerosis and has few side-effects. The suppressant for atherosclerosis according to the present invention is characterized in comprising an anti-HMGB1 monoclonal antibody binding to C-tail of HMGB1 as an active component.

Abstract: The objective to be solved by the present invention is to provide a method for effectively suppressing cerebral edema. The method for suppressing cerebral edema according to the present invention is characterized in comprising a step of administering an anti-HMGB 1 antibody recognizing 208EEEDDDDE215 (SEQ ID NO:1) as an HMGB1 epitope.

Abstract: An object of the present invention is to provide a cerebral infarction suppressant which is effective for brain tissue necrosis after long-time ischemia as in actual cerebral infarction and has fewer side effects. The cerebral infarction suppressant of the present invention is characterized in that histidine is contained and the cerebral infarction is attributed to long-time ischemia.

Abstract: An objective of the present invention is to provide a suppressant for cerebral infarction occurred after long-term ischemia associated with actual cerebral infarction, and has fewer side effects. The cerebral infarction suppressant of the present invention is characterized in comprising an anti-HMGB1 monoclonal antibody as an active ingredient.

Abstract: An object of the present invention is to provide a cerebral infarction suppressant which is effective for brain tissue necrosis attributed to long-time ischemia as in actual cerebral infarction and has fewer side effects. The suppressant for cerebral infarction attributed to long-time ischemia according to the present invention is characterized in that a histidine and an H3-receptor blocker or a histidine and a histamine N-methyltransferase inhibitor are comprised as active ingredients.