TY - JOUR
T1 - Pathophysiological Roles of G-CSF
AU - Ozawa, K.
AU - Watari, K.
AU - Tsuruta, T.
AU - Takahashi, S.
AU - Ogura, H.
AU - Yoshikubo, T.
AU - Nishikawa, M.
AU - Shimane, M.
AU - Okamoto, S.
AU - Tojo, A.
AU - Tani, K.
AU - Asano, S.
PY - 1992
Y1 - 1992
N2 - G-CSF is produced by a variety of cells. In situ hybridization showed that only a small proportion of stromal cells expressed G-CSF after stimulation with LPS or IL-1. The measurement of serum G-CSF level by enzyme immunoassay provided valuable information as to the pathophysiological roles of G-CSF. In aplastic anemia, there was an inverse correlation between blood neutrophil count and serum G-CSF level. Similarly, the G-CSF level rose during the neutropenic phase of cyclic neutropenia. These findings suggest that the serum G-CSF level is regulated by a feedback mechanism. In some cases, the reduced G-CSF production by stromal cells may underlie the pathogenesis of neutropenia. On the other hand, infections and cancers sometimes caused high serum G-CSF levels in association with increased blood neutrophils, presumably reflecting reactive and aberrant production of G-CSF, respectively. Expression of G-CSF by myeloid leukemia cells may partly contribute to their abnormal growth through the autocrine mechanism.
AB - G-CSF is produced by a variety of cells. In situ hybridization showed that only a small proportion of stromal cells expressed G-CSF after stimulation with LPS or IL-1. The measurement of serum G-CSF level by enzyme immunoassay provided valuable information as to the pathophysiological roles of G-CSF. In aplastic anemia, there was an inverse correlation between blood neutrophil count and serum G-CSF level. Similarly, the G-CSF level rose during the neutropenic phase of cyclic neutropenia. These findings suggest that the serum G-CSF level is regulated by a feedback mechanism. In some cases, the reduced G-CSF production by stromal cells may underlie the pathogenesis of neutropenia. On the other hand, infections and cancers sometimes caused high serum G-CSF levels in association with increased blood neutrophils, presumably reflecting reactive and aberrant production of G-CSF, respectively. Expression of G-CSF by myeloid leukemia cells may partly contribute to their abnormal growth through the autocrine mechanism.
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U2 - 10.3177/jnsv.38.Special_345
DO - 10.3177/jnsv.38.Special_345
M3 - Article
C2 - 1284303
AN - SCOPUS:17544400501
SN - 0301-4800
VL - 38
SP - 345
EP - 348
JO - The Journal of vitaminology
JF - The Journal of vitaminology
ER -