BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Pages 818-824 Tumor Necrosis Factor-lnduced Alterations in Circulating Leukocyte Populations

نویسندگان

  • Daniel G. Remick
  • Steven L. Kunkel
چکیده

Tumor necrosis factor is a potent agent possessing diverse biological functions. We investigated the effects of intravenous administration of human recombinant tumor necrosis factor (TNF) on immune cell populations in CBA/J mice. The animals developed a significant lymphopenia and neutrophilia both reaching a maximum at 4 hours post-injection with a trend towards resolution to normal values by 6 hours. The lymphopenia was both relative and absolute. Similarly, the neutrophilia was both relative and absolute and was due to the presence of both immature and mature neutrophils. As the neutrophilia and lymphopenia occurred concomitantly, there was no difference at any time point in the total number of peripheral blood white cells. Extensive controls were done to rule out LPS contamination in the TNF preparation. These data demonstrate the potent effects of intravenous administration of human recombinant tumor necrosis factor on peripheral blood constituents. © 1986 Academic Press, Inc.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Tumor necrosis factor stimulates interleukin-1 and prostaglandin E2 production in resting macrophages.

We have investigated the effect of tumor necrosis factor on the release of interleukin-1 and PGE2 from murine resident peritoneal macrophages. Tumor necrosis factor causes an increase in the production of interleukin-1 and PGE2 with a maximum induction for both noted at 5.9 X 10(-8) M. While indomethacin decreased tumor necrosis factor induced PGE2 production, this cyclooxygenase inhibitor augm...

متن کامل

Regulation of macrophage tumor necrosis factor production by prostaglandin E2.

We have studied the role of prostaglandin E2 on the modulation of tumor necrosis factor by immunologically elicited and lipopolysaccharide treated murine macrophages. Indomethacin, a potent inhibitor of prostaglandin E2 production, caused a dose dependent augmentation of lipopolysaccharide induced tumor necrosis factor production (2-3 fold at 10(-7) molar). Tumor necrosis factor was released in...

متن کامل

Characterization of chicken TNFR superfamily decoy receptors, DcR3 and osteoprotegerin.

Tumor necrosis factor (TNF) family ligands bind to death domain-containing TNF receptors (death receptors), which can subsequently activate intracellular signaling pathways to initiate caspase activity and apoptotic cell death. Decoy receptors, without intracellular death domains, have been reported to prevent cytotoxic effects by binding to and sequestering such ligands, or by interfering with...

متن کامل

Monocyte chemotactic protein gene expression by cytokine-treated human fibroblasts and endothelial cells.

A number of cytokines are active during the evolution of an inflammatory response, including tumor necrosis factor-alpha, interleukin-1, and novel chemotactic cytokines. This latter group of mediators belong to supergene families of inflammatory signals that play a key role in the selective recruitment of immune cells. In this presentation, we present data demonstrating, for the first time, end...

متن کامل

Kinetics of TNF, IL-6, and IL-8 gene expression in LPS-stimulated human whole blood.

While the production of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in septic shock and other inflammatory states is well established, the role of interleukin-8 (IL-8), a recently described neutrophil chemoattractant and activator, has yet to be fully elucidated. Using lipopolysaccharide (LPS)-stimulated human whole blood as an ex vivo model of sepsis, the kinetics of messenger RNA (mR...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2005