No abstract available.
Mast Cells*

No abstract available.
Vibrio vulnificus* ; Vibrio*

The present study was undertaken to investigate the effect of ethanol administration on the resistance of mice to Cryptococcus neoformans, IL-2 production of murine splenocytes, active systemic anaphylaxis induced by ovalbumin (OVA), serum TNF-alpha production, nitric oxide (NO) production by peritoneal machrophages and B16F10 melanoma colonization in lungs in mice. It was found that ethanol administration significantly inhibited the resistance of mice to C. neoformans infection, IL-2 production, active systemic anaphylaxis induction, serum TNF- alpha production and NO production. Ethanol administration significantly enhanced lung colonization when it was administered before i.v. melanoma inoculation. These results demonstrate that ethanol may play a critical role in tumorigenesis and immunoregulation as an immunomodulator.
Anaphylaxis* ; Animals ; Carcinogenesis ; Colon ; Cryptococcus neoformans ; Cytokines* ; Ethanol ; Interleukin-2 ; Lung ; Melanoma* ; Mice ; Nitric Oxide* ; Ovalbumin ; Tumor Necrosis Factor-alpha

No abstract available.
Animals ; Ethanol* ; Interleukin-2* ; Interleukin-6* ; Rats*

No abstract available.
Animals ; Euonymus* ; Mice*

Septic shock is one of the leading cause of death in hospitalized patients and mortality rates of up to 50 % have been reported. Despite all efforts, no regimen today seems to be successful in the treatment of septic shock. The endogenous opioid system (EOS) includes three major families of peptides: dynorphins, endorphins and enkephalins. Several lines of evidence indicate that EOS is implicated in the pathophysiology of anaphylactic and endotoxic shock. An opioid receptor blocker naloxone has been used extensively in studies for the role of EOS or endogenous opiod peptides (EOP). However, there have been few, if any, detailed investigative studies regarding the effect of naloxone on TNF-a production and the lethality in response to endotoxin, and tumorigenesis. ...continue...
Carcinogenesis* ; Cause of Death ; Dynorphins ; Endorphins ; Enkephalins ; Humans ; Melanoma ; Mortality ; Naloxone* ; Nitric Oxide ; Peptides ; Receptors, Opioid* ; Shock, Septic*

Thl cloned cell line 28-4 which is an I-A + KLH - specific Th1 type clone of (C57BU6xC 3H) F1 origin was kindly provided by professor Tomio Tada. In these studies, employing these cloned cells, the author investigated both proliferation responses of Thl cells in the presence of various concentrations of cytokines, such as IL-2, IL-4 or IL-6 and proliferation of Thl cells to various concentration of mitogens such as PHA, ConA or PWM. In addition, the author also investigated the proliferation response of Th1 cells to the optimal dose of PHA, ConA or PWM in the presence or absence of above mentioned cytokines. It was found that IL-2, IL-4 or IL-6 alone their growth stimulation degree was dependent on cytokine concentration and that PHA, ConA or PWM stimulated Thl cell proliferation and optimal dose of PHA ConA and PWM was 3 g, 4 g and 2 g per ml, respectively. In addition, proliferation response of Th1 cells to ConA or PWM in the presence of IL-2 was significantly enhanced, but the proliferation response to PHA was not increased significantly. However, IL-4 did not significantly modulate mitogen-activated Thl cell proliferation response. Interestingly, IL-6 decreased PHA- or ConA-activated proliferation of Thl cells, but did not change PWM-activated proliferation. Taken together, these studies strongly suggested that IL-2, IL-4 or IL-6 itself clone stimulated the Thl cell proliferation and that PHA, ConA or PWM also stimulated Thl cell proliferation. In addition, these studies also indicated that IL-2 increased ConA- or PWM-activated Thl cell proliferation, but IL6 inhibited PHA- or ConA-activated Th1 cell proliferation and that IL-4 did not significantly change the mitogen-activated Th1 cell proliferation.
Cell Line ; Cell Proliferation ; Clone Cells ; Cytokines* ; Interleukin-2 ; Interleukin-4 ; Interleukin-6 ; Mitogens ; Th1 Cells*

No abstract available.
Animals ; Interleukin-2* ; Interleukin-6* ; Mice* ; Pseudomonas aeruginosa* ; Pseudomonas*

No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*

No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*