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Results for “Reactive Inhibition”

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At least 217 records · Page 12Linked to original sources
PubMed1994

Mitogen- and antigen-specific proliferation of T cells in murine toxoplasmosis is inhibited by reactive nitrogen intermediates.

Acute and chronic infections with Toxoplasma gondii result in a nonspecific suppression of immunologic function in mice and humans. Proliferation of spleen cells in response to concanavalin A (ConA) and toxoplasma lysate antigen (TLA) was studied during the course of infection in mice susceptible (CBA/Ca) and resistant (BALB/c) to development of toxoplasmic encephalitis to determine if reactive nitrogen intermediates (RNI) are involved in the suppression of the proliferative responses. Maximal suppression of proliferation of spleen cells in response to ConA and TLA was observed on days 7 and 14 after infection and correlated with elevated levels of nitrite in spleen cell culture supernatants. By day 68 postinfection in BALB/c mice, proliferative responses returned to normal levels, whereas in CBA/Ca mice, they remained suppressed. The addition of an inhibitor of production of RNI (NG-monomethyl-L-arginine) increased proliferation of spleen cells in response to both ConA and TLA at days 7, 14, and 21 after infection. Depletion of adherent cells from spleen cell preparations obtained from acutely infected mice followed by their repletion with adherent spleen cells from uninfected mice resulted in increased proliferation of spleen cells from infected mice and a significant decrease in nitrite in the cultures. These results indicate that production of RNI by macrophages contributes significantly to the suppression of the spleen cell proliferation observed in the acute stage of toxoplasmosis.

Animals↗
PubMed2006

Inhibition of reactive nitrogen species production in COPD airways: comparison of inhaled corticosteroid and oral theophylline.

BACKGROUND: Reactive nitrogen species (RNS) are thought to be one of the important factors in the pathogenesis of chronic obstructive pulmonary disease (COPD). A study was undertaken to examine the effects of theophylline and fluticasone propionate (FP) on RNS production in subjects with COPD. METHODS: Sixteen COPD subjects participated in the study. Theophylline (400 mg/day orally) or FP (400 mug/day inhalation) were administered for 4 weeks in a randomised crossover manner with a washout period of 4 weeks. Induced sputum was collected at the beginning and end of each treatment period. 3-nitrotyrosine (3-NT), which is a footprint of RNS, was quantified by high performance liquid chromatography with an electrochemical detection method as well as by immunohistochemical staining. RESULTS: Theophylline significantly reduced the level of 3-NT in the sputum supernatant as well as the number of 3-NT positive cells (both p<0.01). FP also reduced 3-NT formation, but the effect was smaller than that of theophylline. Theophylline also significantly reduced the neutrophil cell counts in the sputum (p<0.01), while FP treatment had no effect on the number of inflammatory cells in the sputum, except eosinophils. CONCLUSIONS: Theophylline reduces nitrative stress and neutrophil infiltration in COPD airways to a larger extent than inhaled corticosteroid.

Administration, Inhalation↗
PubMed2006

Targeting the expression of platelet-derived growth factor receptor by reactive stroma inhibits growth and metastasis of human colon carcinoma.

The stromal cells within colon carcinoma express high levels of the platelet-derived growth factor receptor (PDGF-R), whereas colon cancer cells do not. Here, we examined whether blocking PDGF-R could inhibit colon cancer growth in vivo. KM12SM human colon cancer cells were injected subcutaneously (ectopic implantation) into the cecal wall (orthotopic implantation) or into the spleen (experimental liver metastasis) of nude mice. In the colon and liver, the tumors induced active stromal reaction, whereas in the subcutis, the stromal reaction was minimal. Groups of mice (n=10) received saline (control), the tyrosine kinase inhibitor imatinib, irinotecan, or a combination of imatinib and irinotecan. Four weeks of treatment with imatinib and irinotecan significantly inhibited tumor growth (relative to control or single-agent therapy) in the cecum and liver but not in the subcutis. The combination therapy completely inhibited lymph node metastasis. Imatinib alone or in combination with irinotecan inhibited phosphorylation of PDGF-Rbeta of tumor-associated stromal cells and pericytes. Combination therapy also significantly decreased stromal reaction, tumor cell proliferation, and pericyte coverage of tumor microvessels and increased apoptosis of tumor cells and tumor-associated stromal cells. These data demonstrate that blockade of PDGF-R signaling pathways in tumor-associated stromal cells and pericytes inhibits the progressive growth and metastasis of colon cancer cells.

Animals↗
PubMed1991

The effect of serum from patients with acute myocardial infarction on in vitro lymphocyte reactivity. II. Inhibition of IL-2 production.

Culture supernatants from concanavalin-A (con-A)-activated peripheral blood lymphocytes from healthy controls grown in the presence of sera from 20 patients 24 hours and 1 week after acute myocardial infarction (AMI) were tested for their mitogenic activity and for the presence of interleukin-2 (IL-2). Binding of exogenous IL-2 to activated lymphocytes from 10 patients was also determined. In supernatants prepared in the presence of patients' as compared to control sera, a significantly decreased mitogenic activity and IL-2 content were found. The mitogenic activity and IL-2 content in culture supernatants prepared with patients' sera collected 24 hours after the AMI (AMI I) and one week thereafter (AMI II) were significantly suppressed, and the degree of suppression in the 24-hour sera was significantly higher than in those collected after one week. No significant differences were observed in the binding capacity to exogenous IL-2 of activated patients' and control lymphocytes. The possibility is that immunosuppressive factors in the patients' sera, including cortisol, may suppress the patients' immune response acting through inhibition of IL-2 production.

Aged↗
PubMed1991

The effect of serum from patients with acute myocardial infarction on in vitro lymphocyte reactivity. I. Inhibition of mitogen stimulation.

Sera from 20 patients obtained within 24 hours and one week after acute myocardial infarction (AMI) were tested for their immunomodulating effect on concanavalin-A (con-A) stimulated lymphocyte cultures from 11 healthy unrelated donors. Individual control sera from 21 healthy donors and 5 pools of control sera were used for comparison. Cortisol levels were tested in patients' and controls' sera. A significantly higher suppressive effect was seen in the presence of patients' sera taken at 24 hours than corresponding sera taken one week later. However, the suppressive effect after one week was increased as compared to control sera. A significant correlation between the degree of suppression and the cortisol level in corresponding sera was observed. An increased immunosuppression was observed with increased cortisol levels.

Adjuvants, Immunologic↗