Search PubMed⌕ Search

Biomedical subjects

A Cerny

Publications and source records attributed to A Cerny.

62 records · Page 4Linked to original sources
PubMed1986

Suppressive effects of B-lactam-antibiotics on in vitro generation of cytotoxic T-cells.

The in vitro effect of several compounds containing the B-lactam structure (including 6-aminopenicillanic acid, piperacillin, 7-aminocephalosporanic acid, ceftazidime and clavulanic acid) on the generation of cytotoxic lymphocytes was investigated in two different in vitro systems: (1) generation of virus specific cytotoxic T-cells and (2) proliferation of lymphocytes were assessed in secondary in vitro anti-viral immune responses. Both activities were suppressed by B-lactams in a dose-dependent manner. In these experiments, as found previously with human in vitro granulopoesis and proliferation of the human erythroleukaemic cell line K-562, cephalosporins and clavulanic acid were five to twenty times more suppressive than penicillins. Since concentrations that were effective in vitro are being achieved, particularly with cephalosporins, in the serum of patients, the possible clinical consequences of our findings may have to be taken into consideration.

Animals↗
PubMed1986

Generation of agammaglobulinaemic mice by prenatal and postnatal exposure to polyclonal or monoclonal anti-IgM antibodies.

Improved experimental conditions are described for the treatment of mice with anti-IgM antibody, which subsequently lead to B-cell deficiency and agammaglobulinaemia. Antibody transmitted via maternal milk alone was found to be more efficient in inducing suppression of serum immunoglobulin isotypes than prenatal transmission or postnatal intraperitoneal injections alone. However, the combined treatment by all three routes of exposure to anti-IgM resulted in total B-cell suppression associated with undetectable levels of all serum immunoglobulin isotypes. Furthermore, suppression of B-cell generation was also achieved with a rat monoclonal mu-specific antibody. The possibility of generating agammaglobulinaemic mice may be useful for investigating the influence of B cells on the generation of T-cell reactivities, and for analysing the effects of monoclonal antibodies in the absence of interfering serum immunoglobulin.

Agammaglobulinemia↗
PubMed1986

Effect of cyclosporin A on immunity to Listeria monocytogenes.

The effect of the immunosuppressive drug cyclosporin A (CS-A) on immunity to the facultative intracellular bacterium Listeria monocytogenes was investigated in unprimed and primed mice. Different treatment protocols were followed to evaluate the time dependence of CS-A-mediated immune suppression and the effect of CS-A on immunological memory to L. monocytogenes. The effect of CS-A was observed only during and after activation of T cell-mediated immunity, whereas early resistance exerted by macrophages assessed 6 and 70 min after challenge remained unaffected. CS-A suppressed efficient elimination of L. monocytogenes even when given after day 3 of a primary infection. This contrasts with findings in other models, including viral infections, where CS-A must be administered very early in an immune response to suppress it. CS-A suppressed antibacterial resistance in mice primed at various times before challenge; suppression of protection was time dependent and was virtually complete in livers, whereas CS-A-resistant memory persisted in spleens for up to 10 months.

Animals↗
PubMed1986

Effects of cyclosporin A on humoral immune response and resistance against vesicular stomatitis virus in mice.

The effect of cyclosporin A (CS-A) on the antiviral humoral response was studied by using vesicular stomatitis virus (VSV); VSV provided the opportunity to simultaneously assess both T-independent and T-dependent antibody responses. The T-independent anti-VSV immunoglobulin M (IgM) response was virtually unaffected, whereas the T-dependent primary anti-VSV IgG response was suppressed by CS-A; in contrast, the secondary IgG response was highly resistant to CS-A. Moreover, once the switch from IgM to IgG had occurred, the primary response also became refractory to suppression by CS-A. We concluded that the effect of CS-A on the primary anti-VSV antibody response was mediated via impairment of a T-dependent mechanism; in contrast, memory T cells or memory B cells or both were quite resistant to the suppressive effects of CS-A. CS-A treatment rendered mice highly susceptible to VSV infection; under CS-A treatment, mortality was 100% after infection via footpads, whereas immunocompetent mice survived. Since CS-A does not impair induction of early T-independent anti-VSV IgM neutralizing antibodies, this high mortality in CS-A treated mice illustrates the crucial role of CS-A-sensitive cells in resistance against VSV.

Animals↗
PubMed1985

Suppression by cyclosporin A of murine T-cell-mediated immunity against viruses in vivo and in vitro.

The immunosuppressive effect of Cyclosporin A on T-cell-mediated antiviral immune responses was examined. When administered intraperitoneally CS-A abrogated anti-vaccinia virus, anti-lymphocytic choriomeningitis virus (LCMV), and anti-vesicular stomatitis virus (VSV) T-cell responses in a dose-dependent fashion. Usually 50-60 mg/kg were efficient in suppressing primary T-cell responses completely. In contrast, 10-20 mg/kg often enhanced T-cell responses significantly when compared with controls. Suppression was observed if CS-A treatment was started before virus injection and up to 12 hr after infection; CS-A given 24 hr after the virus still suppressed T-cell activity partially. A 50 mg/kg dose of CS-A suppressed secondary anti-vaccinia virus or anti-VSV T-cell responses in vivo by a factor of about 10. This dose suppressed the primary T-cell-dependent footpad swelling induced by local LCMV infection and prevented T-cell-mediated immunopathological death due to LCM when LCMV was injected intracerebrally. In addition, clearance of LCMV was delayed drastically by CS-A treatment. When added to cultures of in vivo-primed antiviral T cells that were restimulated in vitro, CS-A inhibited both proliferation as well as generation of virus-specific cytotoxic T cells in a dose-dependent way. The results show that in CS-A-treated mice primary and secondary antiviral T-cell responses are strongly inhibited; acute viral infections with cytopathic viruses may therefore be more dramatic. In contrast immunopathological T-cell-mediated disease caused by noncytopathic viruses such as LCMV may be prevented or attenuated.

Animals↗
PubMed1985

Suppression of B cell development and antibody responses in mice with polyclonal rabbit and monoclonal rat anti-IgM antibodies. I. Characterization of the suppressed state.

Mice treated from birth with polyclonal, crude or affinity purified rabbit or monoclonal rat anti-mouse IgM antibodies [b-7-6 and C-2-23: Eur. J. Immunol. 14: 753-757, 1984] were found to be heavily suppressed with respect to B-cell activities. Crude or affinity purified rabbit or monoclonal rat anti-mouse IgM gave comparable results as follows: serum IgM was below detectable levels; serum IgG was reduced to about 1-3% of normal levels; free anti-IgM was always detectable; IgM and/or kappa-light-chain positive cells as well as IgM-secreting cells were absent in various lymphoid organs; the B-cell mitogen lipopolysaccharide was unable to induce proliferative responses; primary antibody responses could not be induced against sheep red blood cells and phosphorylcholine; lymphoid organs were reduced in size and B-cell areas were not populated with lymphocytes; besides a 40% reduction in absolute lymphocyte numbers in the blood, we found increased platelet counts and a 10% eosinophilia in anti-IgM-treated mice.

Animals↗