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J Salát

Publications and source records attributed to J Salát.

8 recordsLinked to original sources

Antibodies enhance the protective effect of CD4+ T lymphocytes in SCID mice perorally infected with Encephalitozoon cuniculi.

The role of antibodies in the immune response to microsporidiosis was studied using a novel anti-exospore monoclonal antibody (MAb) P5/H1, which recognizes surface antigens of Encephalitozoon cuniculi. The effect of the MAb on microsporidial infection in vivo was to prolong the survival of previously CD4+ reconstituted, perorally infected and intraperitoneally MAb-treated SCID mice. The MAb decreased the numbers of E. cuniculi spores in peritoneal smears obtained post mortem. These results suggest a possible role for antibodies in protection against perorally acquired E. cuniculi infection.

Animals↗

Anti-tumour necrosis factor-alpha activity in Ixodes ricinus saliva.

Tumour necrosis factor-alpha (TNF-alpha) is one of the most prominent inflammatory mediators playing a central role in starting off the inflammatory reactions of the innate immune system. We identified a TNF-alpha-inhibitory activity in the saliva and salivary gland extract (SGE) from partially fed Ixodes ricinus ticks. Using mouse and human TNF-alpha specific ELISA, we showed that tick saliva or SGE markedly reduced the level of detectable cytokine. Both saliva and SGE inhibited the cytotoxic effect of TNF-alpha in a bioassay. Elimination of the TNF-alpha-inhibitory activity in SGE by trypsin digestion demonstrated that the anti-TNF-alpha factor is a protein. Fast protein liquid chromatography fractionation of SGE showed one peak of TNF-alpha-inhibitory activity corresponding to a protein with estimated molecular mass 23 kDa. The likely mechanism of the inhibitory effect is a direct binding of the cytokine. The TNF-alpha-inhibitory molecule seems to play an important role in the anti-inflammatory effect of tick saliva at the tick feeding site, providing a gateway to the host for tick-borne pathogens.

Animals↗

Co-inoculation of Borrelia afzelii with tick salivary gland extract influences distribution of immunocompetent cells in the skin and lymph nodes of mice.

The impact of Ixodes ricinus salivary gland extract (SGE) on inflammatory changes in the skin and draining lymph nodes of mice, elicited by the infection with the important human pathogen, B. afzelii, was determined using flow cytometry. SGE injected together with spirochetes reduced the numbers of leukocytes and gammadelta-T lymphocytes in infected epidermis at early time-points post infection. In draining lymph nodes, the anti-inflammatory effect of SGE was manifested by the decrease of total cell count compared with that in mice treated with inactivated SGE. Changes in subpopulations of immunocompetent cells apparently reflected the effect of SGE on the proliferation of spirochetes in the host. The significance of tick saliva anti-inflammatory effect for saliva activated transmission of B. afzelii is shown.

Animals↗

Etiprednol dicloacetate, a new soft glucocorticoid drug candidate. Development of chemistry.

During development of chemistry of the soft drug candidate etiprednol dicloacetate (BNP-166) 1) optimization studies on the three-step chemical synthesis resulted in a process that could be scaled-up to the kg level, 2) the impurity profile was determined, 3) synthetic routes were developed for the preparation of the radiolabeled target compound, and 4) a series of hydroxylated metabolites was prepared.

Adrenal Cortex Hormones↗

[Encephalitozoon cuniculi and Encephalitozoon intestinalis--causes of opportunistic infections].

Microsporidia (phylum Microsporidia) are intracellular parasites that infect a wide range of protozoa, invertebrates and vertebrate hosts. Over a 1000 species have been classified into approximately 100 genera. Historically, microsporidial infections in silkworms, honey bees, and salmonid fish have been responsible for significant economic losses. More recently, microsporidiosis has been recognized as an important opportunistic infection in immunologically compromised patients. In this review there is information on the immunobiology of microsporidia Encephalitozoon cuniculi and Encephalitozoon intestinalis which were identified as the most common causative agents of microsporidiosis in mammals. Most of what is known about the immunology of microsporidiosis is based on experiments with the microsporidian Encephalitozoon cuniculi.

Animals↗

CD8+ T lymphocytes protect SCID mice against Encephalitozoon cuniculi infection.

Microsporidia are obligate intracellular parasites that cause opportunistic infections in immunocompromised patients. The role of two main T cell subsets in anti-microsporidial immunity has been studied using an Encephalitozoon cuniculi-severe combined immunodeficient (SCID) mouse model. Whereas SCID mice reconstituted with CD4+ T lymphocyte-depleted naive BALB/c splenocytes resolved the infection, adoptive transfer of CD8+ T cell-depleted splenocytes failed to protect the animals against a lethal E. cuniculi infection. Splenocytes from E. cuniculi-immune mice specifically killed syngeneic infected macrophages in a short-term 51Cr-release assay. These results suggest the crucial role of cytotoxic T lymphocytes in the protection against E. cuniculi infection.

Adoptive Transfer↗

Experimental infection of immunocompetent and immunodeficient mice with Encephalitozoon cuniculi.

An experimental infection with the microsporidian Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923 was studied using a model of immunocompetent BALB/c mice and immunodeficient SCID mice. The course of infection after intraperitoneal inoculation of E. cuniculi spores was evaluated using the presence of spores in peritoneal macrophages as a criterion. First significant decrease in the proportion of infected cells was recorded on day 9 post infection (p.i.) in BALB/c mice. From day 14 p.i. no spores were observed in macrophages from BALB/c mice, while the number of infected macrophages from SCID mice increased until the death of the mice. The natural killer (NK) cell activity of mouse splenocytes was compared with the production of interferon gamma (IFN-gamma) by these cells. While in BALB/c mice NK activity peaked on days 9 and 14 p.i., in SCID mice the marked increase of NK activity was recorded close before death of mice, on day 21 p.i. in correlation with the production of IFN-gamma. Production of specific antibodies was demonstrated from day 9 p.i. in sera from BALB/c mice. It is concluded that intraperitoneal infection of SCID mice with spores of E. cuniculi results in the marked increase in the number of peritoneal exudate cells and in the percentage of infected cells close before death of mice. Neither high activity of NK cells nor increased production of IFN-gamma are sufficient for the recovery of SCID mice from an E. cuniculi infection.

Animals↗

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Amino Acids↗