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Biomedical subjects

M J Rios

Publications and source records attributed to M J Rios.

11 recordsLinked to original sources
PubMed1993

Decrease in susceptibility to oral tolerance induction and occurrence of oral immunization to ovalbumin in 20-38-week-old mice. The effect of interval between oral exposures and rate of antigen intake in the oral immunization.

Maturation into adulthood, from 8 to 24 weeks of age, significantly influences the induction of oral tolerance in different strains of mice. Animals from strains which are susceptible to the induction of oral tolerance to ovalbumin (OVA) at 8 weeks of age become refractory at 24 weeks of age. Furthermore, in several strains, intermittent exposure to OVA exclusively by gavage resulted in high titres of circulating anti-OVA antibodies. However, the voluntary intake of similar doses of OVA at the same intervals failed to immunize mice of one of the most responsive strains, H-III.

Administration, Oral↗
PubMed1992

Interleukin-4 inhibits human macrophage activation by tumor necrosis factor, granulocyte-monocyte colony-stimulating factor, and interleukin-3 for antileishmanial activity and oxidative burst capacity.

Interleukin (IL)-4 has been implicated in the pathogenesis of leishmaniasis in a murine model. Experiments were done to examine the effect of IL-4 on cytokine activation of macrophages. Interferon (IFN)-gamma, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF alpha), and IL-3 activate macrophages to inhibit replication of leishmaniae. IL-4 abrogated in a dose- and time-dependent manner the induction of antileishmanial activity by these cytokines. The depression of oxidative burst capacity is one mechanism by which IL-4 inhibits macrophage activation. IL-4 diminished in a dose- and time-dependent manner the TNF alpha enhancement of oxidative capacity. Pretreatment with IL-4 for 48, 24, or 0 h, respectively, inhibited the generation of superoxide induced by TNF alpha by 90%, 60%, and 40%. Furthermore, IL-4 abrogated the enhancement of oxidative capacity by IFN-gamma, GM-CSF, and IL-3. These data suggest that IL-4 is a potent deactivator of macrophage antimicrobial functions and may contribute to the pathogenesis of visceral leishmaniasis.

Animals↗
PubMed1990

[Double outlet left ventricle with pulmonary atresia].

A case of double outlet left ventricle with pulmonary atresia is reported. The hypoplasia of the left ventricule produced by the almost total absence of its trabecular zone has not been previously reported.

Heart Ventricles↗
PubMed1988

Tolerance induction and immunological priming initiated by mucosal contacts with protein antigens in inbred strains of mice.

1. We show that mouse strains differ widely in susceptibility to tolerance induction and/or immunization (priming) following contact of protein antigens (ovalbumin, human or bovine gamma globulins) with different mucosal surfaces. 2. When compared to a control group pretreated with saline, mice pretreated by the oral (intragastric) route with antigen became significantly less responsive to subsequent parenteral immunization (i.e., tolerant). This was observed in most, but not all, antigen/strain combinations. 3. Similar, although less prominent changes were induced by pretreatments with antigen by the ocular (conjunctival) route. 4. No significant effects were observed following pretreatments by the nasal, vaginal or rectal routes. 5. Genes present in strains selected for multispecific "high" or "low" responsiveness are included among those involved in tolerance induction following mucosal contacts with protein antigens.

Animals↗
PubMed1987

Genetics of susceptibility to oral tolerance to ovalbumin.

Inbred mouse strains vary widely in their susceptibility to the induction of tolerance following oral (intragastric) administration of ovalbumin. Marked differences were found between strains that form a congenic pair differing at the H-2 complex: C3H/HeJ (H-2k) and C3H.SW (H-2b)-which were very susceptible and resistant to tolerance induction, respectively. In contrast, no significant differences were found between A/J (H-2a) and A.BY (H-2b) congenics, which were both susceptible, nor among C57BL/10J congenics, which were uniformly resistant to tolerance induction. We conclude that H-2-linked genes determine tolerance susceptibility in conjunction with background genes.

Administration, Oral↗