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Biomedical subjects

L Baranda

Publications and source records attributed to L Baranda.

23 records · Page 2Linked to original sources
PubMedDate not supplied

Natural killer cell-mediated cytotoxicity in cryptococcal meningitis.

There are evidences regarding the role of NK cytotoxic activity in the resistance against experimental C. neoformans infection. To assess the status of NK cell activity in human C. neoformans infection, we studied the peripheral blood of twelve patients with cryptococcal meningitis, six patients with CNS disease different to cryptococcal meningitis, and twelve healthy subjects. The number of CD16+cells and the NK cytotoxic activity of peripheral blood mononuclear cells was studied. The in vitro effect of exogenous IL-2 and interferon gamma on such cytotoxic activity was also studied. The number of CD16+ cells was not significantly different in patients compared to controls. However, cryptococcal patients exhibited a significant lower NK activity compared to both control groups (p less than 0.05 in both cases). The low NK activity of cryptococcal patients was fully reconstituted in vitro with the addition of rIL-2 but not with rIFN gamma. In vitro experiments suggest that the low NK activity of cryptococcal meningitis patients is not due to amphotericin B therapy or blockade of NK cells by C. neoformans-derived molecules. The results of this study suggests that patients with cryptococcal meningitis have a defective NK cytotoxic function and may aid to understand the pathogenesis of this disease.

Adult↗
PubMedDate not supplied

Plasma levels and in vitro production of tumor necrosis factor-alpha and interleukin-6 in patients with amebic liver abscess.

We studied the plasma levels of tumor necrosis factor-alpha (TNF-alpha) interleukin-6 (IL-6) as well as the in vitro production of these cytokines by peripheral blood mononuclear cells, in 10 patients with amebic liver abscess (ALA) and seven healthy controls. TNF-alpha was measured using a bioassay with L929 fibroblasts; IL-6 was quantitated by the B9 cell line assay. In both assays, the number of viable cells was estimated by the conversion of MTT to formazan. TNF-alpha plasma levels were nondetectable (< 20 pg/mL) in ALA patients, as well as in the majority of healthy controls. The in vitro production of TNF induced by lipopolysaccharide was significantly decreased in ALA patients. Most ALA patients (8/10) had increased plasma levels of IL-6. Furthermore, the spontaneous production of IL-6 in vitro was significantly increased in ALA patients compared to controls. In the acute stage of the ALA, a negative relationship was found between the raised plasma levels of IL-6 and the in vitro diminished production of TNF-alpha. After recovery, ALA patients showed both normal plasma levels and in vitro production of TNF and IL-6. Our data corroborate previous reports regarding plasma levels of TNF in ALA, and suggest that E. histolytica induces the in vivo production of IL-6 through a TNF-independent pathway. The raised levels of IL-6 might in turn down-regulate the production of TNF in ALA patients.

Acute Disease↗
PubMedDate not supplied

An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of langerhans cells to UV light.

Actinic prurigo is an inflammatory disease of the skin that appears to be mediated by an abnormal immune response. Cell adhesion molecules play a key role in the induction of the immune response as well as in the pathogenesis of inflammation. We investigated the expression of cell adhesion and activation molecules, as well as the density of Langerhans cells in skin from patients with actinic prurigo. Skin biopsies from ultraviolet light-induced lesions, and non-irradiated areas from 10 actinic prurigo patients were studied; in addition, several spontaneous skin lesions were studied. Skin biopsies from normal individuals were used as controls. The expression of ICAM-1, ICAM-3, LFA-3, CD2, LFA-1, VLA-4, CD1a, VCAM-1, CD69, and activated b1 integrins were assessed by immunostaining. An increased expression of LFA-1, LFA-2, ICAM-3, VLA-4, and activated b1 integrins was observed in the cell infiltrate of actinic prurigo lesions and an up-regulated expression of ICAM-1 was detected in keratinocytes from these specimens. Interestingly, the number of Langerhans cells (CD1a + ) in actinic prurigo skin was not significantly affected by ultraviolet irradiation, a phenomenon that was not observed in normal controls. The increased expression of adhesion molecules in the cell infiltrate of actinic prurigo, indicates that these cells are activated and suggests that they are involved in the skin damage seen in these patients. The resistance of Langerhans cells from patients with actinic prurigo to ultraviolet light may have an important role in the pathogenesis of this condition. The involvement of keratinocytes in the pathogenesis of actinic prurigo is suggested by the expression of ICAM-1 on these cells.

Antibodies, Monoclonal↗