Nov

25

The diverse biofilms of the Borrelia species

November 25, 2009 | Comments Off

From here :

The diverse biofilms of Borrelia……
the majority of bacteria in nature exist attached to a substratum.

Nov

18

From Here :

Psoriasis :
Several studies have examined the responses of psoriasis patients to Malassezia. One of the early studies (375) noted that if dense suspensions of Malassezia were applied to the shaved skin of rabbits, lesions similar to psoriasis resulted. The lesions persisted as long as Malassezia continued to be applied but otherwise resolved within 3 to 4 days. Further work by the same group used patch testing with Malassezia to study the response in 10 patients with psoriasis and 10 controls (259). All of the patients developed psoriatic lesions when challenged with Malassezia, and biopsy specimens showed features consistent with psoriasis. Therefore, Malassezia was able to elicit psoriasiform lesions in both animals and humans.

Additional support for the role of Malassezia in psoriasis comes from successful use of ketoconazole in patients (374). Although ketoconazole may act by a direct antifungal mode of action, it has also been shown to suppress Malassezia-induced proliferation of lymphocytes from psoriatic patients (13), thus reducing the response to antigenic stimulation in lesions.

The first study to characterize the humoral immune response to Malassezia in patients with psoriasis was carried out by Squiquera et al. (417). This study included 15 patients, of whom 8 had active disease, and 10 healthy controls. SDS-PAGE of Malassezia extracts was performed, and the test sera were immunoblotted. The sera from psoriatic patients bound to a 120-kDa band (11 of 15) and a 100-kDa band (7 of 15), but none of the control sera recognized these bands. Consequently, the authors suggested that antibodies to the 100- and 120-kDa proteins were specific serologic markers for psoriasis. These antibodies were subsequently shown to recognize the N-acetylglucosamine terminals of glycoproteins present in Malassezia (276). However, both of these proteins are recognized by sera from patients with AD (256, 312), and so they are not specific markers for psoriasis.

Neutrophils form part of the inflammatory infiltrate in the dermis of psoriatic lesions (90). A study examining the chemotaxis of neutrophils from psoriatic patients and controls demonstrated that Malassezia induced significantly more chemotaxis in neutrophils from psoriatics than other groups (75). The effect was specific, since Staphylococcus epidermidis did not affect chemotaxis, and was due to a protein. Psoriatic lesions often develop at sites of trauma (the Koebner phenomenon [294]), and the increased chemotactic response of neutrophils to Malassezia was suggested to play a role in this event.

Only one study has examined the cellular immune responses to Malassezia in patients with psoriasis (36). All the psoriatic patients included (n = 13) had lesions on the scalp, with disease durations ranging from 2 months to 20 years. Proliferation of PBMC was seen in response to Malassezia in all of the patients tested. However, since no healthy controls were included in the study, it is not possible to determine whether the responses differed from those of normal individuals. The response of PBMC was due to CD4+ T lymphocytes and required antigen presentation by HLA-DR+ cells, and so it was not mitogenic stimulation. T-lymphocyte lines were established from psoriatic and nonpsoriatic patients and were stimulated with Malassezia. Similar patterns of response were obtained whether the patient had psoriasis or not, and the authors concluded that Malassezia-specific T lymphocytes were not involved in psoriasis.

Consequently, the role that Malassezia plays in psoriasis is, as yet, undetermined. Although it may contribute to the inflammation associated with the disease, via complement activation and neutrophil recruitment, convincing evidence that it is of prime importance in the pathogenesis of the disease is still lacking.

Overall, it is difficult to rationalize and explain the wide range of results documented for humoral and cellular immune responses to Malassezia in patients with PV, SD, folliculitis, AD, and other superficial diseases. The use of different techniques, different antigenic preparations, and organisms from different classifications makes comparison of results unreliable and may partly explain the disparity in the findings. However, many of these limitations can now be overcome. The characterization of several antigens from Malassezia and the ability to produce them in vitro should provide a reliable source of defined antigen for use in future immunological studies. The unification of different classifications of Malassezia into one scheme should removed the uncertainty about whether similar strains or species are being studied. Lastly, the finding that, at least in AD, there is significant cross-reactivity between mannans of different yeasts may encourage the use of protein antigens in immunological assays used to define the response specific to Malassezia. Although our understanding of the immune response to Malassezia in superficial diseases has advanced significantly over the last 10 years, there are still many interesting questions awaiting an answer.

November 2009
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