(1/746) Treponema brennaborense sp. nov., a novel spirochaete isolated from a dairy cow suffering from digital dermatitis.

A novel Treponema species was isolated from an ulcerative lesion of a cow suffering from digital dermatitis (DD), a disease which causes painful ulcerations along the coronary band. Among other anaerobic bacteria, high numbers of spirochaetes have been regularly found in DD lesions. Here data are presented of a spirochaete isolated from a DD ulcer. By chemotaxonomy, protein analysis and comparative 16S rDNA sequence analysis this isolate was classified as a treponeme that differed from all Treponema species described previously. The only isolate, DD5/3T, for which the name Treponema brennaborense is proposed, is designated the type strain of the novel species. The strain is a small, highly motile spirochaete that has two periplasmic flagella, one flagellum being attached at each cell pole. Strain DD5/3T exhibits alpha-glucosidase and N-acetyl-beta-glucosaminidase activity and growth is inhibited by rabbit serum. T. brennaborense was phylogenetically most closely related (89.5% 16S rRNA similarity) to Treponema maltophilum, an oral spirochaete isolated from a periodontitis patient.  (+info)

(2/746) Characteristics of spontaneous erythema appeared in hairless rats.

The hairless rat (WBN/Kob-Ht), a dominant mutant rat derived from the Wistar strain, rarely develops spontaneous erythema of a progressive nature on its skin. Erythema was first observed at 8 weeks of age and the incidence at 20 weeks of age was about 4% in both males and females. Histopathologically, erythema was characterised by dermatitis induced by an immunological reaction. Areas of erythema in the skin were decreased by treatment with dexamethasone (1 mg/kg) or ciclosporin (25 or 50 mg/kg). These results suggested that erythema on the hairless rat could be used as an animal model of spontaneous dermatitis.  (+info)

(3/746) Dermatitis with invasive ciliated protozoa in dolphins that died during the 1987-1988 Atlantic Bottlenose Dolphin morbilliviral epizootic.

Dermatitis with intradermal cilated protozoa was identified in 18 of 95 (19%) Atlantic Bottlenose Dolphins (Tursiops truncatus) that died during the 1987-1988 Atlantic-dolphin morbillivirus epizootic. The lesions were characterized by focally extensive suppurative and histiocytic dermatitis and cellulitis with ulceration and variable numbers of dermal and hypodermal ciliates. Vasculitis, thrombosis, and/or intravascular ciliates were rarely present. In one dolphin, there was an associated lymphadenitis with ciliates, and in another, bronchopneumonia with rare intrabronchiolar ciliates. Ten of the dolphins were female, and eight were male. The animals ranged in length from 148 to 260 cm. Eleven were from Virginia, four were from New Jersey, and three were from Florida. In 13 dolphins, results of immunohistochemical and/or polymerase chain reaction (PCR) tests were positive for morbillivirus infection. Results of immunohistochemical tests were negative in four dolphins that were not also tested with PCR. Results were also negative in one dolphin tested using both methods. Nine dolphins had concomitant bacterial, fungal, and/or other protozoal infections. Fourteen other dolphins with ciliate-associated dermatitis were identified from 414 Atlantic bottlenose dolphin cases (3%) archived at the Armed Forces Institute of Pathology. The incidence of dermatitis with invasive ciliates is much greater in dolphins that died during the 1987-1988 epizootic.  (+info)

(4/746) The neutral cysteine protease bleomycin hydrolase is essential for epidermal integrity and bleomycin resistance.

The papain superfamily member bleomycin hydrolase (Blmh) is a neutral cysteine protease with structural similarity to a 20S proteasome. Bleomycin (BLM), a clinically used glycopeptide anticancer agent, is deaminated in vitro by Blmh. We used gene targeting to generate mice that lack Blmh and demonstrated that Blmh is the sole enzyme required for BLM deamination. Although some Blmh null mice were viable and reproduced, only about 65% of the expected number survived the neonatal period, revealing an important role for Blmh in neonatal survival. Mice lacking Blmh exhibited variably penetrant tail dermatitis that resembled rodent ringtail. The histopathology of the tail dermatitis was similar to skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Compared with controls, Blmh null mice were more sensitive to acute BLM lethality and developed pulmonary fibrosis more readily following BLM treatment. Thus, we have established that Blmh is an essential protectant against BLM-induced death and has an important role in neonatal survival and in maintaining epidermal integrity.  (+info)

(5/746) Absence of Peyer's patches and abnormal lymphoid architecture in chronic proliferative dermatitis (cpdm/cpdm) mice.

The chronic proliferative dermatitis (cpdm) mutation causes inflammation in multiple organs, most prominently in the skin. Examination of the immune system revealed severe abnormalities in the architecture of lymphoid tissues. Peyer's patches were absent. In contrast, the spleen, lymph nodes, and nasal-associated lymphoid tissues were present. The spleen had normal numbers of T and B cells, but the spleen, lymph nodes, and nasal-associated lymphoid tissues had poorly defined follicles and lacked germinal centers and follicular dendritic cells. The marginal zone in the spleen was absent. The total concentration of serum IgG, IgA, and IgE in cpdm/cpdm mice was significantly decreased, whereas serum IgM was normal. Fecal IgA was low to undetectable in mutant mice, and the concentration of fecal IgM was increased. The titer of DNP-specific Abs following immunization with DNP-keyhole limpet hemocyanin was significantly decreased for all IgG subclasses. In contrast, T cell function appeared normal as assessed by evaluation of the contact hypersensitivity response in cpdm/cpdm mice. The cpdm mutation causes a complex phenotype that is characterized by multiorgan inflammation and the defective development of lymphoid tissues. The cpdm/cpdm mouse may be a useful model to study the factors that control the development of lymphoid tissues, in particular the Peyer's patches, and the mechanisms that control the humoral immune response.  (+info)

(6/746) Antioxidant modulation of skin inflammation: preventing inflammatory progression by inhibiting neutrophil influx.

OBJECTIVE: To test the hypothesis that antioxidants might affect local inflammation by impairing inflammatory cell influx. DESIGN: A laboratory study using a Swiss-Webster mouse model of local inflammation. SETTING: A university-affiliated hospital. METHODS: Intradermal injection of 30 micrograms of S. minnesota endotoxin (LPS) to Swiss-Webster mice initiates a local inflammatory reaction characterized by an early rise in vascular permeability and a later infux of neutrophils. Animals were pretreated intraperitoneally with either pyrrolidine dithiocarbamate (PDTC, 2 mmol/kg), which inhibits free radical generation, or dimethylthiourea (DMTU, 450 mg/kg), a free radical scavenger. MAIN OUTCOME MEASURES: Histologic findings of tissue samples taken at sites of injection; local changes in tissue vascular permeability (PI) determined by iodine-125 albumin injection before sacrifice; neutrophil accumulation quantified by tissue myeloperoxidase levels; tissue levels of the endothelial adhesion molecules intercellular adhesion molecule-1 protein (ICAM-1) and vascular cell adhesion molecule-1 protein (VCAM-1) assessed by immunohistochemistry and Western blot, respectively. RESULTS: Neither antioxidant had a significant effect on the early increase in PI, but both decreased the late rise in PI and reduced neutrophil influx. Both ICAM-1 and VCAM-1 were upregulated in response to LPS; however, only the increase in VCAM-1 was attenuated by antioxidant pretreatment. CONCLUSION: These data suggest that antioxidants disrupt the propagation phase of an inflammatory response possibly by altering neutrophil migration.  (+info)

(7/746) Selective antibody blockade of lymphocyte migration to mucosal sites and mast cell adhesion.

The integrins alpha4beta7 and alpha4beta1 mediate adhesion to the mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and the vascular cell adhesion molecule-1 (VCAM-1) and are important in T cell and allergic inflammatory reactions in the rat. The relative contributions of alpha4beta7 and alpha4beta1 in these reactions is unknown. To examine the role of alpha4beta7 in the rat a new mAb, TA-6, was developed. TA-6 inhibited adhesion to MAdCAM-1 but not to VCAM-1, a characteristic of alpha4beta7 adhesion, and immunofluorescence and immunoprecipitation studies were compatible with binding to alpha4beta7. TA-6 blocked rat lymphocyte adhesion to mesenteric lymph nodes and T cell migration to mucosal lymphoid tissues and it bound to rat mucosal mast cells. TA-6 did not inhibit lymphocyte adhesion to peripheral lymph nodes and T cell migration to peripheral lymphoid tissues or cutaneous inflammatory sites, and was not expressed on connective tissue mast cells.  (+info)

(8/746) A central role for alpha beta T cells in the pathogenesis of murine lupus.

We have previously shown that female transgenic mice expressing IFN-gamma in the epidermis, under the control of the involucrin promoter, develop inflammatory skin disease and a form of murine lupus. To investigate the pathogenesis of this syndrome, we generated female IFN-gamma transgenic mice congenitally deficient in either alpha beta or gamma delta T cells. TCR delta-/- transgenics continued to produce antinuclear autoantibodies and to develop severe kidney lesions. In contrast, TCR beta-/- IFN-gamma transgenic mice failed to produce antinucleosome, anti-dsDNA, or antihistone autoantibodies, and kidney disease was abolished. Both alpha beta- and gamma delta-deficient transgenics continued to develop IFN-gamma-associated skin disease, lymphadenopathy, and splenomegaly. The data show that the autoantibody-mediated pathology of murine lupus in IFN-gamma transgenic mice is completely alpha beta T cell dependent and that gamma delta T cells cannot drive autoantibody production. These results imply that production of antinuclear autoantibodies in IFN-gamma transgenic animals is Ag driven, and we identified clusters of apoptotic cells in the epidermis of the mice as a possible source of self Ags. Our findings emphasize the relevance of this murine lupus model to the human disease.  (+info)