cholecalciferol and Skin-Diseases--Bacterial

Clostridial dermatitis (CD) is a production disease of commercial turkeys that is characterized by sudden mortality in market-aged male birds and by lesions that include fluid and air bubbles under the skin of the thigh, breast, and tail area. We have developed a model for CD using dexamethasone (Dex) injection that suggests this disease may be related to stressors during the last stages of turkey production. Male turkeys were provided with control feed and water or with feed supplemented with a commercial yeast extract (YE) product, water supplemented with vitamin D (VD), or the combination. At 6, 11, and 15 wk of age birds were treated with three intramuscular injections of Dex over a 5-day period. Both YE and VD, but not the combination, decreased early mortality. At week 7 mortality was increased by VD, and cellulitis lesions were seen in 7/8 mortalities. Mortality at week 12 was decreased by both YE and the combination of YE and VD, and cellulitis lesions were seen in 8/17 mortalities. There were no significant differences in mortality at week 16. Total mortality was 66 birds, and 23 of these had cellulitis lesions (38%). There were no YE-treated birds with CD lesions; however, 67% of VD-treated birds had CD lesions. This study suggests that feed supplementation with YE may improve the ability of turkeys to withstand the stressors during late production and provide protection against the development of CD; however, high levels of VD supplementation may be detrimental.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Cholecalciferol; Clostridium; Clostridium Infections; Dexamethasone; Dietary Supplements; Drinking Water; Immunocompromised Host; Immunosuppressive Agents; Male; Poultry Diseases; Skin Diseases, Bacterial; Turkeys; Yeasts

Immune defence against microbes depends in part on the production of antimicrobial peptides, a process that occurs in a variety of cell types but is incompletely understood. In this study, the mechanisms responsible for the induction of cathelicidin and beta-defensin antimicrobial peptides were found to be independent and specific to the cell type and stimulus. Vitamin D3 induced cathelicidin expression in keratinocytes and monocytes but not in colonic epithelial cells. Conversely, butyrate induced cathelicidin in colonic epithelia but not in keratinocytes or monocytes. Distinct factors induced beta-defensin expression. In all cell types, vitamin D3 activated the cathelicidin promoter and was dependent on a functional vitamin D responsive element. However, in colonic epithelia butyrate induced cathelicidin expression without increasing promoter activity and vitamin D3 activated the cathelicidin promoter without a subsequent increase in transcript accumulation. Induction of cathelicidin transcript correlated with increased processed mature peptide and enhanced antimicrobial activity against Staphylococcus aureus. However, induction of beta-defensin-2 expression did not alter the innate antimicrobial capacity of cells in culture. These data suggest that antimicrobial peptide expression is regulated in a tissue-specific manner at transcriptional, post-transcriptional and post-translational levels. Furthermore, these data show for the first time that innate antimicrobial activity can be triggered independently of the release of other pro-inflammatory molecules, and suggest strategies for augmenting innate immune defence without increasing inflammation.

Topics: Antimicrobial Cationic Peptides; Bacterial Infections; beta-Defensins; Blotting, Western; Butyrates; Cathelicidins; Cells, Cultured; Cholecalciferol; Colitis; Epithelial Cells; Gene Expression Regulation; Humans; Immunity, Innate; Immunohistochemistry; Keratinocytes; Monocytes; Mutagenesis, Site-Directed; Promoter Regions, Genetic; Reverse Transcriptase Polymerase Chain Reaction; Skin Diseases, Bacterial; Transfection