In situ detection and quantification of bursa of fabricius cellular proliferation or apoptosis in normal or steroid-treated neonatal chicks

Abstract

Apoptosis, or programmed cell death, is believed to be the mechanism for depletion of lymphocytes recognizing self-antigens following clonal expansion in the bursa of Fabricius. Although bursal apoptosis has previously been shown to increase following in vivo exposure to glucocorticoids, the microanatomical site of induced or normal apoptosis has not been unequivocally established. Presently, we adapted the existing terminal deoxynucleotidal transferase-mediated dUTP nick-end labeling (TUNEL) assay for use with neonatal bursae. Similar to previous reports, TUNEL revealed that normal apoptosis is preferentially, but not exclusively, ongoing in bursal follicular cortical cells. Administration of a single dose of a synthetic glucocorticoid (dexamethasone) or androgen (19-nortestosterone) did not significantly (P < 0.05) alter follicular lymphocyte numbers or apoptosis per unit of area at the time points evaluated post-administration (6 or 24 h). However, administration of 19-Nortestosterone increased the interfollicular epithelial thickness, a change usually associated with edema, within 6 h following treatment. Additionally, administration of the androgen 19-nortestosterone significantly decreased the number of proliferating cells as detected using mouse anti-proliferating cell nuclear antigen (PCNA) as a primary immunohistochemical antibody. In normal (control) bursal sections, occasional follicles consisting of predominantly apoptotic cells were observed (0.26% of follicles). Such follicles were consistently one-tenth the area of normal follicles. This incidental finding may suggest occasional occurrence of a common signal for deletion, such as a common integral or clonal mistake, viral infection, or an aberrant paracrine signal.

Apoptosis in Lymphoid Organs in Chicken and Duck: A Comparative Study

“…(Rodríguez-Méndez et al, 2010) who demonstrated that there is a developmental wave of apoptosis in the bursa of white Leghorns associated with a greater abundance of TUNEL signals in both the cortical and medullar parts during the involution stage of this organ. In the present study, TUNELpositive cells were found in both the FAE and medulla, indicating that bursal lymphocyte apoptosis can clearly occur in both anatomical locations and closely resembles to that observed in chickens (Higgins et al, 2002). Compared to the present results previous study on cell apoptosis in in chickens and duck's lymphoid organs, the most prominent difference found is that apoptosis seems to be more extensive within the bursa than in the thymus.…”

Immune Recovery Effects of Immunopotentiator from Pantoea agglomerans 1 (IP-PA1) on Low Antibody Productions in Response to Salmonella Enteritidis Vaccine and Sheep Red Blood Cells in Dexamethasone-Treated Stressed Chicken Models

“…Glucocorticoid-mediated immunosuppression is characterized by functional impairment or anatomical defects in immunobiological organs [15,20], peripheral blood lymphopenia and excessive apoptosis of thymic and bursal lymphocytes [17,20,27]. In order to evaluate the usefulness of IP-PA1 in controlling glucocorticoid-mediated immunosuppression in domestic chickens, we investigated the inhibitory effects of IP-PA1 on immunosuppression in dexamethasone-treated stressed chicken models in this study.…”

“…In spite of its strong immune-enhancing effects in vitro, clinical application of LPS from pathological gram-negative bacteria such as Escherichia coli has been limited because they cause severe septic shock when large amounts enter the blood stream directly [17]. However, in contrast to injection, no toxicities of LPS have been reported when administered orally [22].…”

Identification of cells secreting a thymostimulin-like substance and examination of some histoenzymatic pathways in aging avian primary lymphatic organs: II. Bursa of Fabricius

“…The bursa was sensitive to adrenal and gonadal steroid hormones which experimentally may cause its regression (Papermaster and Good, 1962;Erickson and Pincus, 1966;Freeman, 1971;Gasc et al, 1979;Le Douarin et al, 1980;Ylikomi et al, 1987;Wilson and Boyd, 1990;Mase and Oishi, 1991), or decrease the number of proliferating cells (Higgins et al, 2002). Research from the laboratory of Garcia-Espinosa et al, (2002) demonstrated the existence of a bursal anti-steroidogenic peptide (BASP) presenting structural homology to histone H1.…”