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Biomedical subjects

B W Brodersen

Publications and source records attributed to B W Brodersen.

5 recordsLinked to original sources
PubMed1999

Alteration of leukocyte populations in calves concurrently infected with bovine respiratory syncytial virus and bovine viral diarrhea virus.

Bovine viral diarrhea virus (BVDV) infection altered leukocyte populations in calves that were reflected by depression of T, BoCD4+, and BoCD8+ lymphocytes in the thymus and depression of B lymphocytes in Peyer's patches (PP). The present study was based on mononuclear leukocyte preparations from eighteen 9- to 12-month-old crossbred calves that were each exposed to either bovine respiratory syncytial virus (BRSV), BVDV, or BRSV and BVDV concurrently, or served as mock-infected controls. Peripheral blood leukocytes were collected on postinfection days (PID) 0, 2, 4, 6, and 8, and cell populations from thymus, spleen, mesenteric lymph node, and PP were collected at necropsy on PID 9. The leukocytes were analyzed using flow cytometry for lymphocyte subpopulations expressing antigens specific for BoCD2, BoCD4, BoCD8, BoWC1, lambda light chain of bovine immunoglobulin, BoCD11b and major histocompatibility complex (MHC) class II. Concurrent BRSV and BVDV infections caused exaggerated alterations in leukocyte populations with a greater percentage of T-lymphocytes harvested from the PP. Alterations in the leukocyte populations in lymphatic tissues and in peripheral circulation due to BVDV infection may be an important mechanism for causation of clinically severe diseases of the respiratory and digestive tracts during concurrent BRSV and BVDV infections.

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PubMed1998

Effect of concurrent experimentally induced bovine respiratory syncytial virus and bovine viral diarrhea virus infection on respiratory tract and enteric diseases in calves.

OBJECTIVE: To compare experimentally induced concurrent bovine viral diarrhea virus (BVDV) and bovine respiratory syncytial virus (BRSV) infection with single virus infection. ANIMALS: 9- to 12-month-old calves. PROCEDURE: Calves were allotted to 4 groups: 1, mock-infected control (n = 3); 2, BRSV infected (5); 3, BVDV infected (5); and 4, concurrent BRSV and BVDV infected (5). Total and differential WBC counting was done. Concentration and duration of BVDV in nasal secretions and serum, and duration of BRSV in nasal secretions were determined. Concentration of BVDV in various tissues was determined, and isolation of BRSV from lung tissue was attempted. Histologic examination and immunohistochemical analysis were done to detect lesions and distribution of viral antigens, respectively. RESULTS: Calves with concurrent infection developed more severe clinical signs of disease (fever and diarrhea), leukopenia, and more severe lesions. They also shed virus from nasal secretions in greater concentration and for longer duration, and BRSV was isolated from their lungs. Calves with concurrent infection also had more extensive lung lesions. Alimentary epithelial necrosis and severe lymphoid depletion were associated with BVDV infection in calves with or without concurrent BRSV infection. BVDV antigen in lymphatic tissue was detected in stromal cells only. CONCLUSIONS: Concurrent infection with BRSV and BVDV resulted in more severe respiratory tract and enteric disease than did infection with either virus alone, possibly indicating synergistic effect between the viruses. BVDV's role in causing respiratory tract disease is attributable, indirectly, to effects on the host's immune system, not to infection of the lungs.

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PubMed1994

Smoke and viral infection cause cilia loss detectable by bronchoalveolar lavage cytology and dynein ELISA.

The purpose of this study was to quantitate cilia loss following airway epithelial cell injury. Two models of airway injury were used: (1) Ex vivo acute cigarette smoke exposure model: Bovine lungs, obtained directly after slaughter, were ventilated with air or cigarette smoke for 5 min followed immediately by bronchoalveolar lavage (BAL). The bronchi were examined histologically and bronchial and alveolar fractions of BAL fluid were examined for cell counts, cell differentials, and cilia dynein concentrations using a specific 13S dynein ELISA. Smoke exposure resulted in a marked loss of ciliated cells from the bronchial luminal surface (2,364 +/- 351 versus 11,090 +/- 542 ciliated cells/mm2; p = 0.0001), a comparable increase in ciliated cells in the bronchial BAL fraction (0.90 x 10(6) cells/mm3 versus 0.15 x 10(6) cells/mm3; p = 0.0003) and a significant increase in bronchial fluid dynein concentrations (24.5 +/- 6.0 micrograms/ml versus 8.9 +/- 2.2 micrograms/ml; p = 0.03) compared with that in air-exposed lungs. The dynein concentrations strongly correlated with the absolute number of ciliated cells recovered in the bronchial lavage (r = 0.80; p < 0.0001). (2) In vivo viral infection model: Healthy cattle underwent bronchoscopy 3 days before and 7 days after inoculation with bovine respiratory syncytial virus (BRSV). BAL fluid was examined as in the first model. Following BRSV inoculation, airway exfoliation of ciliated cells and squamous metaplasia were observed histologically, bronchial ciliated cell counts doubled (0.011 +/- 0.003 x 10(6) cells/mm3 versus 0.026 +/- 0.006 x 10(6) cells/mm3; p = 0.002) and bronchial dynein concentrations increased threefold (2.2 +/- 1.0 micrograms/ml versus 7.2 +/- 1.9 micrograms/ml; p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

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