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Fluoride (F), a well-recognized harmful substance, is easily absorbed by the intestinal mucosa. The intestinal mucosal immune system is equipped with unique innate and adaptive defense mechanisms that provide a first line of protection against infectious agents. Meanwhile, immunoglobulins are the major secretory products of the adaptive immune system and their levels can be a strong indicator of a disease or condition. In this study, therefore, we investigated the effects of high dietary fluorine on the numbers of immunoglobulin A-positive (IgA(+)) cells in the lamina propria of intestines (duodenum, jejunum and ileum) by immunohistochemistry as well as on the contents of immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) in the mucosa of intestines (duodenum, jejunum, and ileum) by enzyme-linked immunosorbent assay (ELISA). A total of 280 1-day-old healthy avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (fluorine 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg/kg fluorine (high fluorine groups I, II, and III) in the form of sodium fluoride (NaF) for 42 days. The experimental data showed that the numbers of IgA(+) cells as well as the IgA, IgG, and IgM contents were significantly decreased (P < 0.01 or P < 0.05) in the high fluorine groups II and III when compared with those of the control group. It was concluded that dietary fluorine in the range of 800-1,200 mg/kg significantly reduced the numbers of the IgA(+) cells and the contents of aforementioned immunoglobulins in the intestines (duodenum, jejunum, and ileum) of broilers, which could finally impact the mucosal humoral immune function in the intestines by a way that reduces the lymphocyte population and/or lymphocyte activation.

The purpose of this study was to investigate the oxidative damage induced by dietary nickel chloride (NiCl2) in the intestinal mucosa of different parts of the intestine of broilers, including duodenum, jejunum and ileum. A total of 240 one-day-old broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600 or 900 mg/kg NiCl2 during a 42-day experimental period. The results showed that the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (p < 0.05 or p < 0.01) decreased in the 300, 600 and 900 mg/kg groups in comparison with those of the control group. In contrast, malondialdehyde (MDA) content was significantly (p < 0.05 or p < 0.01) higher in the 300, 600 and 900 mg/kg groups than that in the control group. It was concluded that dietary NiCl2 in excess of 300 mg/kg could cause oxidative damage in the intestinal mucosa in broilers, which finally impaired the intestinal functions including absorptive function and mucosal immune function. The oxidative damage might be a main mechanism on the effects of NiCl2 on the intestinal health of broilers.

Porcine pleuropneumonia is a highly contagious respiratory disease that causes great economic losses worldwide. In this study, we aimed to explore the underlying relationship between infection and injury by investigation of the whole porcine genome expression profiles of swine lung tissues post-inoculated with experimentally Actinobacillus pleuropneumoniae. Expression profiling experiments of the control group and the treatment group were conducted using a commercially available Agilent Porcine Genechip including 43,603 probe sets. Microarray analysis was conducted on profiles of lung from challenged versus non-challenged swine. We found 11,929 transcripts, identified as differentially expressed at the p ≤0.01 level. There were 1188 genes annotated as swine genes in the GenBank Data Base. GO term analysis identified a total of 89 biological process categories, 82 cellular components and 182 molecular functions that were significantly affected, and at least 27 biological process categories that were related to the host immune response. Gene set enrichment analysis identified 13 pathways that were significantly associated with host response. Many proinflammatory-inflammatory cytokines were activated and involved in the regulation of the host defense response at the site of inflammation; while the cytokines involved in regulation of the host immune response were suppressed. All changes of genes and pathways of induced or repressed expression not only led to a decrease in antigenic peptides presented to T lymphocytes by APCs via the MHC and alleviated immune response injury induced by infection, but also stimulated stem cells to produce granulocytes (neutrophils, eosinophils, and basophils) and monocyte, and promote neutrophils and macrophages to phagocytose bacterial and foreign antigen at the site of inflammation. The defense function of swine infection with Actinobacillus pleuropneumoniae was improved, while its immune function was decreased.

Fluoride is an environmental and industrial pollutant that affects various organs in humans and animals. The cecal tonsil is an important component of the mucosal immune system and performs important and unique immune functions. In the present study, we investigated the effects of dietary high fluorine on the quantities of IgA+ B cells in the cecal tonsil by immunohistochemistry, and the immunoglobulin A (IgA), immunoglobulin G (IgG) and immunoglobulin M (IgM) contents in the cecal tonsil by ELISA. A total of 280 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as control diet (fluorine 22.6 mg/kg) or the same diet supplemented with 400, 800 and 1,200 mg/kg fluorine (high fluorine groups I, II and III) in the form of sodium fluoride, respectively, throughout a 42-day experimental period. The results showed that the quantities of IgA+ B cells were lower (p < 0.05 or p < 0.01) and the IgA, IgG, and IgM contents were decreased (p < 0.05 or p < 0.01) in high fluorine groups II and III in comparison with those of control group. It was concluded that dietary fluorine, in the 800-1,200 mg/kg range, could reduce the numbers of the IgA+ B cells and immunoglobulin contents in the cecal tonsil, implying the local mucosal immune function was ultimately impacted in broilers.

Fluorine (F) bioaccumulation has been reported in the organs and tissues of organisms, including intestine. The intestinal mucosa is very important to the immune development. Meanwhile, cytokines are present in the normal intestinal mucosal and play an important role in the immune function. Thus, changes of the cytokine contents are related to the state of intestinal mucosal immunity. In this study, we investigated the changes in contents of cytokines such as interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interferon gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) induced by dietary high F in the mucosa of different parts of intestines (duodenum, jejunum, and ileum) by enzyme-linked immunosorbent assay. A total of 280 one-day-old healthy avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (F 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg F/kg (high F groups I, II, and III) in the form of sodium fluoride for 42 days. The experimental data showed that the contents of IL-2, IL-4, IL-6, IFN-γ, and TNF-α in the intestinal mucosa were significantly decreased in the high F groups II and III when compared with those of the control group from 14 to 42 days of age. It was concluded that dietary F in the range of 800-1,200 mg/kg significantly reduced the contents of aforementioned cytokines in the intestinal mucosa of broilers, which could impact the function of intestinal mucosal immunity through the pathways that decreased the lymphocyte population and/or lymphocyte activation.

Long-term excessive fluoride intake is known to be toxic and can lead to fluorosis and bone pathologies. However, the cellular mechanisms underlying sodium fluoride-induced cytotoxicity in the cecal tonsil lymphocytes are not well understood. The aims of this study were to investigate the effects of high dietary fluorine on apoptosis and the expression of the Bcl-2, Bax, and caspase-3 in the cecal tonsil lymphocytes of broilers. The broilers were fed on high-fluorine diets containing 0, 400, 800, and 1,200 mg/kg fluorine. As measured by flow cytometry, the percentage of apoptotic lymphocytes was significantly increased in the high-fluorine groups II and III when compared with those in the control group. Meanwhile, immunohistochemical tests showed that the Bcl-2 protein expression decreased, and the Bax and caspase-3 protein expression increased in the high-fluorine groups II and III. In conclusion, dietary fluorine in the range of 800-1,200 mg/kg increased lymphocyte apoptosis in the cecal tonsil of broilers, suggesting that the lymphocyte apoptosis in the cecal tonsil was mediated by direct effects of fluoride on the expression of Bcl-2, Bax, and caspase-3.

Cytokines are immunoregulatory proteins which play an important role in the immune system. The purpose of this study was to examine the serum cytokine contents including interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) induced by dietary nickel chloride in broilers by enzyme-linked immunospecific assay. A total of 240 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of nickel chloride. During the experimental period of 42 days, the results showed that the serum IL-2, IL-4, IL-6, IL-10, IFN-γ and TNF-α contents were lower (p < 0.05 or p < 0.01) in the 300, 600, 900 mg/kg groups than those in the control group. It was concluded that dietary nickel chloride in the range of 300 to 900 mg/kg could reduce the serum cytokine contents, which could finally impact the immune function in broilers.

The purpose of this 42-day study was to examine the effect of dietary vanadium on intestinal microorganism diversity in the duodenum, ileum, cecum, and rectum segments of broilers by the plate count and polymerase chain reaction-denaturing gradient gel electrophoresis (DGGE). A total of 420 1-day-old avian broilers were divided into six groups and fed on a control diet or the same diet supplemented with vanadium at the doses of 5, 15, 30, 45, and 60 mg/kg in the form of ammonium metavanadate. In comparison with control group, the dietary vanadium at the doses of 45 and 60 mg/kg could decrease the counts of Bifidobacterium spp. in the intestinal tract at 21 and 42 days of age. With increasing level in dietary vanadium, the counts of Escherichia coli were significantly increased in the ileum, cecum, and rectum and were decreased in the duodenum at 21 and 42 days of age. However, the counts of Lactobacilli were decreased in the cecum and rectum and increased in the ileum of 45 and 60 mg/kg groups. The colonization of these three bacteria could be affected by dietary vanadium. DGGE analysis showed that the number of bands in duodenum, ileum, cecum, and rectum were obviously decreased in the 30, 45, and 60 mg/kg groups at 21 and 42 days of age. In conclusion, the dietary vanadium in excess of 30 mg/kg could alter the amount and diversity of intestinal bacteria in broilers, implying that the structure and initial balance in the intestinal microbiota were disrupted.

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on histopathological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative status of the spleen. One hundred twenty 1-day-old avian broilers were randomly divided into two groups of 60 each and were fed on a low Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. The weight and relative weight of the spleen were significantly decreased in the low Se group when compared with those of the control group. Histopathologically, splenic lesions in low-Se chicken were characterized by lymphocyte depletion and congestion of red pulp. As measured by flow cytometry, splenocytes in G(0)/G(1) phase were significantly increased, while splenocytes in S phase and G(2) + M phase were obviously decreased in the low Se group. The percentage of apoptotic splenocytes was greatly increased in the low Se group when compared with that of control group. At the same time, the occurrence frequencies of apoptotic splenocytes was markedly increased in the low Se group with the appearance of condensed nucleus ultrastructurally. Oxidative stress in the spleens of the low Se group was evidenced by decrease in glutathione peroxidase and catalase activities and increase in malondialdehyde contents. The results showed that low Se diet intake caused increased apoptosis, arrested cell cycle, and obvious oxidative stress, which provided a possible pathway for the injured structure and immune function of the spleen in chickens.

The cecal tonsil of broiler is known as a secondary lymphoid tissue, which is involved in antigen-specific humoral immune responses. The purpose of this study was to investigate the effects of dietary vanadium on the tissue distribution and quantity of immunoglobulin A-positive (IgA(+)) cell in the cecal tonsil by immunohistochemistry. Simultaneously, the changes in interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) contents in the cecal tonsil were also quantified by enzyme-linked immunosorbent assay (ELISA). A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet (control diet) or the same diet supplemented respectively with 5, 15, 30, 45, and 60 mg/kg of vanadium in the form of ammonium metavanadate for 42 days. The results showed that the population of the IgA(+) cells in the cecal tonsil were significantly lower (p < 0.05 or p < 0.01) in the 45 and 60 mg/kg groups than that in the control group. Meanwhile, IL-10, IFN-γ and TNF-α contents in the cecal tonsil were significantly decreased (p < 0.05 or p < 0.01) in the 30, 45 and 60 mg/kg groups in comparison with those of the control group. However, IL-6 content in the cecal tonsil was only decreased (p < 0.05 or p < 0.01) in 60 mg/kg at 14 and 28 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg reduced the numbers of the IgA(+) cells and changed the contents of the abovementioned cytokines in the cecal tonsil, which may finally impact the function of local mucosal humoral immunity in broilers.

The purpose of this 42-day study was to examine the effect of dietary vanadium on the ileac T cells and contents of cytokines including interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon-gamma (IFN-γ) in broilers by flow cytometry and enzyme-linked immunosorbent assay. A total of 420 one-day-old avian broilers were divided into six groups (seven replicates in each group and ten broilers in each replicate) and fed on control diet or the same diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium in the form of ammonium metavanadate. The results showed that the percentages of CD3(+), CD3(+)CD4(+), and CD3(+)CD8(+) T cells in both ileac lamina propria lymphocytes (LPLs) and intraepithelial lymphocytes (IELs) were significantly lower (P < 0.05 or P < 0.01) in the 45- and 60-mg/kg groups than in the control group from 14 to 42 days of age. The CD4(+)/CD8(+) ratio was increased in ileac LPLs in the 60-mg/kg group at 28 days of age, and in ileac IELs in the 60-mg/kg group at 28 days of age and in the 45-mg/kg group at 42 days of age. Meanwhile, the ileac IL-2, IL-6 contents were decreased (P < 0.05 or P < 0.01) in the 60-mg/kg group from 14 to 42 days of age and in the 45-mg/kg group from 28 to 42 days of age in comparison with those of the control group. It was concluded that dietary vanadium in excess of 30 mg/kg reduced the ileac T cell population and percentages of T cell subsets, and IL-2, IL-6, and IFN-γ contents, implying that the immune function of local intestinal mucosa in broilers could be affected by the dietary vanadium.

The purpose of this 42-day study was to investigate the apoptosis in the bursa of Fabricius induced by different levels of dietary vanadium. A total of 420 1-day-old avian broilers were divided into 6 groups in which there were 7 replicates in each group and 10 broilers in each replicate and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg) or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate (NH(4)VO(3)). Ultrastructurally, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed in the 30, 45, and 60 mg/kg groups. As measured by flow cytometry, the percentages of apoptotic lymphocytes were significantly increased in the 15-, 30-, 45-, and 60-mg/kg groups when compared with those of control group. Meanwhile, the terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end-labeling assay showed that there were increased numbers of apoptotic cells in the 30-, 45-, and 60-mg/kg groups. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein in the 15-, 30-, 45-, and 60-mg/kg groups. The vanadium content of the bursa was found to be significantly increased in the 30-, 45-, and 60-mg/kg groups. These results suggested that dietary vanadium in excess of 15 mg/kg could cause lymphocyte apoptosis in the bursa of Fabricius and impact humoral immunity in broilers. Lymphocyte apoptosis in the bursa induced by high levels of dietary vanadium is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3.

The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30-60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.

Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium supplied as sodium selenite (n = 60/group). In comparison with those of 0.2 mg/kg selenium group, the percentages of annexin V-positive splenocytes were increased in 5, 10, and 15 mg/kg selenium groups. TUNEL assay revealed that apoptotic cells with brown-stained nuclei distributed within the red pulp and white pulp of the spleens with increased frequency of occurrence in 10 and 15 mg/kg selenium groups in comparison with that of 0.2 mg/kg Se group. Sodium selenite-induced oxidative stress in spleens of chickens was evidenced by decrease in glutathione peroxidase, superoxide dismutase, and catalase activities and increase in malondialdehyde contents. The results indicate that excess dietary selenium in the range of 5-15 mg/kg of feed causes oxidative stress, which may be mainly responsible for the increased apoptosis of splenocytes in chickens.

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on cellular immune function by determining cell cycle of thymus, serum IL-2 content, and mitogenesis of peripheral blood T-lymphocytes. One hundred twenty 1-day-old Avian broilers were randomly assigned to two groups of 60 each and were fed on a low-Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. Cell cycle analysis by flow cytometry showed that low-Se diet caused an increase in G(0)G(1) phase cells that corresponded to a decrease in S-phase cells in thymus. Ultrastructurally, mitochondria injury and increased apoptotic cells with condensed nuclei were observed. Low-Se diet decreased the serum IL-2 contents and mitogenesis of peripheral blood lymphocytes to concanavalin A in comparison with those of control group. These data indicate that low-Se diet inhibits the development of thymus by arresting the cell cycle and decreasing the IL-2 content.

Selenium is an essential trace element possessing immune-stimulatory properties. The purpose of this 42-day study was to investigate the effects of excess dietary selenium on cellular immune function by determining morphological changes of thymus and peripheral blood T-cell subset. Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, 15 mg/kg selenium supplied as sodium selenite (n = 60/group). Pathological lesions were progressed with the dietary Se level increased. Grossly, the volume of thymus was decreased. Histopathologically, lymphopenia and congestion were observed. Ultrastructurally, mitochondria injury was observed. In comparison with that of control group, 5, 10 and 15 mg/kg dietary Se decreased the percentage of CD3(+), CD3(+)CD4(+) and CD3(+)CD8(+) T cells of the peripheral blood, as measured by flow cytometry. The results showed that excess selenium (more than 5 mg/kg) intake could cause lesions of thymus and decrease of T-cell subsets. The cellular immune function was finally impaired in broilers.

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on spleen growth and lesions by determining morphological changes and cell cycle of spleen. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, 60 ppm of vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of spleen was significantly raised in 5- and 15-ppm groups, but depressed in 45- and 60-ppm groups. The gross lesions of spleen showed obvious atrophy with decreased volume and pale color in 45- and 60-ppm groups. Histopathologically, lymphocytes in splenic corpuscle and periarterial lymphatic sheath were variously decreased in number in 30-, 45-, and 60-ppm groups. The percentage of static phase (G0/G1) was significantly decreased, and the percentage of synthesis period (S) phase and the proliferating index (PI) were significantly increased in 5- and 15-ppm groups. The percentage of G0/G1 phase was significantly increased, and the percentage of mitotic phase (G2+M), S phase, and PI significantly decreased in 45- and 60-ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of spleen and induce lesions in spleen in chicken.

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining changes of the subsets and proliferation function of splenic T cells. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 ppm of vanadium supplied as ammonium metavanadate. When compared with those of the control group, the percentage of CD3+, CD3+CD4+, and CD3+CD8+ of splenic T cells were decreased in the 45 and 60 ppm groups; however, the percentage of CD3+ and CD3+CD4+ were increased in the 5 ppm group, and the CD4+/CD8+ ratios were raised in the 5 and 15 ppm groups at 14 days of age. Meanwhile, the proliferation of splenic T cells were depressed in the 45 and 60 ppm groups but raised in the 5 and 15 ppm groups. Also, the serum interleukin-2 (IL-2) and interleukin-6 (IL-6) contents were decreased in the 45 and 60 ppm groups and increased in the 5 ppm group. It was concluded that dietary vanadium in excess of 30 ppm changed the percentages of splenic T cell subsets and inhibited the proliferation of splenic T cells and reduced the serum IL-2 and IL-6 contents. The cellular immune function was finally impaired in broilers.

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining the morphological changes and cell cycle of bursa of Fabricius, and the serum Ig contents. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet, or the same diet amended to contain 5, 15, 30, 45, and 60 ppm vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of bursa was significantly increased in the 15 ppm group from 14 to 35 days of age and increased in the 5 ppm group at 42 days of age, and significantly decreased in the 60 ppm group from 14 to 42 days of age and decreased in 30 and 45 ppm groups from 35 to 42 days of age. Pathological lesions progressed as the dietary vanadium increased. The gross lesions of bursa showed obvious atrophy with decreased volume and pale color in 45 and 60 ppm groups. Histopathologically, widened cortex and increased number of lymphocytes appeared in 5 and 15 ppm groups, and reduced lymphocytes and connective tissue hyperplasia appeared in 45 and 60 ppm groups. The bursal cells in static phase (G(0)/G(1)) were decreased, and those in the mitotic phase (G(2) + M) and the proliferating index (PI) were increased in 5 and 15 ppm groups. However, bursal cells in the G(0)/G(1) phase were increased, and those in G(2) + M phase, synthesis phase (S) and the PI were decreased in 45 and 60 ppm groups. Also, the serum IgG and IgA contents were increased in 5 and 15 ppm groups, and the serum IgG, IgA, and IgM contents were decreased in 45 and 60 ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of bursa of Fabricius and impair humoral immunity in chicken.

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on immune function by determining histopathological changes of thymus, apoptosis of thymic cells, and subpopulation of peripheral blood T cells. One hundred twenty 1-day-old avian broilers were randomly assigned to two groups of 60 each and were fed on a low Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. The relative weight of thymus was significantly decreased in low Se group from 21 days of age in time-dependent manner when compared with that of control group. Histopathologically, lymphopenia in the cortex and medulla of thymus was observed in low Se group. In comparison with those of control group, the percentage of Annexin-V positive cells was increased, and the percentages of CD3(+) and CD3(+)CD8(+) T cells of the peripheral blood were decreased in low Se group, as measured by flow cytometry. These data suggested that low dietary Se induced histological lesions of thymus, increased apoptosis of thymic cells, and decreased T cell subsets. The cellular immune function was finally impaired in broilers.

The experiment was conducted with the objective of examining the effects of high molybdenum (Mo) on the apoptosis of splenic lymphocytes in broilers by the methods of experimental pathology and flow cytometry (FCM). Three hundred 1-day-old avian broilers were divided into four groups of 75 each and were fed on control diet (Mo 13 mg/kg) and high Mo diets (Mo 500 mg/kg, high Mo group I; Mo 1,000 mg/kg, high Mo group II; and Mo 1,500 mg/kg, high Mo group III) for 42 days. The results showed that the relative weight of spleen was decreased, and lymphocytes were histopathologically decreased in high Mo groups II and III. Ultrastructurally, the apoptotic cells showed typical condensed nuclei with dark-round, petal-like, and horseshoe-like shapes. The mitochondria were swelled, and the endoplasmic reticulum and the Golgi apparatus were dilated in high Mo groups II and III. The statistical analyses by FCM indicated that the percentage of cellular apoptosis was higher in high Mo groups II and III than in control group. Also, the TUNEL staining was consistent with the results of FCM. It was concluded that dietary molybdenum in 1,000 and 1,500 mg/kg caused splenic lesions and lymphocyte apoptosis, which could inhibit the development of spleen and could impair immune function in broilers.

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining changes of the subsets and proliferation function of peripheral blood T cells. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 ppm vanadium supplied as ammonium metavanadate. In comparison with those of the control group, the percentages of CD (3) (+) , CD (3) (+) CD (4) (+) , and CD (3) (+) CD (8) (+) were decreased in 45 and 60 ppm groups from 14 to 42 days of age, and the percentages of CD (3) (+) and CD (3) (+) CD (4) (+) were increased in 5 ppm group at 42 days of age. The CD (4) (+) /CD (8) (+) ratio was increased in 45 and 60 ppm groups at 28 days of age. Meanwhile, the proliferation function of peripheral blood T cell were decreased in 30, 45, and 60 ppm groups from 14 to 42 days of age. Also, the serum interleukin-2 contents were decreased in 45 and 60 ppm groups from 14 to 42 days of age and increased in 5 ppm group at 28 days of age. Histopathologically, hypocellularity appeared in the thymus in 45 and 60 ppm groups. It was concluded that dietary vanadium in excess of 30 ppm reduced the percentages of peripheral blood T-cell subsets and the proliferation function and serum interleukin-2 contents. The cellular immune function was finally impaired in broilers.

The purpose of this 42-day study was to investigate the effects of excess dietary selenium on immune function by determining morphological changes of spleen and cell cycle of splenocyte. Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium (Se) supplied as sodium selenite (n = 60/group). Anatomically, the spleens were shrunken in volume with pallecent color. Histopathologically, lymphopenia in splenic nodules and periarterial lymphatic sheaths and congestion of the red pulp were observed in 5, 10, and 15 mg/kg Se group. By flow cytometry method, the percentage of G(0)/G(1) phase splenocytes was significantly increased, whereas the percentages of S phase and G(2)+M phase splenocytes and the proliferation index were markedly decreased in 5, 10, and 15 mg/kg Se groups when compared with those of 0.2 mg/kg group. The results confirmed that excess dietary Se as sodium selenite in the range of 5~15 mg/kg caused growth retardation of spleen by cell cycle blockage in young chickens.