Deficiencies in Selenium and/or Vitamin E Lower the Resistance of Mice to Heligmosomoides polygyrus Infections

Smith, Allen; Madden, Kathleen B.; Yeung, Karla J. Au; Zhao, Aiping; Elfrey, Justin; Finkelman, Fred D.; Levander, Orville A.; Shea‐Donohue, Terez; Urban, Joseph F.

doi:10.1093/jn/135.4.830

Cited by 39 publications

(39 citation statements)

References 44 publications

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“…For example, J774.1 mouse macrophages cultured in media with 1% fetal bovine serum (FBS) and no added Se exhibit decreased phagocytic capacity compared with Se-adequate controls (media supplemented with 0.1 ppm Se) (211). The requirement of antioxidant nutrients such as Se and vitamin E for resistance against nematode infections highlight the importance of redox balance in phagocytes (232). For example, mice fed torula yeast-based low Se diets exhibited decreased resistance to Heligmosomoides polygyrus compared with adequate Se diets (0.2 ppm Se) on secondary infection (11).…”

Section: The Effects Of Se Intake On Camentioning

confidence: 99%

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

658

496

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Dietary selenium (]Se), mainly through its incorporation into selenoproteins, plays an important role in inflammation and immunity. Adequate levels of Se are important for initiating immunity, but they are also involved in regulating excessive immune responses and chronic inflammation. Evidence has emerged regarding roles for individual selenoproteins in regulating inflammation and immunity, and this has provided important insight into mechanisms by which Se influences these processes. Se deficiency has long been recognized to negatively impact immune cells during activation, differentiation, and proliferation. This is related to increased oxidative stress, but additional functions such as protein folding and calcium flux may also be impaired in immune cells under Se deficient conditions. Supplementing diets with above-adequate levels of Se can also impinge on immune cell function, with some types of inflammation and immunity particularly affected and sexually dimorphic effects of Se levels in some cases. In this comprehensivearticle, the roles of Se and individual selenoproteins in regulating immune cell signaling and function are discussed. Particular emphasis is given to how Se and selenoproteins are linked to redox signaling, oxidative burst, calcium flux, and the subsequent effector functions of immune cells. Data obtained from cell culture and animal models are reviewed and compared with those involving human physiology and pathophysiology, including the effects of Se levels on inflammatory or immune-related diseases including anti-viral immunity, autoimmunity, sepsis, allergic asthma, and chronic inflammatory disorders. Finally, the benefits and potential adverse effects of intervention with Se supplementation for various inflammatory or immune disorders are discussed. Antioxid. Redox Signal. 16, 705-743.

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Section: The Effects Of Se Intake On Camentioning

confidence: 99%

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

658

496

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“…Previous work with mice established that deficiencies in selenium and/or vitamin E altered the normal physiological response and intestinal clearance of a parasitic nematode, Heligmosomoides polygyrus (1,49). A secondary H. polygyrus infection induced a potent T-helper cell 2 (Th2) immune (memory) response, and both single and double deficiencies in selenium and vitamin E delayed adult worm expulsion, increased fecundity (egg production), and impaired some, but not all, IL-4 receptor-dependent changes to the small intestine.…”

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confidence: 99%

The Pathogenicity of an EntericCitrobacter rodentiumInfection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E

et al. 2011

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The pathogenesis of a Citrobacter rodentium infection was evaluated in mice fed diets with a single deficiency in either selenium or vitamin E or with a double deficiency in both selenium and vitamin E compared to mice on nutritionally adequate diets. Mice fed the selenium-and vitamin E-deficient diet for 6 weeks had increased loads of C. rodentium in the colon and spleen, which were not observed in mice fed either of the singly deficient diets or the adequate diet. Infected mice fed the doubly deficient diet had increased colon crypt hyperplasia and an influx of infiltrating cells along with gross changes to crypt architecture, including ulceration and denuding of the epithelial layer. Cytokine and chemokine mRNA levels in the colon were measured by real-time PCR. Expression of proinflammatory cytokines and chemokines was upregulated on day 12 after infection with C. rodentium in mice fed the doubly deficient diet compared to mice fed the control diet. Heme oxygenase 1, an enzyme upregulated by oxidative stress, also was more highly induced in infected mice fed the doubly deficient diet. Production of C. rodentium antigen-specific IgM and IgG antibodies was not affected by feeding the doubly deficient diet. The results indicated that selenium and vitamin E play an important role in host resistance and in the pathology induced by C. rodentium, an infection that mimics disease caused by common food-borne bacterial pathogens in humans.

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“…There has been evidence that GIN specifically produce and secrete a number of protective antioxidant enzymes in response to host generated RONS (Kotze, 2003;Dzik, 2006;Lees et al, 2011). Some studies have demonstrated the requirement for effective host antioxidant defenses for the development of immunity against GIN infection (Smith et al, 2005).…”

Section: Oxidative Statusmentioning

confidence: 99%

Immune and other factors modulating host resistance against gastrointestinal nematode parasites in sheep

Arsenopoulos

Symeonidou

Papadopoulos

2018

J Hellenic Vet Med Soc

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Infection of small ruminants with gastrointestinal nematode (GIN) parasites is a significant problem with crucial impact on meat and milk production. The strategy of administrating anthelminthic drugs has been implemented for many years and has resulted in the development of resistant strains of parasites. Meanwhile, consumers demand for free of drugs products have led to the adoption of alternative control methods, which involve the selective breeding of animals, which are resistant to parasitism. The development of immunity and therefore, resistance against gastrointestinal parasites is based on the activation of specific host genes. Gene analysis has revealed areas (QTLs), which affect resistance or susceptibility of sheep to gastrointestinal infestations between animals of different breeds and between individuals of the same breed. The role of cytokines and T helper cells has been enhanced as research, strongly, supports the connection of Th2 cells with resistance and Th1 cells with susceptibility against GIN. Latest data implicates T regulatory cells and a specific cell type, Th17, in immune response mechanisms. Specific adhesion molecules (integrins, lectins, cadherins) are produced in the gut lumen in sufficient amounts and appear to boost immunity and reduce clinical signs in sheep. Additionally, the immunoglobulins IgA and IgE have been positively correlated with increased resistance against GIN. In several cases of GIN, where an increased number of eosinophils and mast cells in the intestinal epithelium have been recorded, the animals had a reduced number of parasite eggs in their feces. The genes of the Major Histocompatibility Complex have been referred to as potential resistance or susceptibility markers. Other enzymes, like chitinases, enhance the resilience of animals and protect them effectively. Animal’s nutritional status is another determinant factor of immune capability against GIN in sheep, both systemic, as well as locally. Regarding the effect of reactive oxygen and nitrogen species, some researchers support their direct effect against GIN, resulting in a natural reduction of their number, while others claim the indirect action in the intestinal epithelium by reducing local immunity. Consequently, the detection of genes associated with resistance or susceptibility to gastrointestinal infestations is promising and in line with modern requirements.

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Deficiencies in Selenium and/or Vitamin E Lower the Resistance of Mice to Heligmosomoides polygyrus Infections

Cited by 39 publications

References 44 publications

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

The Pathogenicity of an EntericCitrobacter rodentiumInfection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E

Immune and other factors modulating host resistance against gastrointestinal nematode parasites in sheep

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