phenylephrine-hydrochloride and Vitamin-A-Deficiency

phenylephrine-hydrochloride has been researched along with Vitamin-A-Deficiency* in 3 studies

Other Studies

3 other study(ies) available for phenylephrine-hydrochloride and Vitamin-A-Deficiency

ArticleYear
Vitamin A deficient mice exhibit increased viral antigens and enhanced cytokine/chemokine production in nasal tissues following respiratory virus infection despite the presence of FoxP3+ T cells.
    International immunology, 2016, Volume: 28, Issue:3

    The World Health Organization (WHO) estimates that 250 million children under the age of five suffer from vitamin A deficiencies (VAD). Individuals with VAD experience higher rates of mortality and increased morbidity during enteric and respiratory infections compared with those who are vitamin A sufficient. Previously, our laboratory has demonstrated that VAD mice have significantly impaired virus-specific IgA and CD8(+) T-cell responses in the airways. Here, we demonstrate that VAD mice experience enhanced cytokine/chemokine gene expression and release in the respiratory tract 10 days following virus infection compared with control vitamin A sufficient animals. Cytokines/chemokines that are reproducibly up-regulated at the gene expression and protein levels include IFNγ and IL-6. Despite previous indications that cytokine dysregulation in VAD animals might reflect low forkhead box P3 (FoxP3)-positive regulatory T-cell frequencies, we found no reduction in FoxP3(+) T cells in VAD respiratory tissues. As an alternative explanation for the high cytokine levels, we found that the extent of virus infection and the persistence of viral antigens were increased on day 10 post-infection in VAD animals compared with controls, and consequently that respiratory tract tissues had an increased potential to activate virus-specific T cells. Results encourage cautious management of viral infections in patients with VAD, as efforts to enhance FoxP3(+) T cell frequencies and quell immune effectors could potentially exacerbate disease if the virus has not been cleared.

    Topics: Animals; Antigens, Viral; Diet Therapy; Female; Forkhead Transcription Factors; Humans; Interferon-gamma; Interleukin-6; Male; Mice; Mice, Inbred C57BL; Nose; Pregnancy; Respirovirus Infections; Sendai virus; T-Lymphocytes, Regulatory; Up-Regulation; Viral Load; Vitamin A; Vitamin A Deficiency

2016
The development of lesions in vitamin A-deficient adult fowl.
    British journal of experimental pathology, 1969, Volume: 50, Issue:2

    Topics: Animals; Beak; Body Weight; Bone and Bones; Cerebrospinal Fluid; Chickens; Epithelium; Female; Male; Manometry; Nerve Degeneration; Nervous System; Nose; Periosteum; Spinal Canal; Vitamin A Deficiency

1969
Experimentally induced changes in nasal mucous secretory systems and their effect on virus infection in chickens. I. Effect on mucosal mrphology and function.
    The Journal of experimental medicine, 1969, Jul-01, Volume: 130, Issue:1

    The domestic chicken was used as an experimental model in which to demonstrate morphological and functional relationships of nasal organ systems, principally of mucous systems. Mucous secretions of olfactory, respiratory, lacrimal, and accessory areas were found to have clear histochemical differences, yet were sufficiently miscible in normal circumstances to form an unbroken, synchronously moving sheet. Changes induced experimentally in host physiology did not all affect the mucous components of given areas in the same way or to the same degree. Mucosal changes were produced by the following methods: Topically administered cocaine 20%, in a single application, temporarily paralyzed the cilia, and the consequently reduced traction apparently held mucus in the acini and effected a temporary lag in mucus excretion. Three successive applications caused acute acinar depletion and ciliary paralysis. Hexylcaine chloride 5% immediately desquamated all intranasal epithelia, damaged the proximal portion of the acini, and induced acinar exhaustion and mucosal inflammation-effects not overcome within 5(1/2) days. Internal dehydration produced progressively viscous mucus, severe acinar gaping with mucus anchored in the acini, a heavy surface sheet, and deceleration or arrest of mucociliary flow. Avitaminosis A induced reduction in the height (about 50%) of all mucosae and acini, especially the inner lining of the maxillary concha, caused an actual 50% reduction in the number of cells per acinus, and retarded the mucociliary flow rate about 50%. Pilocarpine induced initial hypersecretion, later exhaustion, and, still later, slow production of densely staining mucus in the acinar cells; also acinar gaping. Breeding in a germfree environment produced a greatly reduced mucosal depth throughout the nasal fossa, an extraordinary reduction in the number of cells per acinus, relative reduction in the number of acinar neck cells, and concomitant increase in ciliated cells in that region. Exposure to a temperature of -20 degrees C for 1 hr caused blanching of all secretory cells, acinar gaping, and temporary reduction of mucosal depth.

    Topics: Amino Alcohols; Animals; Chickens; Cilia; Cocaine; Cold Temperature; Dehydration; Ethers; Germ-Free Life; Mucus; Nasal Mucosa; Nose; Pilocarpine; Virus Diseases; Vitamin A Deficiency

1969