T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis.

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Abstract Text:

Maoxiang Li,Jack R Harkema,Zahidul Islam,Chistopher F Cuff,James J Pestka,

Exposure to immunosuppressive environmental contaminants is a possible contributing factor to increased occurrence of viral respiratory diseases. The objective of this study was to test the hypothesis that the trichothecene mycotoxin T-2 toxin (T-2), a frequent food contaminant, alters host resistance to lung infection by reovirus, a model respiratory virus. Balb/c mice (4 week old) were treated intraperitoneally with T-2 toxin (1.75 mg/kg bw) or saline vehicle and then intranasally instilled 2 h later with 10(7) plaque forming unit (PFU) of reovirus, strain Lang (T1/L) or saline vehicle. At 10 days post-instillation (PI), both virus plaque-forming responses and reovirus L2 gene expression were 10-fold higher in lungs of T-2-treated mice compared to controls. No-effect and lowest-effect levels for T-2-induced suppression of reovirus clearance were 20 and 200 microg/kg bw, respectively. Respiratory reovirus infection resulted in a mild bronchiolitis with minimal alveolitis, which was markedly exacerbated by T-2 pretreatment. Reovirus exposure induced marked increases in total cells, neutrophils and lymphocytes at 3 and 7 days PI in bronchial alveolar lavage fluid (BALF) whereas macrophages were increased only at 7 days PI. Although prior T-2 exposure attenuated total cell and macrophage counts in BALF of control and infected mice at 3 days PI, the toxin potentiated total cell, macrophage, neutrophil and lymphocyte counts in infected mice at 7 days PI. At 3 days PI, T-2 suppressed reovirus-induced IFN-gamma elevation in BALF, but enhanced production of IL-6 and MCP-1. T-2 pretreatment also suppressed reovirus-specific mucosal IgA responses in lung and enteric tract, but potentiated serum IgA and IgG responses. Taken together, T-2 increased lung viral burden, bronchopneumonia and pulmonary cellular infiltration in reovirus-infected mice. These effects might be attributable to reduced alveolar macrophage levels as well as modulated cytokine and mucosal Ig responses.

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Publishing Authors By Initials

M Li,JR Harkema,Z Islam,CF Cuff,JJ Pestka,

For similar investigative techniques: clinical laboratory techniques: microbiological techniques: viral load research abstracts see: investigative techniques: clinical laboratory techniques: microbiological techniques: viral load research

PUBMED ID PMID:

MEDLINE DATE:

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Toxicology and applied pharmacology

VOLUME: 217

Page Numbers: 76-85

Journal Abbreviation: Toxicol. Appl. Pharmacol.

ISSN: 0041-008X

DAY: 12

MONTH: 08

YEAR: 2006

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 416575

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Keywords Mesh Terms:

KEYWORDS: Viral Load

MESH TERMS: analysis

Chemical & Substance for Abstract: T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis. Information

Substance Name: Interferon Type II

Registry Number: 82115-62-6

Grant and Affiliation Information for T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis.

AFFILIATION: Center for Integrative Toxicology, Michigan State University, East Lansing, MI 48824-1224, USA.

Country: United States

AGENCY: United States NIEHS

GRANT: ES03553

ACRONYM: ES

MEDLINETA: Toxicol Appl Pharmacol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis Related Publications

• Comparative induction of 28S ribosomal RNA cleavage by ricin and the trichothecenes deoxynivalenol and T-2 toxin in the macrophage.
• Deoxynivalenol exacerbates viral bronchopneumonia induced by respiratory reovirus infection.
• Deoxynivalenol induces p38 interaction with the ribosome in monocytes and macrophages.
• Double-Stranded RNA-Activated Protein Kinase Mediates Induction of Interleukin-8 Expression by Deoxynivalenol, Shiga Toxin 1, and Ricin in Monocytes.
• Historical developments in the research of interferon receptors.
• Neurotoxicity and inflammation in the nasal airways of mice exposed to the macrocyclic trichothecene mycotoxin roridin a: kinetics and potentiation by bacterial lipopolysaccharide coexposure.
• Protein arginine methyltransferases: evolution and assessment of their pharmacological and therapeutic potential.
• Purification and cloning of interferon alpha.
• Satratoxin G-induced apoptosis in PC-12 neuronal cells is mediated by PKR and caspase independent.
• Sequencing and bacterial expression of a novel murine alpha interferon gene.
• Simultaneous screening of fumonisin B1, aflatoxin B1, and zearalenone by line immunoblot: a computer-assisted multianalyte assay system.
• T-2 toxin impairs murine immune response to respiratory reovirus and exacerbates viral bronchiolitis.
• The interferons: 50 years after their discovery, there is much more to learn.
• Tissue distribution and proinflammatory cytokine induction by the trichothecene deoxynivalenol in the mouse: Comparison of nasal vs. oral exposure.
• Transcriptional regulation of deoxynivalenol-induced IL-8 expression in human monocytes.