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Ovalbumin sensitization changes the inflammatory response to subsequent parainfluenza infection. Eosinophils mediate airway hyperresponsiveness, m(2) muscarinic receptor dysfunction, and antiviral effects.

Adamko DJ, Yost BL, Gleich GJ, Fryer AD, Jacoby DB - J. Exp. Med. (1999)

Bottom Line: Asthma exacerbations, many of which are virus induced, are associated with airway eosinophilia.An additional and unexpected finding was that sensitization to ovalbumin caused a marked (80%) reduction in the viral content of the lungs.This was reversed by the antibody to IL-5, implicating a role for eosinophils in viral immunity.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Health Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.

ABSTRACT
Asthma exacerbations, many of which are virus induced, are associated with airway eosinophilia. This may reflect altered inflammatory response to viruses in atopic individuals. Inhibitory M(2) muscarinic receptors (M(2)Rs) on the airway parasympathetic nerves limit acetylcholine release. Both viral infection and inhalational antigen challenge cause M(2)R dysfunction, leading to airway hyperresponsiveness. In antigen-challenged, but not virus-infected guinea pigs, M(2)R dysfunction is due to blockade of the receptors by the endogenous antagonist eosinophil major basic protein (MBP). We hypothesized that sensitization to a nonviral antigen before viral infection alters the inflammatory response to viral infection, so that M(2)R dysfunction and hyperreactivity are eosinophil mediated. Guinea pigs were sensitized to ovalbumin intraperitoneally, and 3 wk later were infected with parainfluenza. In sensitized, but not in nonsensitized animals, virus-induced hyperresponsiveness and M(2)R dysfunction were blocked by depletion of eosinophils with antibody to interleukin (IL)-5 or treatment with antibody to MBP. An additional and unexpected finding was that sensitization to ovalbumin caused a marked (80%) reduction in the viral content of the lungs. This was reversed by the antibody to IL-5, implicating a role for eosinophils in viral immunity.

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Administration of AbMBP before viral infection of sensitized animals protected the ability of pilocarpine to inhibit vagally induced bronchoconstriction. Pilocarpine (1–100 μg·kg−1 intravenous) inhibited vagally induced bronchoconstriction in sensitized control animals (open circles, n = 7), but not in sensitized virus-infected animals (filled circles, n = 10), unless they were pretreated with AbMBP (filled diamonds, n = 5; P = 0.005). Each point is the mean, with SEM shown by vertical bars.
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Figure 3: Administration of AbMBP before viral infection of sensitized animals protected the ability of pilocarpine to inhibit vagally induced bronchoconstriction. Pilocarpine (1–100 μg·kg−1 intravenous) inhibited vagally induced bronchoconstriction in sensitized control animals (open circles, n = 7), but not in sensitized virus-infected animals (filled circles, n = 10), unless they were pretreated with AbMBP (filled diamonds, n = 5; P = 0.005). Each point is the mean, with SEM shown by vertical bars.

Mentions: Pretreatment with an AbIL5 did not prevent virus-induced M2R dysfunction in nonsensitized guinea pigs (Fig. 2 A). In contrast, pretreatment with AbIL5 did prevent virus-induced M2R dysfunction in virus-infected guinea pigs sensitized to OVA (Fig. 2 B). Likewise, pretreatment of sensitized guinea pigs with AbMBP before viral infection also protected the function of the neuronal M2Rs (Fig. 3).


Ovalbumin sensitization changes the inflammatory response to subsequent parainfluenza infection. Eosinophils mediate airway hyperresponsiveness, m(2) muscarinic receptor dysfunction, and antiviral effects.

Adamko DJ, Yost BL, Gleich GJ, Fryer AD, Jacoby DB - J. Exp. Med. (1999)

Administration of AbMBP before viral infection of sensitized animals protected the ability of pilocarpine to inhibit vagally induced bronchoconstriction. Pilocarpine (1–100 μg·kg−1 intravenous) inhibited vagally induced bronchoconstriction in sensitized control animals (open circles, n = 7), but not in sensitized virus-infected animals (filled circles, n = 10), unless they were pretreated with AbMBP (filled diamonds, n = 5; P = 0.005). Each point is the mean, with SEM shown by vertical bars.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2195693&req=5

Figure 3: Administration of AbMBP before viral infection of sensitized animals protected the ability of pilocarpine to inhibit vagally induced bronchoconstriction. Pilocarpine (1–100 μg·kg−1 intravenous) inhibited vagally induced bronchoconstriction in sensitized control animals (open circles, n = 7), but not in sensitized virus-infected animals (filled circles, n = 10), unless they were pretreated with AbMBP (filled diamonds, n = 5; P = 0.005). Each point is the mean, with SEM shown by vertical bars.
Mentions: Pretreatment with an AbIL5 did not prevent virus-induced M2R dysfunction in nonsensitized guinea pigs (Fig. 2 A). In contrast, pretreatment with AbIL5 did prevent virus-induced M2R dysfunction in virus-infected guinea pigs sensitized to OVA (Fig. 2 B). Likewise, pretreatment of sensitized guinea pigs with AbMBP before viral infection also protected the function of the neuronal M2Rs (Fig. 3).

Bottom Line: Asthma exacerbations, many of which are virus induced, are associated with airway eosinophilia.An additional and unexpected finding was that sensitization to ovalbumin caused a marked (80%) reduction in the viral content of the lungs.This was reversed by the antibody to IL-5, implicating a role for eosinophils in viral immunity.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Health Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.

ABSTRACT
Asthma exacerbations, many of which are virus induced, are associated with airway eosinophilia. This may reflect altered inflammatory response to viruses in atopic individuals. Inhibitory M(2) muscarinic receptors (M(2)Rs) on the airway parasympathetic nerves limit acetylcholine release. Both viral infection and inhalational antigen challenge cause M(2)R dysfunction, leading to airway hyperresponsiveness. In antigen-challenged, but not virus-infected guinea pigs, M(2)R dysfunction is due to blockade of the receptors by the endogenous antagonist eosinophil major basic protein (MBP). We hypothesized that sensitization to a nonviral antigen before viral infection alters the inflammatory response to viral infection, so that M(2)R dysfunction and hyperreactivity are eosinophil mediated. Guinea pigs were sensitized to ovalbumin intraperitoneally, and 3 wk later were infected with parainfluenza. In sensitized, but not in nonsensitized animals, virus-induced hyperresponsiveness and M(2)R dysfunction were blocked by depletion of eosinophils with antibody to interleukin (IL)-5 or treatment with antibody to MBP. An additional and unexpected finding was that sensitization to ovalbumin caused a marked (80%) reduction in the viral content of the lungs. This was reversed by the antibody to IL-5, implicating a role for eosinophils in viral immunity.

Show MeSH
Related in: MedlinePlus