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Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
Published on: July 23, 2012
Allergic airway sensitization impairs antibacterial IgG antibody responses during bacterial respiratory tract
Arthur H Totten1, Li Xiao2, Danlin Luo1
1Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Ala.
Background:
Mycoplasma pneumoniae, an atypical human pathogen, has been associated with asthma initiation and exacerbation. Asthmatic patients have been reported to have higher carriage rates of M pneumoniae compared with nonasthmatic subjects and are at greater risk for invasive respiratory infections.
Objective:
We sought to study whether prior allergen sensitization affects the host response to chronic bacterial infection.
Methods:
BALB/cJ and IL-4 receptor α-/- mice were sensitized with ovalbumin (OVA) and then infected with M pneumoniae or Streptococcus pneumoniae. Immune parameters were analyzed at 30 days postinfection and included cellular profiles in bronchoalveolar lavage fluid (BALF) and serum IgG and IgE antibody levels to whole bacterial lysate, recombinant P1 adhesin, and OVA. Total lung RNA was examined for transcript levels, and BALF was examined for cytokine protein profiles.
Results:
Anti-M pneumoniae antibody responses were decreased in allergen-sensitized, M pneumoniae-infected animals compared with control animals, but OVA-specific IgG responses were unaffected. Similar decreases in anti-S pneumoniae antibody levels were found in OVA-sensitized animals. However, M pneumoniae, but not S pneumoniae, infection augmented anti-OVA IgE antibody responses. Loss of IL-4 receptor signaling partially restored anti-M pneumoniae antibody responses in IgG2a and IgG2b subclasses. Inflammatory cytokine levels in BALF from OVA-sensitized, M pneumoniae-infected or S pneumoniae-infected animals were reduced compared with those in uninfected OVA-sensitized control animals. Unexpectedly, airway hyperreactivity to methacholine was essentially ablated in M pneumoniae-infected, OVA-sensitized animals.
Conclusions:
An established type 2-biased host immune response impairs the host immune response to respiratory bacterial infection in a largely pathogen-independent manner. Some pathogens, such as M pneumoniae, can augment ongoing allergic responses and inhibit pulmonary type 2 cytokine responses and allergic airway hyperreactivity.
Insights
Prior allergen sensitization impairs the immune response to respiratory bacterial infections like Mycoplasma pneumoniae. However, M. pneumoniae infection can paradoxically reduce allergic airway hyperreactivity.
Area of Science:
- Immunology
- Microbiology
- Respiratory Medicine
Background:
- Mycoplasma pneumoniae is linked to asthma development and worsening.
- Asthma patients show higher M. pneumoniae carriage rates and increased risk of respiratory infections.
Purpose of the Study:
- To investigate if prior allergen sensitization influences the host's response to chronic bacterial infection.
- To understand the interaction between allergic responses and bacterial pathogens in the respiratory tract.
Main Methods:
- Mice were sensitized with ovalbumin (OVA) then infected with M. pneumoniae or Streptococcus pneumoniae.
- Immune responses were assessed via bronchoalveolar lavage fluid (BALF) cellular profiles, serum antibody levels (IgG, IgE), lung RNA transcript levels, and BALF cytokine profiles.
- IL-4 receptor signaling knockout mice were used to explore its role in immune responses.
Main Results:
- Allergen-sensitized animals showed reduced antibody responses to M. pneumoniae and S. pneumoniae.
- M. pneumoniae infection, but not S. pneumoniae, increased anti-OVA IgE antibody levels.
- Loss of IL-4 receptor signaling partially restored anti-M. pneumoniae IgG responses.
- Inflammatory cytokine levels were reduced in infected, sensitized animals.
- Airway hyperreactivity was significantly reduced in M. pneumoniae-infected, OVA-sensitized mice.
Conclusions:
- A type 2-biased immune response, typical of allergies, hinders the host's ability to fight respiratory bacterial infections.
- Mycoplasma pneumoniae can exacerbate allergic responses while simultaneously suppressing pulmonary type 2 cytokines and allergic airway hyperreactivity.
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