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Pneumocystis infection in an immunocompetent host can promote collateral sensitization to respiratory antigens.

Authors: Swain, SD  Meissner, N  Han, S  Harmsen, A 
Citation: Swain SD, etal., Infect Immun. 2011 Feb 22.
Pubmed: (View Article at PubMed) PMID:21343358
DOI: Full-text: DOI:10.1128/IAI.01273-10

Infection with the opportunistic fungal pathogen Pneumocystis is assumed to pass without persistent pathology in immunocompetent hosts. However, when immunocompetent BALB/c mice were inoculated with Pneumocystis, a vigorous Th2-like pulmonary inflammation ensued, which peaked at 14 days post infection. This coincided with a 10 fold increase in the number of antigen presenting cells (APCs) in the lung, and these cells were capable of presenting antigen in vitro, as well as greater uptake of antigen in vivo. When mice were presented with exogenous antigen at the 14 day time point of the infection, they developed respiratory sensitization to that antigen, in the form of increased airway hyperresponsiveness upon a later challenge, whereas mice not infected but presented with antigen did not. Like other forms of collateral sensitization, this response was dependent on IL-4 receptor signaling. This ability to facilitate sensitization to exogenous antigen has been previously reported for other infectious diseases, however, Pneumocystis appears uniquely capable in this respect, as a single i.n. dose without added adjuvant, when administered at the appropriate time, was sufficient to initiate sensitization. Pneumocystis infection probably occurs in most humans during the first few years of life, and in the vast majority of cases, fails to cause any overt direct pathology. However, as we show here, Pneumocystis can be an agent of co-morbidity at this time, by facilitating respiratory sensitization that may relate to the later development or exacerbation of obstructive airway disease.

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CRRD Object Information
CRRD ID: 5128506
Created: 2011-03-07
Species: All species
Last Modified: 2011-03-07
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.