alexa Hypersensitivity Pneumonitis Caused by House Cricket, A
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
Open Access

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Research Article

Hypersensitivity Pneumonitis Caused by House Cricket, Acheta domesticus

Mijeong Park1,2, Emma L Boys1,2, Max Yan3, Katherine Bryant1, Barbara Cameron1, Anup Desai2, Paul S Thomas1,2* and Nicodemus T Tedla1*
1Inflammation and Infection Research Centre, Department of Pathology, UNSW, Sydney, NSW 2052, Australia
2Department of Respiratory Medicine, Prince of Wales Hospital, Sydney, NSW 2031, Australia
3Department of Anatomical Pathology, SEALS, Prince of Wales Hospital, Sydney, NSW 2031, Australia
Corresponding Authors : Paul S Thomas, MD
Department of Respiratory Medicine, Prince of Wales Hospital
Sydney, NSW 2031, Australia
Tel: +61 2 9382 4620
Fax: +61 2 9382 4627
E-mail: [email protected]
  Nicodemus Tedla MD, PhD
Inflammation and Infection Research Centre
Faculty of Medicine, university of New South Wales
Sydney, NSW 2052, Australia
Tel: +61 2 93852919
Fax: +61 2 93851389
E-mail: [email protected]
Received June 16, 2014; Accepted August 15, 2014; Published August 25, 2014
Citation: Park M, Boys EL, Yan M, Bryant K, Cameron B, et al. (2014) Hypersensitivity Pneumonitis Caused by House Cricket, Acheta domesticus. J Clin Cell Immunol 5:248. doi: 10.4172/2155-9899.1000248
Copyright: © 2014 Park M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Hypersensitivity pneumonitis (HP) is characterized by extensive interstitial lung inflammation primarily driven by activated T lymphocytes in response to exogenous antigens. The purpose of this study was to investigate whether chronic exposure to Acheta domesticus commonly known as house cricket was the underlying cause of HP in a 63 year old patient. HP was diagnosed by the history, spirometry high resolution computed tomography (HRCT) of the chest, bronchoalveolar lavage and trans-bronchial biopsy. Ouchterlony double diffusion assay, direct ELISA and Western blotting were used to detect immuno-reactive precipitins/antigens and anti-cricket antibodies. Mass spectrometry was used to identify the major putative antigens. T cell-mediated response to cricket antigens was assessed by in vitro cytokine production assays. HRCT showed extensive bilateral and ground glass opacification throughout the lungs with some sparing at the bases, while bronchoalveolar lavage showed lymphocyte predominant leukocyte infiltration. A lung biopsy showed diffuse chronic interstitial inflammation with poorly defined granulomas consisting lymphocytes and occasional giant cells. There were high titer antibodies against cricket protein extracts and specific antigen-antibody precipitins. Western blotting showed 4 specific immuno-reactive bands. Tryptic peptide digest and mass spectrometry revealed arginine kinase as a potential antigen. Multistep chromatography enriched cricket arginine kinase induced strong in-vitro interferon-γ response by PBMC obtained from the patient but not in other cricket-exposed and non-exposed healthy control subjects. This is the first study to report a case of subacute HP in response to prolonged exposure to house cricket antigens.

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