Hypersensitivity pneumonitis

@article{Mohr2004HypersensitivityP,
  title={Hypersensitivity pneumonitis},
  author={Lawrence C. Mohr},
  journal={Current Opinion in Pulmonary Medicine},
  year={2004},
  volume={10},
  pages={401-411}
}
  • L. Mohr
  • Published 1 September 2004
  • Medicine, Biology
  • Current Opinion in Pulmonary Medicine
Purpose of review Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is a granulomatous, inflammatory disease of the lungs caused by the inhalation of antigenic organic particles or fumes. The disease may present as an acute, subacute, or chronic illness. Episodes of acute and subacute HP usually resolve following cessation of antigen exposure. Chronic HP may be progressive, irreversible, and result in debilitating fibrotic lung disease. This review discusses… 

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Hypersensitivity pneumonitis (HP), or extrinsic allergic alveolitis, is due to a hypersensitivity reaction after repeated inhalation of finely dispersed antigens, mainly organic particles or low

Hypersensitivity pneumonitis: current concepts and future questions.

TLDR
This review is limited to the disease caused by airborne allergens and focuses on its immunopathogenesis, eliciting agents, clinical manifestations, diagnosis, management, and prognosis.

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TLDR
The history of occupational and environmental pulmonary diseases associated with exposure to organic dusts and what I believe to be the present state-of-the-art related to this subject are discussed.

IL-12 modulates expression of hypersensitivity pneumonitis.

TLDR
It is suggested that the IL-12 response to Ag may modulate in part the expression ofHypersensitivity pneumonitis.

Mediators of hypersensitivity pneumonitis.

TLDR
It is concluded that chemokines and cytokines induced by intratracheal administration of S. rectivirgula precede BALF neutrophilia and lymphocytosis and may cause differentiation of Th1 cells; it is also concluded that pulmonary macrophages represent a potential source of these substances.

Mechanisms accounting for granulomatous responses in hypersensitivity pneumonitis.

TLDR
CD8+ T cells, the most predominant cell in the lesions of HP, may modulate the granuloma formation via the production of Th1-like or Th2-like cytokines.

Increase of lung neutrophils in hypersensitivity pneumonitis is associated with lung fibrosis.

TLDR
It is suggested that in HP lungs there is a persistent traffic of neutrophils loaded with gelatinase B and collagenase-2 that may play a role in the lung damage and in the fibrotic response.

Interleukin-10 modulates the severity of hypersensitivity pneumonitis in mice.

TLDR
These studies show that IL-10 has important anti-inflammatory properties in HP, and that lack of this cytokine leads to a more severe granulomatous inflammatory response.

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TLDR
Modulation of experimental granulomatous lesions by several of the means previously discussed may offer some important clues to the incidence and clinical course of AA in man and to future therapy and/or prevention of the disease.

Interferon-gamma is necessary for the expression of hypersensitivity pneumonitis.

TLDR
It is shown that IFN-gamma is essential for the expression of hypersensitivity pneumonitis and replaced this mediator via intraperitoneal injections developed granulomatous inflammation in the lung.
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