The role of viruses in the pathogenesis of hypersensitivity pneumonitis

Cormier, Yvon; Israël-Assayag, Évelyne

doi:10.1097/00063198-200009000-00006

Cited by 32 publications

(20 citation statements)

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“…Animal and vegetable proteins, as well as bacteria, fungi and chemical compounds can cause HP [1]. For example, farmer's lung, one of the most common forms of HP, is often caused by Saccharopolyspora rectivirgula actinomycetes found in poorly conserved hay, straw or grain [2].…”

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confidence: 99%

Impaired function of regulatory T-cells in hypersensitivity pneumonitis

Girard

Israël-Assayag²,

Cormier³

2010

European Respiratory Journal

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Hypersensitivity pneumonitis (HP) is characterised by lung lymphocytosis. Most individuals exposed to HP antigens remain asymptomatic. The mechanisms involved in the impaired immune tolerance leading to HP are unclear. Normally, T-regulatory (Treg)-cells control the immune response. The aim of the present study was to determine whether Treg-cell suppressive function deficiency can explain the uncontrolled inflammation in HP.Bronchoalveolar lavage (BAL) and blood samples were obtained from normal subjects, asymptomatic individuals and HP patients. BAL and blood Treg-cells were isolated. The ability of Treg-cells to suppress T-cell proliferation and the role of interleukin (IL)-17 was verified.BAL and blood Treg-cells from normal subjects suppressed the proliferative response of activated T-cells by 47.1 and 42%, respectively. BAL and blood Treg-cells from asymptomatic subjects had a slightly decreased activity and suppressed proliferation by 29.4 and 31.8%, respectively. BAL and blood Treg-cells from HP patients were totally nonfunctional and unable to suppress proliferation. Low levels of IL-17 were detected in sera and BAL from both normal and asymptomatic individuals, whereas measurable levels were found in patients.Treg-cells may be involved in antigen tolerance in asymptomatic subjects. Defective Treg-cell function, potentially caused by increased IL-17 production, could account for the exacerbated immune response characteristic of HP.

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confidence: 99%

Impaired function of regulatory T-cells in hypersensitivity pneumonitis

Girard

Israël-Assayag²,

Cormier³

2010

European Respiratory Journal

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“…Causative agents, mostly organic in nature, include animal proteins, microbial products and plant particles [1]. The disease is characterised by a pulmonary infiltration and proliferation of activated lymphocytes [2].…”

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confidence: 99%

Mature CD11c+ cells are enhanced in hypersensitivity pneumonitis

Girard¹,

Israël-Assayag²,

Cormier³

2009

European Respiratory Journal

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The present study verified the hypothesis that enhanced maturation of antigenpresenting CD11c+ cells could explain the viral-induced exacerbated immune response to Saccharopolyspora rectivirgula (SR), the main antigen responsible for farmer's lung, a classic form of hypersensitivity pneumonitis (HP). Four groups of mice were studied: group 1 received intranasal instillations of saline; group 2 received instillations of SR for 12 weeks; group 3 received instillations of saline and a single infection with Sendai virus on week 3; and group 4 received instillations of SR for 12 weeks with a single administration of Sendai virus on week 3. On week 13, mice were sacrificed and bronchoalveolar lavage was performed. Lungs were harvested, digested with enzymes, and CD11c + cells were analysed in flow cytometry with anti-CD11c, anti-CD86 and anti-major histocompatibility complex class II markers. Immunofluorescence studies were also performed with the same cell surface markers. Both flow cytometry and immunofluorescence results demonstrate that mature CD11c + cells are significantly enhanced in SR-challenged mice simultaneously infected with Sendai virus, compared with other groups. These CD11c + cells persist in the lung for 9 weeks after the virus infection. Maturation of CD11c + cells could explain, at least in part, the virus-induced increased immune response to SR antigens in this model of HP, but mechanisms have still to be elucidated.

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“…Viruses may also play a role in the development of HP [88][89][90][91][92][93]. Many patients report a viral type illness and flu-like symptoms with an episode of acute HP.…”

Section: Virusesmentioning

confidence: 99%

“…The antigenic response in HP may be enhanced in patients with an acute viral infection for several reasons. Viruses are able to increase the antigen presentation ability of alveolar macrophages, decrease clearance of antigens and induce the release of pro-inflammatory cytokines [89]. Through an increase in the production of IFN-γ, viral infections may promote the antigen presenting ability of macrophages by increasing the expression of major histocompatibility class I and II molecules [89].…”

Section: Virusesmentioning

confidence: 99%

“…Viruses are able to increase the antigen presentation ability of alveolar macrophages, decrease clearance of antigens and induce the release of pro-inflammatory cytokines [89]. Through an increase in the production of IFN-γ, viral infections may promote the antigen presenting ability of macrophages by increasing the expression of major histocompatibility class I and II molecules [89]. Influenza viral infection has also been shown to upregulate CD80 (B7-1) and CD86 (B7-2) molecules on alveolar macrophages, thus increasing their antigen-presenting ability and leading to increased activation and proliferation of T cells [48,89].…”

Section: Virusesmentioning

confidence: 99%

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Hypersensitivity Pneumonitis

Temprano¹,

Knutsen²,

Slavin³

2005

CPR

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Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an immunological mediated hypersensitivity reaction to a variety of inhaled allergens that may cause an acute and subacute interstitial pneumonitis and may lead to a chronic end-stage lung disease. Though more common in adults, hypersensitivity pneumonitis needs to be considered in the differential diagnosis of interstitial pneumonitis in children. In children, the most common antigens are from residential exposure to birds, humidifiers and indoor molds. Clinical features are dependent upon stage of disease, and can include fevers, chills, cough, dyspnea, fatigue and weight loss. Physical examination often reveals rales, and dyspnea and hypoxemia are usually present. Routine laboratory testing demonstrates a moderately elevated erythrocyte sedimentation rate, leukocyte count, total IgG level and a positive rheumatoid factor. Though serum IgG antibodies are elevated to the inhaled antigen(s) in hypersensitivity pneumonitis, they may be present in asymptomatic exposed individuals. The immunopathogenesis involves cellular immunity to inhaled allergens, especially CD8+ cytotoxic T cells, multinucleated giant cells, and ultimately granulomas. The role of antigen-specific IgG antibodies is unclear, but may be involved in antibody-dependent-cellular-cytotoxicity (ADCC) and/or interaction with FcRγ on dendritic cells and monocytes that enhance a Th1 response. Pulmonary function studies demonstrate a restrictive pattern with a diffusion defect resulting in hypoxemia. Radiographic changes vary according to the stage of the disease and are best evaluated by high resolution computerized tomography. Bronchoalveolar lavage demonstrates a lymphocytosis with characteristic increase of CD8+ T cells and NK cells. However, recent literature suggests that the CD4+/CD8+ ratio may not be decreased in children as found in adults. Treatment of hypersensitivity pneumonitis is antigen avoidance and systemic corticosteroids, and prognosis depends on early recognition of the disease.

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The role of viruses in the pathogenesis of hypersensitivity pneumonitis

Cited by 32 publications

References 23 publications

Impaired function of regulatory T-cells in hypersensitivity pneumonitis

Impaired function of regulatory T-cells in hypersensitivity pneumonitis

Mature CD11c+ cells are enhanced in hypersensitivity pneumonitis

Hypersensitivity Pneumonitis

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