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Interleukin 12, interleukin 18, and tumor necrosis factor alpha release by alveolar macrophages: acute and chronic hypersensitivity pneumonitis.
Ann Allergy Asthma Immunol. 2009 Feb; 102(2):149-54.AA

Abstract

BACKGROUND

Hypersensitivity pneumonitis (HP) is characterized by a granulomatous inflammation and may show various forms of clinical presentation, such as the acute, subacute, and chronic forms. The TH1-associated cytokines interleukin (IL) 12 and IL-18 and tumor necrosis factor alpha (TNF-alpha) may be involved in the pathogenesis of both the acute and chronic forms of HP.

OBJECTIVE

To compare the release of IL-12, IL-18, and TNF-alpha from bronchoalveolar lavage (BAL) macrophages in these 2 forms of HP.

METHODS

Patients underwent BAL 0 to 6 days after the last antigen exposure. Alveolar macrophages (AMs) from BAL in 6 patients with acute HP, 16 with chronic HP, and 11 controls were cultured for 24 hours. Cytokines in the culture supernatants were measured by enzyme-linked immunosorbent assay.

RESULTS

The production of IL-12, IL-18, and TNF-alpha by AMs was increased in patients with both acute and chronic forms in either the absence or presence of lipopolysaccharide compared with controls. The levels of IL-12, IL-18, and TNF-alpha showed no difference between patients with acute and chronic HP. The spontaneous production of IL-12, IL-18, and TNF-alpha did not correlate with the CD4/CD8 ratio in BAL. The spontaneous and lipopolysaccharide-stimulated release of IL-12 showed a positive correlation with the percentage of lymphocytes (r = .470, P = .03; r = .496, P = .02; respectively) in BAL.

CONCLUSIONS

This study demonstrates that an increased release of IL-12, IL-18, and TNF-alpha by AMs is associated with both the acute and chronic forms of HP.

Authors+Show Affiliations

Department of Pneumology and Allergology, Ruhrlandklinik, Medical Faculty, University of Duisburg-Essen, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19230467

Citation

Ye, Qiao, et al. "Interleukin 12, Interleukin 18, and Tumor Necrosis Factor Alpha Release By Alveolar Macrophages: Acute and Chronic Hypersensitivity Pneumonitis." Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology, vol. 102, no. 2, 2009, pp. 149-54.
Ye Q, Nakamura S, Sarria R, et al. Interleukin 12, interleukin 18, and tumor necrosis factor alpha release by alveolar macrophages: acute and chronic hypersensitivity pneumonitis. Ann Allergy Asthma Immunol. 2009;102(2):149-54.
Ye, Q., Nakamura, S., Sarria, R., Costabel, U., & Guzman, J. (2009). Interleukin 12, interleukin 18, and tumor necrosis factor alpha release by alveolar macrophages: acute and chronic hypersensitivity pneumonitis. Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology, 102(2), 149-54. https://doi.org/10.1016/S1081-1206(10)60246-3
Ye Q, et al. Interleukin 12, Interleukin 18, and Tumor Necrosis Factor Alpha Release By Alveolar Macrophages: Acute and Chronic Hypersensitivity Pneumonitis. Ann Allergy Asthma Immunol. 2009;102(2):149-54. PubMed PMID: 19230467.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin 12, interleukin 18, and tumor necrosis factor alpha release by alveolar macrophages: acute and chronic hypersensitivity pneumonitis. AU - Ye,Qiao, AU - Nakamura,Shinobu, AU - Sarria,Rafael, AU - Costabel,Ulrich, AU - Guzman,Josune, PY - 2009/2/24/entrez PY - 2009/2/24/pubmed PY - 2009/3/11/medline SP - 149 EP - 54 JF - Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology JO - Ann Allergy Asthma Immunol VL - 102 IS - 2 N2 - BACKGROUND: Hypersensitivity pneumonitis (HP) is characterized by a granulomatous inflammation and may show various forms of clinical presentation, such as the acute, subacute, and chronic forms. The TH1-associated cytokines interleukin (IL) 12 and IL-18 and tumor necrosis factor alpha (TNF-alpha) may be involved in the pathogenesis of both the acute and chronic forms of HP. OBJECTIVE: To compare the release of IL-12, IL-18, and TNF-alpha from bronchoalveolar lavage (BAL) macrophages in these 2 forms of HP. METHODS: Patients underwent BAL 0 to 6 days after the last antigen exposure. Alveolar macrophages (AMs) from BAL in 6 patients with acute HP, 16 with chronic HP, and 11 controls were cultured for 24 hours. Cytokines in the culture supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: The production of IL-12, IL-18, and TNF-alpha by AMs was increased in patients with both acute and chronic forms in either the absence or presence of lipopolysaccharide compared with controls. The levels of IL-12, IL-18, and TNF-alpha showed no difference between patients with acute and chronic HP. The spontaneous production of IL-12, IL-18, and TNF-alpha did not correlate with the CD4/CD8 ratio in BAL. The spontaneous and lipopolysaccharide-stimulated release of IL-12 showed a positive correlation with the percentage of lymphocytes (r = .470, P = .03; r = .496, P = .02; respectively) in BAL. CONCLUSIONS: This study demonstrates that an increased release of IL-12, IL-18, and TNF-alpha by AMs is associated with both the acute and chronic forms of HP. SN - 1081-1206 UR - https://www.unboundmedicine.com/medline/citation/19230467/Interleukin_12_interleukin_18_and_tumor_necrosis_factor_alpha_release_by_alveolar_macrophages:_acute_and_chronic_hypersensitivity_pneumonitis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1081-1206(10)60246-3 DB - PRIME DP - Unbound Medicine ER -