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Original Research: CHEST INFECTIONS |

Presence of Activated Airway T Lymphocytes in Human Puumala Hantavirus DiseaseAirway T Lymphocytes in Puumala Hantavirus Disease

Johan Rasmuson, MD; Jamshid Pourazar, PhD; Mats Linderholm, MD, PhD; Thomas Sandström, MD, PhD; Anders Blomberg, MD, PhD; Clas Ahlm, MD, PhD
Author and Funding Information

From Infectious Diseases, Department of Clinical Microbiology (Drs Rasmuson, Linderholm, and Ahlm), and Respiratory Medicine, Department of Public Health and Clinical Medicine (Drs Pourazar, Sandström, and Blomberg), Umeå University, Umeå, Sweden.

Correspondence to: Johan Rasmuson, MD, Infectious Diseases, Department of Clinical Microbiology, Umeå University, SE-901 85, Umeå, Sweden; e-mail: johan.rasmuson@climi.umu.se


Funding/Support: This work was supported with grants from the Swedish Heart Lung Foundation, the Heart Foundation of Northern Sweden, the County Councils of Northern Sweden, the County Council of Västerbotten, and the Medical Faculty of Umeå University. Dr Blomberg is the holder of the Lars Werkö Distinguished Research Fellowship from the Swedish Heart Lung Foundation.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(3):715-722. doi:10.1378/chest.10-2791
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Background:  Hantaviruses cause two clinical syndromes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The clinical spectrum in HFRS also often involves respiratory symptoms. As information about the pulmonary pathogenesis in HFRS is limited, we aimed to further study the local airway immune response in the lower airways.

Methods:  Bronchoscopy was performed in 15 hospitalized patients with HFRS, with sampling of endobronchial mucosal biopsies and BAL fluid. Biopsies were stained for leukocytes, lymphocyte subsets, and vascular endothelial adhesion molecules. BAL fluid and blood lymphocyte subsets were determined using flow cytometry. Fourteen healthy volunteers acted as a control group.

Results:  Compared with control subjects, endobronchial mucosal biopsies from patients with HFRS revealed increased numbers of CD8+ T cells in both epithelium and submucosa (P ≤ .001), along with an increase in submucosal CD4+ T cells (P = .001). In contrast, patients’ submucosal neutrophil and eosinophil numbers were reduced (P < .001). The expression of vascular cell adhesion molecule-1 (VCAM-1) was enhanced in patients with HFRS (P < .001). In patients with HFRS, analyses of T-cell subsets in BAL fluid showed higher proportions of CD3+ and CD8+ T cells (P = .011 and P = .025) and natural killer cells (P < .001), together with an increased expression of activation markers human leukocyte antigen-DR (HLA-DR) and CD25 on T cells (P < .001 and P < .001).

Conclusions:  The present findings indicate a local immune response in terms of activated T lymphocytes in the lungs of patients with HFRS. The elevated expression of activation markers and VCAM-1 further implies the importance of cytotoxic lymphocytes in the pathogenesis of pulmonary involvement in HFRS.

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