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Infection and Immunity, December 2000, p. 6962-6969, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Dose-Dependent Activation of Lymphocytes in Endotoxin-Induced Airway Inflammation

Roland Larsson,1 David Rocksén,1 Bo Lilliehöök,1 Åsa Jonsson,1 and Anders Bucht1,2,*

Department of Biomedicine, Division of NBC Defence, Defence Research Establishment, Umeå,1 and Department of Medicine, Karolinska Institute, Stockholm,2 Sweden

Received 18 May 2000/Returned for modification 30 June 2000/Accepted 6 September 2000

Recruitment of neutrophils to lung tissue and airspaces is a hallmark of inflammatory events following inhalation of endotoxins. We studied the role of different lymphocyte subsets in this inflammation, which is assumed to primarily involve the innate immune system. Inhalation of aerosolized Escherichia coli lipopolysaccharide (LPS) in mice induced a dose-dependent increase in neutrophils in bronchoalveolar lavage fluid, reaching a maximum after 12 h at a low dose and after 24 h at a high dose. Profiles of gene expression in lung tissue indicated an early (2 h) and transient onset of proinflammatory cytokines and chemokines by a low dose of LPS, while a high dose caused more delayed and sustained (6 to 12 h) activation. Gamma interferon, interleukin-2 (IL-2), RANTES, and the alpha  chain of the IL-2 receptor were not expressed at a low dose, whereas a high dose of LPS induced a strong expression of these genes, indicating a dose-dependent activation of T cells. A similar pattern was observed for IL-17, supporting a contribution of T cells to the neutrophilic inflammation only at high-dose exposure to LPS. The involvement of lymphocytes in the inflammatory response was further studied using mice with functional deficiencies in defined lymphocyte subsets. Both gamma delta T-cell- and B-cell-deficient mice displayed a response similar to that of the corresponding wild-type strains. Selective depletion of NK cells by in vivo administration of the pk136 antibody did not significantly affect the recruitment of neutrophils into airspaces. Thus, neither NK cells, B cells, nor gamma delta T cells appeared to participate in the host response, suggesting that among the lymphocyte subsets, alpha beta T cells are exclusively involved in endotoxin-induced airway inflammation.

* Corresponding author. Mailing address: Division of NBC Defence, Department of Biomedicine, Defence Research Establishment, SE-901 82, Umeå, Sweden. Phone: 46 90 106634. Fax: 46 90 106803. E-mail: anders.bucht{at}ume.foa.se.

Infection and Immunity, December 2000, p. 6962-6969, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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