Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes

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Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes. / Andersson, A; Qvarfordt, I; Laan, M; Sjostrand, M; Malmhall, C; Riise, GC; Cardell, Lars-Olaf; Linden, A.

I: Clinical and Experimental Immunology, Vol. 138, Nr. 1, 2004, s. 75-82.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Andersson, A, Qvarfordt, I, Laan, M, Sjostrand, M, Malmhall, C, Riise, GC, Cardell, L-O & Linden, A 2004, 'Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes', Clinical and Experimental Immunology, vol. 138, nr. 1, s. 75-82. https://doi.org/10.1111/j.1365-2249.2004.02580.x

APA

Andersson, A., Qvarfordt, I., Laan, M., Sjostrand, M., Malmhall, C., Riise, GC., Cardell, L-O., & Linden, A. (2004). Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes. Clinical and Experimental Immunology, 138(1), 75-82. https://doi.org/10.1111/j.1365-2249.2004.02580.x

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MLA

Vancouver

Author

Andersson, A ; Qvarfordt, I ; Laan, M ; Sjostrand, M ; Malmhall, C ; Riise, GC ; Cardell, Lars-Olaf ; Linden, A. / Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes. I: Clinical and Experimental Immunology. 2004 ; Vol. 138, Nr. 1. s. 75-82.

RIS

TY - JOUR

T1 - Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes

AU - Andersson, A

AU - Qvarfordt, I

AU - Laan, M

AU - Sjostrand, M

AU - Malmhall, C

AU - Riise, GC

AU - Cardell, Lars-Olaf

AU - Linden, A

PY - 2004

Y1 - 2004

N2 - CD4(+) and CD8(+) lymphocytes are mobilized in severe chronic obstructive pulmonary disease (COPD) and the CD8(+) cytokine interleukin (IL)-16 is believed to be important in regulating the recruitment and activity of CD4(+) lymphocytes. In the current study, we examined whether tobacco smoke exerts an impact not only on IL-16 in the lower airways but also in CD4(+) or CD8(+) lymphocytes or in lymphoid tissue. The concentration of IL-16 protein was measured by enzyme-linked immunosorbent assay (ELISA) in concentrated bronchoalveolar lavage fluid (BALF) collected from 33 smokers with chronic bronchitis (CB), eight asymptomatic smokers (AS) and seven healthy never-smokers (NS). The concentrations of IL-16 and soluble IL-2 receptor alpha (sIL-2Ralpha) protein were also measured in conditioned medium from human blood CD4(+) and CD8(+) lymphocytes stimulated with tobacco smoke extract (TSE) in vitro. IL-16 mRNA was assessed in vitro as well, using reverse transcription-polymerase chain reaction (RT-PCR). Finally, the intracellular immunoreactivity for IL-16 protein (IL-16IR) was assessed in six matched pairs of palatine tonsils from smokers and non-smokers. BALF IL-16 was higher in CB and AS than in NS. TSE substantially increased the concentration of IL-16 but not sIL-2Ralpha in conditioned medium from CD4(+) and CD8(+) lymphocytes. There was no corresponding effect on IL-16 mRNA. IL-16IR in tonsils was lower in smokers than in non-smokers. The current findings demonstrate that tobacco smoke exerts a wide impact on the CD8(+) cytokine IL-16, in the airway lumen, in blood CD4(+) and CD8(+) lymphocytes and in lymphoid tissue. The effect on IL-16 release may be selective for preformed IL-16 in CD4(+) lymphocytes. New clinical studies are required to evaluate whether tobacco smoke mobilizes T lymphocytes via IL-16 in the lower airways and whether this mechanism can be targeted in COPD.

AB - CD4(+) and CD8(+) lymphocytes are mobilized in severe chronic obstructive pulmonary disease (COPD) and the CD8(+) cytokine interleukin (IL)-16 is believed to be important in regulating the recruitment and activity of CD4(+) lymphocytes. In the current study, we examined whether tobacco smoke exerts an impact not only on IL-16 in the lower airways but also in CD4(+) or CD8(+) lymphocytes or in lymphoid tissue. The concentration of IL-16 protein was measured by enzyme-linked immunosorbent assay (ELISA) in concentrated bronchoalveolar lavage fluid (BALF) collected from 33 smokers with chronic bronchitis (CB), eight asymptomatic smokers (AS) and seven healthy never-smokers (NS). The concentrations of IL-16 and soluble IL-2 receptor alpha (sIL-2Ralpha) protein were also measured in conditioned medium from human blood CD4(+) and CD8(+) lymphocytes stimulated with tobacco smoke extract (TSE) in vitro. IL-16 mRNA was assessed in vitro as well, using reverse transcription-polymerase chain reaction (RT-PCR). Finally, the intracellular immunoreactivity for IL-16 protein (IL-16IR) was assessed in six matched pairs of palatine tonsils from smokers and non-smokers. BALF IL-16 was higher in CB and AS than in NS. TSE substantially increased the concentration of IL-16 but not sIL-2Ralpha in conditioned medium from CD4(+) and CD8(+) lymphocytes. There was no corresponding effect on IL-16 mRNA. IL-16IR in tonsils was lower in smokers than in non-smokers. The current findings demonstrate that tobacco smoke exerts a wide impact on the CD8(+) cytokine IL-16, in the airway lumen, in blood CD4(+) and CD8(+) lymphocytes and in lymphoid tissue. The effect on IL-16 release may be selective for preformed IL-16 in CD4(+) lymphocytes. New clinical studies are required to evaluate whether tobacco smoke mobilizes T lymphocytes via IL-16 in the lower airways and whether this mechanism can be targeted in COPD.

KW - chronic bronchitis

KW - CD8(+)

KW - CD4(+)

KW - BAL

KW - tonsil

U2 - 10.1111/j.1365-2249.2004.02580.x

DO - 10.1111/j.1365-2249.2004.02580.x

M3 - Article

VL - 138

SP - 75

EP - 82

JO - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 1

ER -