Increased levels of interleukin-16 in the airways of tobacco smokers: relationship with peripheral blood T lymphocytes

Laan, Martti; Qvarfordt, Ingemar; Riise, Gerdt C.; Åndersson, Bengt; Larsson, S; Lindén, Anders

doi:10.1136/thx.54.10.911

Cited by 22 publications

(20 citation statements)

References 27 publications

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“…Many of these effects of smoking may result from the ability of nicotine to suppress immune system function [18,19]. Thus, nicotine has been reported to increase IL-16 levels, which may influence systemic immunomodulation by altering the number and responsiveness of systemic T lymphocytes in humans [20,21]. Nicotine has also been reported to differentially effect mouse splenocyte proliferation, with production of Th1 versus Th2 cytokines [22,23].…”

Section: Discussionmentioning

confidence: 97%

Correlates of CD4+ and CD8+ Lymphocyte Counts in High-Risk Immunodeficiency Virus (HIV)-Seronegative Women enrolled in the Women’s Interagency HIV Study (WIHS)

et al. 2007

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Section: Discussionmentioning

confidence: 97%

Correlates of CD4+ and CD8+ Lymphocyte Counts in High-Risk Immunodeficiency Virus (HIV)-Seronegative Women enrolled in the Women’s Interagency HIV Study (WIHS)

et al. 2007

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“…Interestingly, IL‐16 may also mediate non‐specific airway hyperresponsiveness, at least in a mouse model of airway allergy [6]. IL‐16 may enhance the proliferative response of co‐stimulated blood CD4 + lymphocytes [7,8]. Thus, IL‐16 constitutes a plausible candidate cytokine for mobilizing CD4 + lymphocytes in severe COPD.…”

Section: Introductionmentioning

confidence: 99%

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

Andersson

Qvarfordt

Laan

et al. 2004

Clinical and Experimental Immunology

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SUMMARY 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-2R a ) 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-2R a 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.

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“…It is known that the concentration of IL‐16 in the airways is increased in patients with allergic asthma [16] as well as in smokers with and without airway symptoms [17]. In bronchoalveolar lavage (BAL) fluid of allergen‐challenged asthmatic patients, IL‐16 accounts for the major part of the chemotactic activity for lymphocytes [18], whereas in smokers the increased airway IL‐16 concentration is associated with decreased number and increased responsiveness of systemic T lymphocytes [17]. At present, however, the airway concentration and function of IL‐16 in lung allograft recipients with AR or OB is not known.…”

Section: Introductionmentioning

confidence: 99%

IL-16 in the airways of lung allograft recipients with acute rejection or obliterative bronchiolitis

Laan

Lindén

Riise

2003

Clinical and Experimental Immunology

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SUMMARYAcute rejection (AR) is the principal risk factor for obliterative bronchiolitis (OB), the major complication of lung transplantation. It is known that activated CD4 + T lymphocytes are involved in the development of AR and that interleukin (IL)-16 can inhibit the activity of CD4 + T lymphocytes. In this study, we evaluated whether the concentration of IL-16 in the airways is altered in AR or OB and, if so, how this IL-16 concentration relates to the number or activity of airway lymphocytes. The concentration of IL-16 protein was measured in bronchoalveolar lavage (BAL) fluid at three time-points in lung allograft recipients with either AR or OB and in matched controls using ELISA. The concentration of soluble IL-2 receptor (R) protein was measured in BAL fluid using ELISA as well, as an indicator of lymphocyte activity. The percentage of airway lymphocytes was evaluated by performing BAL differential cell counts. Lung allograft recipients with AR displayed lower IL-16 concentrations compared with matched control patients and this IL-16 concentration correlated negatively with the sIL-2R concentration, but it did not correlate with the percentage of lymphocytes in BAL fluid. In contrast, in BAL fluid from lung allograft recipients with OB, the IL-16 concentration was not altered compared with matched control patients and it did not correlate with the percentage of lymphocytes or with the sIL-2R concentration. These data are compatible with an increase in IL-16 playing a protective role against AR but not against OB and, hypothetically, this type of protective effect could be exerted via a down-regulation of the activity of T lymphocytes.

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Increased levels of interleukin-16 in the airways of tobacco smokers: relationship with peripheral blood T lymphocytes

Abstract: (Thorax 1999;54:911-916)

Cited by 22 publications

References 27 publications

Correlates of CD4+ and CD8+ Lymphocyte Counts in High-Risk Immunodeficiency Virus (HIV)-Seronegative Women enrolled in the Women’s Interagency HIV Study (WIHS)

Correlates of CD4+ and CD8+ Lymphocyte Counts in High-Risk Immunodeficiency Virus (HIV)-Seronegative Women enrolled in the Women’s Interagency HIV Study (WIHS)

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

IL-16 in the airways of lung allograft recipients with acute rejection or obliterative bronchiolitis

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