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Interleukin‐16 stimulates the expression and production of pro‐inflammatory cytokines by human monocytes
Author(s) -
Mathy N. L.,
Scheuer W.,
Lanzendörfer M.,
Honold K.,
Ambrosius D.,
Norley S.,
Kurth R.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00997.x
Subject(s) - secretion , peripheral blood mononuclear cell , cd14 , tumor necrosis factor alpha , cytokine , monocyte , immune system , endocrinology , interleukin , proinflammatory cytokine , biology , interleukin 10 , stimulation , medicine , immunology , inflammation , chemistry , in vitro , biochemistry
Summary Interleukin‐16 (IL‐16) acts as a chemoattractant for CD4 + cells, as a modulator of T‐cell activation, and plays a key role in asthma. This report describes the cytokine‐inducing effects of IL‐16 on total peripheral blood mononuclear cells (PBMC) and PBMC subpopulations. While CD4 + T lymphocytes did not secrete cytokines in response to rhIL‐16, CD14 + CD4 + monocytes and maturing macrophages secrete IL‐1β, IL‐6, IL‐15 and tumour necrosis factor‐α (TNF‐α) upon rhIL‐16 stimulation. The mRNA species for these four cytokines were detected as early as 4 hr post‐stimulation, with protein being secreted by 24 hr. Secretion of IL‐1β and IL‐6 by total PBMC was dose dependent, with maximal secretion being observed using 50 ng/ml rhIL‐16. However, for IL‐15 or TNF‐α maximal secretion by total PBMC occurred with all concentrations between 5 ng/ml to 500 ng/ml rhIL‐16. Purified monocytes/macrophages secreted maximal concentrations of all four cytokines in the presence of 500 ng/ml rhIL‐16, except for monocytes where maximal secretion of IL‐15 was, interestingly, observed with only 50 ng/ml rhIL‐16. The use of higher concentrations of rhIL‐16 (1000 ng/ml) inhibited secretion of all four cytokines. While these IL‐16‐induced cytokines are likely to be involved in the immune system's response to antigen, the data suggest that IL‐16 may play a key role in initiating and/or sustaining an inflammatory response.