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Cited by 1,498

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

IL-6 is an antiinflammatory cytokine required for controlling local or systemic acute inflammatory responses.

Open access
Xing, Z, Gauldie, J, Cox, G, Baumann, H, Jordana, M, Lei, X F, Achong, M K·1998·Journal of Clinical Investigation
DOI 10.1172/jci1368
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Abstract

IL-6 is induced often together with the proinflammatory cytokines TNFalpha and IL-1 in many alarm conditions, and circulating IL-6 plays an important role in the induction of acute phase reactions. However, whether this endogenous IL-6 plays any additional pro- or antiinflammatory roles in local or systemic responses remains unclear. In this study, the role of IL-6 in acute inflammatory responses was investigated in animal models of endotoxic lung or endotoxemia by using IL-6+/+ and IL-6-/- mice. Aerosol exposure of endotoxin induced increased IL-6 and proinflammatory cytokines TNFalpha and MIP-2 and a neutrophilic response in the lung of IL-6+/+ mice. However, the levels of TNFalpha and MIP-2 and neutrophilia were significantly higher in the lung of IL-6-/- mice. The rate of neutrophil apoptosis in these mice was similar to that in IL-6+/+ mice. A low constitutive level of antiinflammatory cytokine IL-10 was not enhanced by endotoxin and remained similar in the lung in both IL-6+/+ and IL-6-/- mice. Systemically, intraperitoneal delivery of endotoxin resulted in much more pronounced circulating levels of TNFalpha, MIP-2, GM-CSF, and IFNgamma in IL-6-/- mice than in IL-6+/+ mice, and administration of recombinant IL-6 to IL-6-/- mice abolished these differences. In contrast, circulating IL-10 levels were induced to a similar degree in both IL-6+/+ and IL-6-/- mice. Thus, our studies reveal that endogenous IL-6 plays a crucial antiinflammatory role in both local and systemic acute inflammatory responses by controlling the level of proinflammatory, but not antiinflammatory, cytokines, and that these antiinflammatory activities by IL-6 cannot be compensated for by IL-10 or other IL-6 family members.

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Metadata

Authors
Xing, Z., Gauldie, J., Cox, G., Baumann, H., Jordana, M., Lei, X. F., & Achong, M. K.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1998-01-15
Volume
101
Issue
2
Pages
311-320
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci1368
OpenAlex
W1987150557
Cited by
1,498
References
3
FWCI
18.71
Type
journal article
Language
en
Open access
green

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