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Haptoglobin dampens endotoxin‐induced inflammatory effects both in vitro and in vivo
Author(s) -
Arredouani Mohamed S.,
Kasran Ahmad,
Vanoirbeek Jeroen A.,
Berger Frank G.,
Baumann Heinz,
Ceuppens Jan L.
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.02071.x
Subject(s) - haptoglobin , lipopolysaccharide , acute phase protein , tumor necrosis factor alpha , in vivo , immunology , in vitro , sepsis , cytokine , monocyte , stimulation , interleukin , inflammation , medicine , biology , biochemistry , microbiology and biotechnology
Summary We report that haptoglobin, an acute‐phase protein produced by liver cells in response to interleukin‐6 (IL‐6), can modulate the inflammatory response induced by endotoxins. We provide evidence that haptoglobin has the ability to selectively antagonize lipopolysaccharide (LPS) effects in vitro by suppressing monocyte production of tumour necrosis factor‐α, IL‐10 and IL‐12, while it fails to inhibit the production of IL‐6, IL‐8 and IL‐1 receptor antagonist. In two animal models of LPS‐induced bronchopulmonary hyperreactivity and endotoxic shock, haptoglobin knockout mice were more sensitive to LPS effects compared to their wild‐type counterparts. The present data suggest that haptoglobin regulates monocyte activation following LPS stimulation. The increase in haptoglobin levels during an acute‐phase reaction may generate a feedback effect which dampens the severity of cytokine release and protects against endotoxin‐induced effects.