Role of interleukin-6 in immune complex induced models of vascular injury
SD McClintock, AG Barron, EW Olle, MP Deogracias… - Inflammation, 2005 - Springer
SD McClintock, AG Barron, EW Olle, MP Deogracias, RL Warner, M Opp, KJ Johnson
Inflammation, 2005•SpringerPrevious studies have suggested that Interleukin-6 (IL-6) acts as a marker of vasculitis. To
determine the role of IL-6 in vasculitis we utilized two models of immune complex induced
vascular injury (dermal Arthus and acute pulmonary alveolitis) in IL-6 deficient (IL-6−/−) and
IL-6 sufficient (IL-6+/+) mice. Plasma and bronchoalveolar lavage (BAL) levels of IL-6 were
elevated in the injured IL-6+/+ mice with acute alveolitis and in the plasma of IL-6+/+ mice
with dermal Arthus vasculitis. While, IL-6 levels in IL-6−/− mice were near or below the levels …
determine the role of IL-6 in vasculitis we utilized two models of immune complex induced
vascular injury (dermal Arthus and acute pulmonary alveolitis) in IL-6 deficient (IL-6−/−) and
IL-6 sufficient (IL-6+/+) mice. Plasma and bronchoalveolar lavage (BAL) levels of IL-6 were
elevated in the injured IL-6+/+ mice with acute alveolitis and in the plasma of IL-6+/+ mice
with dermal Arthus vasculitis. While, IL-6 levels in IL-6−/− mice were near or below the levels …
Abstract
Previous studies have suggested that Interleukin-6 (IL-6) acts as a marker of vasculitis. To determine the role of IL-6 in vasculitis we utilized two models of immune complex induced vascular injury (dermal Arthus and acute pulmonary alveolitis) in IL-6 deficient (IL-6−/−) and IL-6 sufficient (IL-6+/+) mice. Plasma and bronchoalveolar lavage (BAL) levels of IL-6 were elevated in the injured IL-6+/+ mice with acute alveolitis and in the plasma of IL-6+/+ mice with dermal Arthus vasculitis. While, IL-6 levels in IL-6−/− mice were near or below the levels of detection. Histological examination of the intensity of vascular injury response demonstrated no significant differences between IL-6−/− and IL6+/+ mice. More specifically, lung permeability (total protein in the BAL) in the lung injury model in IL-6−/− mice was the same as injured IL-6+/+ mice. As a corollary, assessment of vascular permeability in both models was the same in the IL-6−/− as the IL-6+/+ mice. Quantification of leukocyte influx into the injured tissues in both models also revealed no differences between the IL-6−/− and IL-6+/+ mice. These data demonstrate that while IL-6 is upregulated in acute vascular injury it does not appear to be critical in the development of the vascular inflammatory response.
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