Endotoxin induces late increase in the production of pulmonary proinflammatory cytokines in murine lupus-like pristane-primed modelp

Abstract

Lupus-like syndrome is characterized by multiple organ injuries including lungs and kidneys. Endotoxin induces a transiently Lupus-like syndrome is characterized by multiple organ injuries including lungs and kidneys. Endotoxin induces a transiently
intent systemic inflammatory response and indirectly transient acute lung injury in normal condition. However, whether endotoxin intent systemic inflammatory response and indirectly transient acute lung injury in normal condition. However, whether endotoxin
may trigger the persistent development of lung injury in chronic, inflammatory lupus-like syndrome compared with normal condition may trigger the persistent development of lung injury in chronic, inflammatory lupus-like syndrome compared with normal condition
remains unclear. We examined the pulmonary vascular permeability and production of proinflammatory cytokines, such as TNF-α, remains unclear. We examined the pulmonary vascular permeability and production of proinflammatory cytokines, such as TNF-α,
IL-6, IL-10 and IFN-λ, which play prominent roles in the pathogenesis of lupus-like tissue injury, 6 h and 72 h afteri.p. lipopolysaccharide (LPS; endotoxin) injection in pristane-primed chronic inflammation ICR mice characterized by a lupus-like IL-6, IL-10 and IFN-λ, which play prominent roles in the pathogenesis of lupus-like tissue injury, 6 h and 72 h afteri.p. lipopolysaccharide (LPS; endotoxin) injection in pristane-primed chronic inflammation ICR mice characterized by a lupus-like
syndrome. These results demonstrated that levels of serum IL-6, IL-10 and IFN-λ and bronchoalveolar lavage (BAL) IL-6 andevels of serum IL-6, IL-10 and IFN-λ and bronchoalveolar lavage (BAL) IL-6 and
IFN-λ were remarkably increased 6 h in LPS-exposed pristane-primed mice compared with pristane-primed controls, while pulmonary IFN-λ were remarkably increased 6 h in LPS-exposed pristane-primed mice compared with pristane-primed controls, while pulmonary
vascular permeability and levels of serum and BAL TNF-α were not. And levels of BAL TNF-α, IL-6 and IL-10 were significantly vascular permeability and levels of serum and BAL TNF-α were not. And levels of BAL TNF-α, IL-6 and IL-10 were significantly
enhanced 72 h in LPS-exposed pristane-primed mice compared of TNF-α, IL-6 and IL-10 by lung cells obtained from LPS-exposed enhanced 72 h in LPS-exposed pristane-primed mice compared of TNF-α, IL-6 and IL-10 by lung cells obtained from LPS-exposed
pristane-primed mice compared with LPS-exposed normal mice. Our findings indicate that LPS may trigger persistent progression pristane-primed mice compared with LPS-exposed normal mice. Our findings indicate that LPS may trigger persistent progression
of lung injury through late overproduction of BAL TNF-α, IL-6, and IL-10 in lupuslike chronic inflammation syndrome compared of lung injury through late overproduction of BAL TNF-α, IL-6, and IL-10 in lupuslike chronic inflammation syndrome compared
with normal condition. with normal condition.