Attenuation of lipopolysaccharide‐induced acute lung injury by treatment with IL‐10

Abstract

Neutrophils appeared to play an important role in ALI. Time-dependent treatment with IL-10 after intra-tracheal instillation of LPS was effective in protecting rats from ALI, probably by suppressing pulmonary infiltration with activated neutrophils.

Analysis of cytotoxicity induced by proinflammatory cytokines in the human alveolar epithelial cell line A549

“…In fact, high levels of IFN-γ has been demonstrated in some populations with clinical systemic inflammation, especially in virus-associated ALI such as SARS (severe acute respiratory syndrome) (8,10). Multiple inflammatory mediators have been proved in the bloodstream and bronchoalveolar lavage fluid of patients with septic ALI (10)(11)(12)(13). The observation that a mediator such as IFN-γ, which has minimal direct toxicity against 76 parenchymal cells, can exert synergistic cytotoxicity in combination with other mediators implies the complex pathophysiology of sepsis and suggests one reason for the failure of antiinflammatory strategies targeting a single mediator such as IL-1β or TNF-α (38).…”

“…In this study, we evaluated the cytotoxicity induced by a mixture of proinflammatory cytokines (IL-1β/ TNF-α/IFN-γ), which have been suggested to play major roles in sepsis or ALI (5,(8)(9)(10)(11)(12)(13), in the human alveolar epithelial cell line A549. Then, to clarify the cytotoxic signaling pathways responsible for alveolar epithelial cell injury, various agents with antiinflammatory or antioxidative properties were screened for cytoprotective effects in an in vitro acute lung injury model (9,(14)(15)(16)(17).…”

Growth Factors and Cytokines in Acute Lung Injury

“…While several of these cytokines have been shown to be necessary to dampen the magnitude of inflammatory cytokine release and limit lung injury (52,129,277), the expression of these molecules can themselves promote disordered reparative responses. For instance, IL-13 and TGF-β stimulate fibroblast effector cell function in vitro and/or or promote fibrogenesis in vivo (22,194), which is of particular relevance to the development of fibroproliferation in ARDS.…”

Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase

“…Among the proinflammatory cytokines, tumor necrosis factor (TNF)-a plays a pivotal role in the development of ALI, participating in both early and later inflammatory responses, initiating and perpetuating the inflammation [5,6]. Interleukin (IL)-10 is one of the anti-inflammatory cytokines protecting the lung from inflammatory injury [7,8]. The balance between proinflammatory and anti-inflammatory cytokines is crucial in the process of ALI.…”