TY - JOUR
T1 - Macrophages and inflammatory mediators in tissue injury
AU - Laskin, Debra L.
AU - Pendino, Kimberly J.
PY - 1995
Y1 - 1995
N2 - Tissue injury induced by a diverse group of xenobiotics appears to involve both direct and indirect damage to target cells. Thus, while chemicals may act directly on target cells resulting in toxicity, they may also act indirectly by recruiting and activating resident and inflammatory tissue macrophages. Macrophages are potent secretory cells that release an array of mediators, including proinflammatory and cytotoxic cytokines and growth factors, bioactive lipids, hydrolytic enzymes, reactive oxygen intermediates, and nitric oxide - each of which has been implicated in the pathogenesis of tissue injury. The potential role of macrophages and their mediators in tissue injury has been extensively investigated in the lung and the liver. In both of these tissues, xenobiotics induce localized macrophage accumulation and mediator release. Furthermore, when macrophage functioning is blocked, pulmonary and hepatic injury-induced agents such as ozone, bleomycin, acetaminophen, carbon tetrachloride, and galactosamine are reduced. These data provide direct support for the hypothesis that macrophages and the mediators they release contribute to xenobiotic-induced tissue injury.
AB - Tissue injury induced by a diverse group of xenobiotics appears to involve both direct and indirect damage to target cells. Thus, while chemicals may act directly on target cells resulting in toxicity, they may also act indirectly by recruiting and activating resident and inflammatory tissue macrophages. Macrophages are potent secretory cells that release an array of mediators, including proinflammatory and cytotoxic cytokines and growth factors, bioactive lipids, hydrolytic enzymes, reactive oxygen intermediates, and nitric oxide - each of which has been implicated in the pathogenesis of tissue injury. The potential role of macrophages and their mediators in tissue injury has been extensively investigated in the lung and the liver. In both of these tissues, xenobiotics induce localized macrophage accumulation and mediator release. Furthermore, when macrophage functioning is blocked, pulmonary and hepatic injury-induced agents such as ozone, bleomycin, acetaminophen, carbon tetrachloride, and galactosamine are reduced. These data provide direct support for the hypothesis that macrophages and the mediators they release contribute to xenobiotic-induced tissue injury.
KW - cytokines
KW - liver
KW - lung
KW - nitric oxide
KW - reactive oxygen intermediates
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U2 - https://doi.org/10.1146/annurev.pa.35.040195.003255
DO - https://doi.org/10.1146/annurev.pa.35.040195.003255
M3 - Review article
C2 - 7598511
SN - 0066-4251
VL - 35
SP - 655
EP - 677
JO - Annual Review of Pharmacology and Toxicology
JF - Annual Review of Pharmacology and Toxicology
ER -