Ischemia-Reperfusion Injury Activates Innate Immunity in Rat Kidneys

Kim, Byung Soo; Lim, Sun Woo; Li, Can; Kim, Jung Shim; Sun, Bo; Ahn, Kyung Ohk; Han, Sang Woo; Kim, Jin; Yang, Chul Woo

doi:10.1097/01.tp.0000158355.83327.62

Cited by 176 publications

(156 citation statements)

References 28 publications

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“…In the present study, the TLR4 mRNA expression levels in the kidneys were markedly increased in the HS5 and HS10 groups compared with the control group, demonstrating that the kidneys were seriously impacted by AHS. In addition, previous research has shown a marked increase in TLR2 and TLR4 expression in renal tubular cells and in renal infiltrating cells caused by ischemia and reperfusion injury compared with control group (Kim et al, 2005;Pedregosa et al, 2011). Cunningham et al (2004) reported that TLR4 expression in the kidneys was critical in mediating LPS-induced acute kidney failure via proinflammatory cytokine release and subsequent kidney damage.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of TLR4 mRNA Expression Levels in Broiler Chickens Under Acute Heat Stress

Huang

2017

Rev. Bras. Cienc. Avic.

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Toll-like receptors (TLRs) are well-characterized in mice and rats, but little is known on their role in broiler chickens during acute heat stress (AHS). The aim of the present study was to estimate the change in TLR4 mRNA expression in the liver, kidney's pleen, heart, and small intestine of broiler chickens under AHS. A total of 240 healthy Arbor Acres (AA) broiler chickens were randomly divided into four groups: control group (22±1°C; 0h), HS2, HS5 and HS10 (38±1°C; 2h, 5h and 10h of heat stress, respectively). As AHS duration increased, TLR4 mRNA expression slightly decreased at HS2 and HS5, but was dramatically elevated in HS10 (p<0.001) compared with the control group in the small intestine, as well as in the spleen at HS2 (p=0.001) and HS10 (p<0.001). The mRNA expression levels of TLR4 significantly increased in the liver, heart, and kidneys (p<0.001) at HS10, and in the kidneys at HS5 (p=0.003). It is found that TLR4 mRNA expression at HS10 in different organs was significantly higher (p<0.001) compared with HS2 and HS5. The results of the present study suggest that AHS may modulate the functional responses of the liver, kidney, spleen, heart, and small intestine of broilers by regulating TLR4 mRNA expression.

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Section: Discussionmentioning

confidence: 99%

Upregulation of TLR4 mRNA Expression Levels in Broiler Chickens Under Acute Heat Stress

Huang

2017

Rev. Bras. Cienc. Avic.

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“…TLR4-deficient mice have reduced myocardial infarction size 24 h after 1-h ligation of the left anterior descending coronary artery (35) and reduced levels of aspartate aminotransferase 1 and 3 h after reperfusion of liver lobes rendered ischemic for 45 min (53). TLRs were implicated in a rat model of renal IRI, but the earliest studies were performed 24 h after reperfusion (25). TLR4 protein and mRNA were elevated for days after renal IRI, and TLR4Ϫ/Ϫ as well as MyD88Ϫ/Ϫ animals had less renal dysfunction and less histological evidence of IRI 24 h after reperfusion (52).…”

Section: Discussionmentioning

confidence: 99%

Novel critical role of Toll-like receptor 4 in lung ischemia-reperfusion injury and edema

Zanotti

Casiraghi

Abano³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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like receptors (TLRs) of the innate immune system contribute to noninfectious inflammatory processes. We employed a murine model of hilar clamping (1 h) with reperfusion times between 15 min and 3 h in TLR4-sufficient (C3H/ OuJ) and TLR4-deficient (C3H/HeJ) anesthetized mice with additional studies in chimeric and myeloid differentiation factor 88 (MyD88)-and TLR4-deficient mice to determine the role of TLR4 in lung ischemia-reperfusion injury. Human pulmonary microvascular endothelial monolayers were subjected to simulated warm ischemia and reperfusion with and without CRX-526, a competitive TLR4 inhibitor. Functional TLR4 solely on pulmonary parenchymal cells, not bone marrow-derived cells, mediates early lung edema following ischemia-reperfusion independent of MyD88. Activation of MAPKs and NF-B was significantly blunted and/or delayed in lungs of TLR4-deficient mice as a consequence of ischemia-reperfusion injury, but edema development appeared to be independent of activation of these signaling pathways. Pretreatment with a competitive TLR4 inhibitor prevented edema in vivo and reduced actin cytoskeletal rearrangement and gap formation in pulmonary microvascular endothelial monolayers subjected to simulated warm ischemia and reperfusion. In addition to its well-accepted role to alter gene transcription, functioning TLR4 on pulmonary parenchymal cells plays a key role in very early and profound pulmonary edema in murine lung ischemiareperfusion injury. This may be due to a novel mechanism: regulation of endothelial cell cytoskeleton affecting microvascular endothelial cell permeability. microvascular permeability; endothelial cell; pulmonary edema ACUTE LUNG INJURY IS A FEATURE of sepsis, systemic inflammatory response, and adult respiratory distress syndrome. Noncardiogenic pulmonary edema and impaired gas exchange are consequences of acute lung injury, irrespective of etiology. The mechanisms causing pulmonary edema due to acute lung injury are not well-understood. Ischemia-reperfusion injury (IRI), a form of acute lung injury occurring immediately following lung transplantation, is a frequent complication causing morbidity and mortality (26). A greater understanding of lung IRI is likely relevant to many types of acute lung injury and thus may benefit not only lung transplant recipients, but also substantial numbers of other patients with lung injury. Such knowledge would also facilitate retrieval of lungs from nonheart-beating cadaver donors for transplant and/or may assist in the salvage of lungs not considered suitable for transplant, thereby reducing the critical shortage of transplantable lungs (8, 11).Reperfusion following an interval of ischemia results in an inflammatory response involving components of the innate immune system, including the complement and coagulation cascades. Both parenchymal and myeloid cells elaborate free radicals, nitric oxide, and pro-and anti-inflammatory cytokines (4, 5). Recently, there has been increasing awareness of the important contribution of the innate immune syst...

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“…These PRR include the toll-like receptor (TLR) family of innate immune receptors (4). In organ transplantation, DAMPs formed as a result of ischemia/reperfusion injury activate the innate immune system (86,94,135). Thus, infection and transplantation generate an inflammatory response by activating the MPS, resulting in the production of cytokines and chemokines and priming of the adaptive immune system (42).…”

Section: The Mononuclear Phagocyte Systemmentioning

confidence: 99%

The Mononuclear Phagocyte System in Homeostasis and Disease: A Role for Heme Oxygenase-1

Hull

Agarwal

George

2014

Antioxidants & Redox Signaling

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Significance: Heme oxygenase-1 (HO-1) is a potential therapeutic target in many diseases, especially those mediated by oxidative stress and inflammation. HO-1 expression appears to regulate the homeostatic activity and distribution of mononuclear phagocytes ( MP) in lymphoid tissue under physiological conditions. It also regulates the ability of MP to modulate the inflammatory response to tissue injury. Recent Advances: The induction of HO-1 within MP-particularly macrophages and dendritic cells-modulates the effector functions that they acquire after activation. These effector functions include cytokine production, surface receptor expression, maturation state, and polarization toward a pro-or anti-inflammatory phenotype. The importance of HO-1 in MP is emphasized by their expression of specific receptors that primarily function to ingest heme-containing substrate and deliver it to HO-1. Critical Issues: MP are the first immunological responders to tissue damage. They critically affect the outcome of injury to many organ systems, yet few therapies are currently available to specifically target MP during disease pathogenesis. Elucidation of the role of HO-1 expression in MP may help to direct broadly applicable therapies to clinical use that are based on the immunomodulatory capabilities of HO-1. Future Directions: Unraveling the complexities of HO-1 expression specifically within MP will more completely define how HO-1 provides cytoprotection in vivo. The use of models in which HO-1 expression is specifically modulated in bone marrow-derived cells will allow for a more complete characterization of its immunoregulatory properties.

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Ischemia-Reperfusion Injury Activates Innate Immunity in Rat Kidneys

Abstract: I/R injury rapidly activates the innate immune response.

Cited by 176 publications

References 28 publications

Upregulation of TLR4 mRNA Expression Levels in Broiler Chickens Under Acute Heat Stress

Upregulation of TLR4 mRNA Expression Levels in Broiler Chickens Under Acute Heat Stress

Novel critical role of Toll-like receptor 4 in lung ischemia-reperfusion injury and edema

The Mononuclear Phagocyte System in Homeostasis and Disease: A Role for Heme Oxygenase-1

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