Abstract
Reactive oxygen species (ROS) are formed as a result of physiologic cellular metabolism, and a homeostatic balance exists between the formation of ROS and their removal by antioxidant scavenging compounds. Host–pathogen interaction results in a variety of responses, which include phagocytosis of the pathogen, release of cytokines, secretion of toxins, as well as production of ROS, leading to oxidative stress in the kidney. Oxidative stress is widely recognized as an important feature of urinary tract infection, pyelonephritis, and in sepsis kidney. Innate immunity toll-like receptors (TLR) are involved in the pathogen recognition and ROS may mediate its initiation and function. Efforts must be made to identify the precise contribution of these factors in infection process in order to clarify the mechanisms associated with kidney disease. This will certainly lead to discovery of therapeutic strategies in the future.
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References
Gutteridge JM, Mitchell J: Redox imbalance in the critically ill. Br Med Bull 1999; 55(1):49–75.
Gutteridge JM: Lipid peroxidation and antioxidants as biomarkers of tissue damage. Clin Chem 1995; 41(12 Pt 2):1819–1828.
Babior BM: Oxygen-dependent microbial killing by phagocytes (second of two parts). N Engl J Med 1978; 298(13):721–725.
Fantone JC, Ward PA: Role of oxygen-derived free radicals and metabolites in leukocyte-dependent inflammatory reactions. Am J Pathol 1982; 107(3):395–418.
Lampert MB, Weiss SJ: The chlorinating potential of the human monocyte. Blood 1983; 62(3):645–651.
Klebanoff SJ: Oxygen metabolism and the toxic properties of phagocytes. Ann Intern Med 1980; 93(3):480–489.
Hasnain SE, Begum R, Ramaiah KV et al.: Host-pathogen interactions during apoptosis. J Biosci 2003; 28(3):349–358.
Kim I, Xu W, Reed JC. Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities. Nat Rev Drug Discov 2008; 7(12):1013–1030.
Malhotra JD, Kaufman RJ: Endoplasmic reticulum stress and oxidative stress: a vicious cycle or a double-edged sword? Antioxid Redox Signal 2007; 9(12):2277–2293.
Kirschbaum B: Total urine antioxidant capacity. Clin Chim Acta 2001; 305(1–2):167–173.
Nathan C, Xie QW: Nitric oxide synthases: roles, tolls, and controls. Cell 1994; 78(6):915–918.
Mulvey MA, Schilling JD, Martinez JJ, Hultgren SJ: Bad bugs and beleaguered bladders: interplay between uropathogenic Escherichia coli and innate host defenses. Proc Natl Acad Sci USA 2000; 97(16):8829–8835.
Kurutas EB, Ciragil P, Gul M, Kilinc M: The effects of oxidative stress in urinary tract infection. Mediators Inflamm 2005; 2005(4):242–244.
Mates JM: Effects of antioxidant enzymes in the molecular control of reactive oxygen species toxicology. Toxicology 2000; 153(1–3):83–104.
McGirr LG, Hadley M, Draper HH: Identification of N alpha-acetyl-epsilon-(2-propenal)lysine as a urinary metabolite of malondialdehyde. J Biol Chem 1985; 260(29):15427–15431.
Gul M, Kurutas E, Ciragil P et al.: Urinary tract infection aggravates oxidative stress in diabetic patients. Tohoku J Exp Med 2005; 206(1):1–6.
Smith SD, Wheeler MA, Weiss RM: Nitric oxide synthase: an endogenous source of elevated nitrite in infected urine. Kidney Int 1994; 45(2):586–591.
Kolodziejska KE, Burns AR, Moore RH, Stenoien DL, Eissa NT: Regulation of inducible nitric oxide synthase by aggresome formation. Proc Natl Acad Sci USA 2005; 102(13):4854–4859.
Rumbo M, Courjault-Gautier F, Sierro F, Sirard JC, Felley-Bosco E: Polarized distribution of inducible nitric oxide synthase regulates activity in intestinal epithelial cells. FEBS J 2005; 272(2):444–453.
Jablonska E, Puzewska W, Marcinczyk M, Grabowska Z, Jablonski J: iNOS expression and NO production by neutrophils in cancer patients. Arch Immunol Ther Exp (Warsz) 2005; 53(2):175–179.
Kawai K, Yamamoto M, Kameyama S et al.: Enhancement of rat urinary bladder tumorigenesis by lipopolysaccharide-induced inflammation. Cancer Res 1993; 53(21):5172–5175.
Vinson JA, Bose P, Proch J, Al Kharrat H, Samman N: Cranberries and cranberry products: powerful in vitro, ex vivo, and in vivo sources of antioxidants. J Agric Food Chem 2008; 56(14):5884–5891.
Valentova K, Stejskal D, Bednar P et al.: Biosafety, antioxidant status, and metabolites in urine after consumption of dried cranberry juice in healthy women: a pilot double-blind placebo-controlled trial. J Agric Food Chem 2007; 55(8):3217–3224.
Gupta A, Sharma S, Nain CK, Sharma BK, Ganguly NK: Reactive oxygen species-mediated tissue injury in experimental ascending pyelonephritis. Kidney Int 1996; 49(1):26–33.
Mittal R, Sharma S, Chhibber S, Harjai K: Contribution of free radicals to Pseudomonas aeruginosa induced acute pyelonephritis. Microb Pathog 2008; 45(5–6):323–330.
Sener G, Tugtepe H, Velioglu-Ogunc A et al.: Melatonin prevents neutrophil-mediated oxidative injury in Escherichia coli-induced pyelonephritis in rats. J Pineal Res 2006; 41(3):220–227.
Macdonald J, Galley HF, Webster NR: Oxidative stress and gene expression in sepsis. Br J Anaesth 2003; 90(2):221–232.
Khan RZ, Badr KF: Endotoxin and renal function: perspectives to the understanding of septic acute renal failure and toxic shock. Nephrol Dial Transplant 1999; 14(4):814–818.
Gullo A: Sepsis and organ dysfunction/failure. An overview. Minerva Anestesiol 1999; 65(7–8):529–540.
Wiesel P, Patel AP, DiFonzo N et al.: Endotoxin-induced mortality is related to increased oxidative stress and end-organ dysfunction, not refractory hypotension, in heme oxygenase-1-deficient mice. Circulation 2000; 102(24):3015–3022.
Lee JG, Lee SH, Park DW et al.: Toll-like receptor 9-stimulated monocyte chemoattractant protein-1 is mediated via JNK-cytosolic phospholipase A2-ROS signaling. Cell Signal 2008; 20(1):105–111.
Azevedo LC, Janiszewski M, Soriano FG, Laurindo FR: Redox mechanisms of vascular cell dysfunction in sepsis. Endocr Metab Immune Disord Drug Targets 2006; 6(2):159–164.
Salvemini D, Cuzzocrea S: Oxidative stress in septic shock and disseminated intravascular coagulation. Free Radic Biol Med 2002; 33(9):1173–1185.
Zager RA, Johnson AC, Hanson SY, Lund S: Ischemic proximal tubular injury primes mice to endotoxin-induced TNF-alpha generation and systemic release. Am J Physiol Renal Physiol 2005; 289(2):F289–F297.
Heemskerk S, Pickkers P, Bouw MP et al.: Upregulation of renal inducible nitric oxide synthase during human endotoxemia and sepsis is associated with proximal tubule injury. Clin J Am Soc Nephrol 2006; 1(4):853–862.
Heemskerk S, Masereeuw R, Russel FG, Pickkers P: Selective iNOS inhibition for the treatment of sepsis-induced acute kidney injury. Nat Rev Nephrol 2009; 5(11):629–640.
Roth E, Manhart N, Wessner B: Assessing the antioxidative status in critically ill patients. Curr Opin Clin Nutr Metab Care 2004; 7(2):161–168.
Frantz S, Kelly RA, Bourcier T: Role of TLR-2 in the activation of nuclear factor kappaB by oxidative stress in cardiac myocytes. J Biol Chem 2001; 276(7):5197–5203.
Paul-Clark MJ, McMaster SK, Sorrentino R et al.: Toll-like receptor 2 is essential for the sensing of oxidants during inflammation. Am J Respir Crit Care Med 2009; 179(4):299–306.
Remer KA, Brcic M, Jungi TW: Toll-like receptor-4 is involved in eliciting an LPS-induced oxidative burst in neutrophils. Immunol Lett 2003; 85(1):75–80.
Lemaitre B, Nicolas E, Michaut L, Reichhart JM, Hoffmann JA: The dorsoventral regulatory gene cassette spatzle/Toll/cactus controls the potent antifungal response in Drosophila adults. Cell 1996; 86(6):973–983.
Medzhitov R: Toll-like receptors and innate immunity. Nat Rev Immunol 2001; 1(2):135–145.
Schwandner R, Dziarski R, Wesche H, Rothe M, Kirschning CJ: Peptidoglycan- and lipoteichoic acid-induced cell activation is mediated by toll-like receptor 2. J Biol Chem 1999; 274(25):17406–17409.
Poltorak A, He X, Smirnova I et al.: Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in TLR4 gene. Science 1998; 282(5396):2085–2088.
Hayashi F, Smith KD, Ozinsky A et al.: The innate immune response to bacterial flagellin is mediated by toll-like receptor 5. Nature 2001; 410(6832):1099–1103.
Hemmi H, Takeuchi O, Kawai T et al.: A toll-like receptor recognizes bacterial DNA. Nature 2000; 408(6813):740–745.
Robson MG: Toll-like receptors and renal disease. Nephron Exp Nephrol 2009; 113(1):e1–e7.
Shishido T, Nozaki N, Takahashi H et al.: Central role of endogenous toll-like receptor-2 activation in regulating inflammation, reactive oxygen species production, and subsequent neointimal formation after vascular injury. Biochem Biophys Res Commun 2006; 345(4):1446–1453.
Ryan KA, Smith MF, Jr., Sanders MK, Ernst PB: Reactive oxygen and nitrogen species differentially regulate toll-like receptor 4-mediated activation of NF-kappa B and interleukin-8 expression. Infect Immun 2004; 72(4):2123–2130.
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Yang, CW. (2011). Infection and the Kidney. In: Miyata, T., Eckardt, KU., Nangaku, M. (eds) Studies on Renal Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press. https://doi.org/10.1007/978-1-60761-857-7_14
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DOI: https://doi.org/10.1007/978-1-60761-857-7_14
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