ProCite
RefWorks
Reference Manager
BibTeX
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-
1
Tait P, Allison D, 2001. Imaging of the gastrointestinal tract. Drugs Today (Barc) 37 :533–557.
-
2
Lomas DJ, 2003. Technical developments in bowel MRI. Eur Radiol 13 :1058–1071.
-
3
Lawler LP, Fishman EK, 2003. Bladder imaging using multidetector row computed tomography, volume rendering, and magnetic resonance imaging. J Comput Assist Tomogr 27 :553–563.
-
4
Bruel JM, Gallix B, 2003. Multidetector CT and MRI in diseases of the GI tract. J Radiol 84 :499–513.
-
5
Boczko J, Tar M, Melman A, Jelicks LA, Wittner M, Factor SM, Zhao D, Hafron J, Weiss LM, Tanowitz HB, Christ GJ, 2005. Trypanosoma cruzi infection induced changes in the innervation, structure and function of the murine bladder. J Urol 173 :1784–1788.
-
6
Kirchhoff LV, 1996. American trypanosomiasis Chagas disease. Gastroenterol Clin North Am 25 :517–533.
-
7
Tanowitz HB, Kirchhoff LV, Simon D, Morris SA, Weiss LM, Wittner M, 1992. Chagas disease. Clin Microbiol Rev 5 :400–419.
-
8
da Silveira AB, Lemos EM, Adad SJ, Correa-Oliveira R, Furness JB, D’Avila Reis D, 2007. Megacolon in Chagas disease: a study of inflammatory cells, enteric nerves, and glial cells. Hum Pathol 38 :1256–1264.
-
9
Madrid AM, Quera R, Defilippi C, Defilippi C, Gil LC, Sapunar J, Henriques A, 2004. Gastrointestinal motility disturbances in Chagas disease. Rev Med Chil 132 :939–946.
-
10
Madrid AM, Defilippi C, 2006. Disturbances of small intestinal motility in patients with chronic constipation. Rev Med Chil 134 :181–186.
-
11
Scremin LH, Corbett CE, Laurenti MD, Nunes EV, Gama-Rodrigues JJ, Okumura M, 1999. Megabladder in experimental Chagas disease: pathological features of the bladder wall. Rev Hosp Clin Fac Med Sao Paulo 54 :43–46.
-
12
Postan M, Cheever AW, Dvorak JA, McDaniel JP, 1986. A histopathological analysis of the course of myocarditis in C3H/He mice infected with Trypanosoma cruzi clone Sylvio-X10/4. Trans R Soc Trop Med Hyg 80 :50–55.
-
13
Postan M, Bailey JJ, Dvorak JA, McDaniel JP, Pottala EW, 1987. Studies of Trypanosoma cruzi clones in inbred mice. III. Histopathological and electrocardiographical responses to chronic infection. Am J Trop Med Hyg 37 :541–549.
-
14
De Rossell RA, Rodriguez AM, De Jesus R, Calcagno M, De Segnini ZM, Diaz S, 2000. Tripomastigotes de sangre y de cultivo celular de Trypanosoma cruzi Y.: II.—Patología de la enfermedad de Chagas en ratones Balb/c. Parasitol Dia 24 :79–87.
-
15
Mori T, Yoon HS, Iizuka FH, Myung JM, Sato HR, Silva MF, Okumura M, 2005. Intestinal transit and opaque enema study in chagasic mice. Rev Hosp Clin Fac Med Sao Paulo 501 :63–66.
-
16
Guillen-Pernia B, Lugo-Yarbuh A, Moreno E, 2001. Digestive tract dilation in mice infected with Trypanosoma cruzi.Invest Clin 42 :195–209.
-
17
de Oliveira GM, de Melo Medeiros M, da Silva Batista W, Santana R, Araújo-Jorge TC, de Souza AP, 2008. Applicability of the use of charcoal for the evaluation of intestinal motility in a murine model of Trypanosoma cruzi infection. Parasitol Res 102 :747–750.
-
18
Garcia SB, Paula JS, Giovannetti GS, Zenha F, Ramalho EM, Zucoloto S, Silva JS, Cunha FQ, 1999. Nitric oxide is involved in the lesions of the peripheral autonomic neurons observed in the acute phase of experimental Trypanosoma cruzi infection. Exp Parasit 93 :191–197.
-
19
Ribeiro U Jr, Safatle-Ribeiro AV, Habr-Gama A, Gama-Rodrigues JJ, Sohn J, Reynolds JC, 1998. Effect of Chagas disease on nitric oxide-containing neurons in severely affected and unaffected intestine. Dis Colon Rectum 41 :1411–1417.
-
20
Aliberti JC, Machado FS, Souto JT, Campanelli AP, Teixeira MM, Gazzinelli RT, Silva JS, 1999. β-Chemokines enhance parasite uptake and promote nitric oxide-dependent microbiostatic activity in murine inflammatory macrophages infected with Trypanosoma cruzi.Infect Immun 67 :4819–4826.
-
21
Holscher C, Kohler G, Muller U, Mossmann H, Schaub GA, Brombacher F, 1998. Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase. Infect Immun 66 :1208–1215.
-
22
Oswald IP, Wynn TA, Sher A, James SL, 1994. NO as an effector molecule of parasite killing: modulation of its synthesis by cytokines. Comp Biochem Physiol Pharmacol Toxicol Endocrinol 108 :11–18.
-
23
Teixeira MM, Gazzinelli RT, Silva JS, 2002. Chemokines, inflammation and Trypanosoma cruzi infection. Trends Parasitol 18 :262–265.
-
24
Vespa GN, Cunha FQ, Silva JS, 1994. Nitric oxide is involved in control of Trypanosoma cruzi induced parasitemia and directly kills the parasite in vitro.Infect Immun 62 :5177–5182.
-
25
Stark ME, Szurszewski JH, 1992. Role of nitric oxide in gastrointestinal and hepatic function and disease. Gastroenterology 103 :1928–1949.
-
26
Mashimo H, Goyal RK, 1999. Lessons from genetically engineered animal models IV. Nitric oxide synthase gene knockout mice. Am J Physiol Gastrointest Liver Physiol 277 :G745–G750.
-
27
Mungrue I, Husain M, Stewart DJ, 2002. The role of NOS in heart failure: lessons from murine genetic models. Heart Fail Rev 7 :407–422.
-
28
Ny L, Persson K, Larsson B, Chan J, Weiss LM, Wittner M, Huang H, Tanowitz HB, 1999. Localization and activity of nitric oxide synthases in the gastrointestinal tract of Trypanosoma cruzi-infected mice. J Neuroimmunol 99 :27–35.
-
29
Ny L, Alm P, Larsson B, Ekstrom P, Andersson KE, 1995. Nitric oxide pathway in cat esophagus: localization of nitric oxide synthase and functional effects. Am J Physiol Gastrointest Liver Physiol 268 :G59–G70.
-
30
Li E, Zhou P, Singer SM, 2006. Neuronal nitric oxide synthase is necessary for elimination of Giardia lamblia infections in mice. J Immunol 176 :516–521.
-
31
Beck PL, Xavier R, Wong J, Ezedi I, Mashimo H, Mizoguchi A, Mizoguchi E, Bhan AK, Podolsky DK, 2004. Paradoxical roles of different nitric oxide synthase isoforms in colonic injury. Am J Physiol Gastrointest Liver Physiol 286 :G137–G147.
-
32
Helmer KS, West SD, Shipley GL, Chang L, Cui Y, Mailman D, Mercer DW, 2002. Gastric nitric oxide synthase expression during endotoxemia: implications in mucosal defense in rats. Gastroenterology 123 :173–186.
-
33
McCafferty DM, Mudgett JS, Swain MG, Kubes P, 1997. Inducible nitric oxide synthase plays a critical role in resolving intestinal inflammation. Gastroenterology 112 :1022–1027.
-
34
Chandra M, Tanowitz HB, Petkova SB, Huang H, Weiss LM, Wittner M, Factor SM, Shtutin V, Jelicks LA, Chan J, Shirani J, 2002. Significance of inducible nitric oxide synthase in acute myocarditis caused by Trypanosoma cruzi (Tulahuen strain). Int J Parasitol 32 :897–905.
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35
Cummings KL, Tarleton RL, 2004. Inducible nitric oxide synthase is not essential for control of Trypanosoma cruzi infection in mice. Infect Immun 72 :4081–4089.
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36
Huang H, Chan J, Wittner M, Jelicks LA, Morris SA, Factor SM, Weiss LM, Braunstein VL, Bacchi CJ, Yarlett N, Chandra M, Shirani J, Tanowitz HB, 1999. Expression of cardiac cytokines and inducible form of nitric oxide synthase (NOS2) in Trypanosoma cruzi-infected mice. J Mol Cell Cardiol 31 :75–88.
-
37
Huang H, Chan J, Wittner M, Weiss LM, Bacchi CJ, Yarlett N, Martinez M, Morris SM, Braunstein VL, Factor SA, Tanowitz HB, 1997. Trypanosoma cruzi infection induces myocardial nitric oxide synthase. Cardiovasc Pathol 6 :161–166.
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38
Jelicks LA, Shirani J, Wittner M, Chandra M, Weiss LM, Factor SM, Bekirov I, Braunstein VL, Chan J, Huang H, Tanowitz HB, 1999. Application of cardiac gated magnetic resonance imaging in murine Chagas disease. Am J Trop Med Hyg 61 :207–214.
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A Magnetic Resonance Imaging Study of Intestinal Dilation in Trypanosoma cruzi–infected Mice Deficient in Nitric Oxide Synthase
Lars Ny
Lars Ny
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Hua Li
Hua Li
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Shankar Mukherjee
Shankar Mukherjee
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Katarina Persson
Katarina Persson
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Bo Holmqvist
Bo Holmqvist
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Dazhi Zhao
Dazhi Zhao
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Vitaliy Shtutin
Vitaliy Shtutin
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Huan Huang
Huan Huang
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Louis M. Weiss
Louis M. Weiss
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Fabiana S. Machado
Fabiana S. Machado
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Stephen M. Factor
Stephen M. Factor
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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John Chan
John Chan
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Herbert B. Tanowitz
Herbert B. Tanowitz
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Linda A. Jelicks
Linda A. Jelicks
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Infection with Trypanosoma cruzi causes megasyndromes of the gastrointestinal (GI) tract. We used magnetic resonance imaging (MRI) to monitor alterations in the GI tract of T. cruzi–infected mice, and to assess the role of nitric oxide (NO) in the development of intestinal dilation. Brazil strain–infected C57BL/6 wild-type (WT) mice exhibited dilatation of the intestines by 30 days post-infection. Average intestine lumen diameter increased by 72%. Levels of intestinal NO synthase (NOS) isoforms, NOS2 and NOS3, were elevated in infected WT mice. Inflammation and ganglionitis were observed in all infected mice. Intestinal dilation was observed in infected WT, NOS1, NOS2, and NOS3 null mice. This study demonstrates that MRI is a useful tool to monitor intestinal dilation in living mice and that these alterations may begin during acute infection. Furthermore, our data strongly suggests that NO may not be the sole contributor to intestinal dysfunction resulting from this infection.
Author Notes
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
Tait P, Allison D, 2001. Imaging of the gastrointestinal tract. Drugs Today (Barc) 37 :533–557.
-
2
Lomas DJ, 2003. Technical developments in bowel MRI. Eur Radiol 13 :1058–1071.
-
3
Lawler LP, Fishman EK, 2003. Bladder imaging using multidetector row computed tomography, volume rendering, and magnetic resonance imaging. J Comput Assist Tomogr 27 :553–563.
-
4
Bruel JM, Gallix B, 2003. Multidetector CT and MRI in diseases of the GI tract. J Radiol 84 :499–513.
-
5
Boczko J, Tar M, Melman A, Jelicks LA, Wittner M, Factor SM, Zhao D, Hafron J, Weiss LM, Tanowitz HB, Christ GJ, 2005. Trypanosoma cruzi infection induced changes in the innervation, structure and function of the murine bladder. J Urol 173 :1784–1788.
-
6
Kirchhoff LV, 1996. American trypanosomiasis Chagas disease. Gastroenterol Clin North Am 25 :517–533.
-
7
Tanowitz HB, Kirchhoff LV, Simon D, Morris SA, Weiss LM, Wittner M, 1992. Chagas disease. Clin Microbiol Rev 5 :400–419.
-
8
da Silveira AB, Lemos EM, Adad SJ, Correa-Oliveira R, Furness JB, D’Avila Reis D, 2007. Megacolon in Chagas disease: a study of inflammatory cells, enteric nerves, and glial cells. Hum Pathol 38 :1256–1264.
-
9
Madrid AM, Quera R, Defilippi C, Defilippi C, Gil LC, Sapunar J, Henriques A, 2004. Gastrointestinal motility disturbances in Chagas disease. Rev Med Chil 132 :939–946.
-
10
Madrid AM, Defilippi C, 2006. Disturbances of small intestinal motility in patients with chronic constipation. Rev Med Chil 134 :181–186.
-
11
Scremin LH, Corbett CE, Laurenti MD, Nunes EV, Gama-Rodrigues JJ, Okumura M, 1999. Megabladder in experimental Chagas disease: pathological features of the bladder wall. Rev Hosp Clin Fac Med Sao Paulo 54 :43–46.
-
12
Postan M, Cheever AW, Dvorak JA, McDaniel JP, 1986. A histopathological analysis of the course of myocarditis in C3H/He mice infected with Trypanosoma cruzi clone Sylvio-X10/4. Trans R Soc Trop Med Hyg 80 :50–55.
-
13
Postan M, Bailey JJ, Dvorak JA, McDaniel JP, Pottala EW, 1987. Studies of Trypanosoma cruzi clones in inbred mice. III. Histopathological and electrocardiographical responses to chronic infection. Am J Trop Med Hyg 37 :541–549.
-
14
De Rossell RA, Rodriguez AM, De Jesus R, Calcagno M, De Segnini ZM, Diaz S, 2000. Tripomastigotes de sangre y de cultivo celular de Trypanosoma cruzi Y.: II.—Patología de la enfermedad de Chagas en ratones Balb/c. Parasitol Dia 24 :79–87.
-
15
Mori T, Yoon HS, Iizuka FH, Myung JM, Sato HR, Silva MF, Okumura M, 2005. Intestinal transit and opaque enema study in chagasic mice. Rev Hosp Clin Fac Med Sao Paulo 501 :63–66.
-
16
Guillen-Pernia B, Lugo-Yarbuh A, Moreno E, 2001. Digestive tract dilation in mice infected with Trypanosoma cruzi.Invest Clin 42 :195–209.
-
17
de Oliveira GM, de Melo Medeiros M, da Silva Batista W, Santana R, Araújo-Jorge TC, de Souza AP, 2008. Applicability of the use of charcoal for the evaluation of intestinal motility in a murine model of Trypanosoma cruzi infection. Parasitol Res 102 :747–750.
-
18
Garcia SB, Paula JS, Giovannetti GS, Zenha F, Ramalho EM, Zucoloto S, Silva JS, Cunha FQ, 1999. Nitric oxide is involved in the lesions of the peripheral autonomic neurons observed in the acute phase of experimental Trypanosoma cruzi infection. Exp Parasit 93 :191–197.
-
19
Ribeiro U Jr, Safatle-Ribeiro AV, Habr-Gama A, Gama-Rodrigues JJ, Sohn J, Reynolds JC, 1998. Effect of Chagas disease on nitric oxide-containing neurons in severely affected and unaffected intestine. Dis Colon Rectum 41 :1411–1417.
-
20
Aliberti JC, Machado FS, Souto JT, Campanelli AP, Teixeira MM, Gazzinelli RT, Silva JS, 1999. β-Chemokines enhance parasite uptake and promote nitric oxide-dependent microbiostatic activity in murine inflammatory macrophages infected with Trypanosoma cruzi.Infect Immun 67 :4819–4826.
-
21
Holscher C, Kohler G, Muller U, Mossmann H, Schaub GA, Brombacher F, 1998. Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase. Infect Immun 66 :1208–1215.
-
22
Oswald IP, Wynn TA, Sher A, James SL, 1994. NO as an effector molecule of parasite killing: modulation of its synthesis by cytokines. Comp Biochem Physiol Pharmacol Toxicol Endocrinol 108 :11–18.
-
23
Teixeira MM, Gazzinelli RT, Silva JS, 2002. Chemokines, inflammation and Trypanosoma cruzi infection. Trends Parasitol 18 :262–265.
-
24
Vespa GN, Cunha FQ, Silva JS, 1994. Nitric oxide is involved in control of Trypanosoma cruzi induced parasitemia and directly kills the parasite in vitro.Infect Immun 62 :5177–5182.
-
25
Stark ME, Szurszewski JH, 1992. Role of nitric oxide in gastrointestinal and hepatic function and disease. Gastroenterology 103 :1928–1949.
-
26
Mashimo H, Goyal RK, 1999. Lessons from genetically engineered animal models IV. Nitric oxide synthase gene knockout mice. Am J Physiol Gastrointest Liver Physiol 277 :G745–G750.
-
27
Mungrue I, Husain M, Stewart DJ, 2002. The role of NOS in heart failure: lessons from murine genetic models. Heart Fail Rev 7 :407–422.
-
28
Ny L, Persson K, Larsson B, Chan J, Weiss LM, Wittner M, Huang H, Tanowitz HB, 1999. Localization and activity of nitric oxide synthases in the gastrointestinal tract of Trypanosoma cruzi-infected mice. J Neuroimmunol 99 :27–35.
-
29
Ny L, Alm P, Larsson B, Ekstrom P, Andersson KE, 1995. Nitric oxide pathway in cat esophagus: localization of nitric oxide synthase and functional effects. Am J Physiol Gastrointest Liver Physiol 268 :G59–G70.
-
30
Li E, Zhou P, Singer SM, 2006. Neuronal nitric oxide synthase is necessary for elimination of Giardia lamblia infections in mice. J Immunol 176 :516–521.
-
31
Beck PL, Xavier R, Wong J, Ezedi I, Mashimo H, Mizoguchi A, Mizoguchi E, Bhan AK, Podolsky DK, 2004. Paradoxical roles of different nitric oxide synthase isoforms in colonic injury. Am J Physiol Gastrointest Liver Physiol 286 :G137–G147.
-
32
Helmer KS, West SD, Shipley GL, Chang L, Cui Y, Mailman D, Mercer DW, 2002. Gastric nitric oxide synthase expression during endotoxemia: implications in mucosal defense in rats. Gastroenterology 123 :173–186.
-
33
McCafferty DM, Mudgett JS, Swain MG, Kubes P, 1997. Inducible nitric oxide synthase plays a critical role in resolving intestinal inflammation. Gastroenterology 112 :1022–1027.
-
34
Chandra M, Tanowitz HB, Petkova SB, Huang H, Weiss LM, Wittner M, Factor SM, Shtutin V, Jelicks LA, Chan J, Shirani J, 2002. Significance of inducible nitric oxide synthase in acute myocarditis caused by Trypanosoma cruzi (Tulahuen strain). Int J Parasitol 32 :897–905.
-
35
Cummings KL, Tarleton RL, 2004. Inducible nitric oxide synthase is not essential for control of Trypanosoma cruzi infection in mice. Infect Immun 72 :4081–4089.
-
36
Huang H, Chan J, Wittner M, Jelicks LA, Morris SA, Factor SM, Weiss LM, Braunstein VL, Bacchi CJ, Yarlett N, Chandra M, Shirani J, Tanowitz HB, 1999. Expression of cardiac cytokines and inducible form of nitric oxide synthase (NOS2) in Trypanosoma cruzi-infected mice. J Mol Cell Cardiol 31 :75–88.
-
37
Huang H, Chan J, Wittner M, Weiss LM, Bacchi CJ, Yarlett N, Martinez M, Morris SM, Braunstein VL, Factor SA, Tanowitz HB, 1997. Trypanosoma cruzi infection induces myocardial nitric oxide synthase. Cardiovasc Pathol 6 :161–166.
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38
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