Skip to main content
Erschienen in: Inflammation 3/2018

28.02.2018 | ORIGINAL ARTICLE

Involvement of Alveolar Macrophages and Neutrophils in Acute Lung Injury After Scorpion Envenomation: New Pharmacological Targets

verfasst von: Hadjer Saidi, Julie Bérubé, Fatima Laraba-Djebari, Djelila Hammoudi-Triki

Erschienen in: Inflammation | Ausgabe 3/2018

Einloggen, um Zugang zu erhalten

Abstract

Androctonus australis hector (Aah) scorpion venom is well known to induce a systemic inflammatory response associated with cell infiltration in lung and edema formation. The present study investigate (i) in vivo the evolution of lung and systemic inflammation triggered by Aah venom and (ii) analyze in vitro the signaling cascade, upstream of inflammatory cytokine expression after Aah venom-stimulated mouse alveolar macrophage (MH-S), the main resident immune cells in the lung. The inflammation induced by Aah venom was assessed in mice through inflammatory cell count, nitric oxide metabolite, and lactate dehydrogenase (LDH) activity in blood, concordantly with neutrophil sequestration in tissue and lung histology. In the in vitro study, MH-S cells are stimulated with Aah venom in the presence of signaling pathway inhibitors, NG25 an inhibitor of transforming growth factor β-activated kinase (TAK1), PD184352 MAP kinase (MKK)1/2 inhibitor, BI605906 an inhibitor of IKκ-β (inhibitor of nuclear factor kappa B), and BIRB0796 an inhibitor of p38 MAPK. Obtained results showed that leukocyte transmigration is important in some area of the lung and is closely associated with systemic increase of nitric oxide and LDH. The in vitro study showed that Aah venom induce significantly an increase of the expression of TNF-α, IL-1β, and MIP-2 in MH-S cells. The pretreatment with inhibitors showed that cytokine increase involves TAK1, IKκ-β, and ERK1/2 pathways, similarly to Toll-like receptor activation. These findings highlight the contribution of alveolar macrophage and their secretory products to tissue damage and made of TAK1 and ERK1/2, an interesting target in scorpion envenomation.
Literatur
1.
Zurück zum Zitat Adi-Bessalem, S., D. Hammoudi-Triki, and F. Laraba-Djebari. 2008. Pathophysiological effects of Androctonus australis hector scorpion venom: tissue damages and inflammatory response. Experimental and Toxicologic Pathology 60: 373–380.CrossRefPubMed Adi-Bessalem, S., D. Hammoudi-Triki, and F. Laraba-Djebari. 2008. Pathophysiological effects of Androctonus australis hector scorpion venom: tissue damages and inflammatory response. Experimental and Toxicologic Pathology 60: 373–380.CrossRefPubMed
2.
Zurück zum Zitat Raouraoua-Boukari, R., S. Sami-Merah, D. Hammoudi-Triki, M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2012. Immunomodulation of the inflammatory response induced by Androctonus australis hector neurotoxins: biomarker interactions. Neuroimmunomodulation 19: 103–110.CrossRefPubMed Raouraoua-Boukari, R., S. Sami-Merah, D. Hammoudi-Triki, M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2012. Immunomodulation of the inflammatory response induced by Androctonus australis hector neurotoxins: biomarker interactions. Neuroimmunomodulation 19: 103–110.CrossRefPubMed
3.
Zurück zum Zitat Saidi, H., S. Adi-Bessalem, D. Hammoudi-Triki, and F. Laraba-Djebari. 2013. Effects of atropine and propranolol on lung inflammation in experimental envenomation: comparison of two buthidae venoms. Journal of Venomous Animals and Toxins Including Tropical Diseases 19: 8.CrossRefPubMedPubMedCentral Saidi, H., S. Adi-Bessalem, D. Hammoudi-Triki, and F. Laraba-Djebari. 2013. Effects of atropine and propranolol on lung inflammation in experimental envenomation: comparison of two buthidae venoms. Journal of Venomous Animals and Toxins Including Tropical Diseases 19: 8.CrossRefPubMedPubMedCentral
4.
Zurück zum Zitat Bekkari, N., M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2015. Complement system and immunological mediators: their involvements in the induced inflammatory process by Androctonus australis hector venom and its toxic components. Experimental and Toxicologic Pathology 67: 389–397.CrossRefPubMed Bekkari, N., M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2015. Complement system and immunological mediators: their involvements in the induced inflammatory process by Androctonus australis hector venom and its toxic components. Experimental and Toxicologic Pathology 67: 389–397.CrossRefPubMed
5.
Zurück zum Zitat Fukahara, Y., M. Reis, R. Dellalibera-Joviliani, F. Cunha, and E. Donadi. 2003. Increased levels of IL-1b, IL-6, IL-8, IL-10 and TNF-a in patients moderately or severely envenomed by Tityus serrulatus scorpion sting. Toxicon 41: 49–55.CrossRef Fukahara, Y., M. Reis, R. Dellalibera-Joviliani, F. Cunha, and E. Donadi. 2003. Increased levels of IL-1b, IL-6, IL-8, IL-10 and TNF-a in patients moderately or severely envenomed by Tityus serrulatus scorpion sting. Toxicon 41: 49–55.CrossRef
6.
Zurück zum Zitat Meki, A.-R., and Z.M. El-Dean. 1998. Serum interleukin-1β, interleukin-6, nitric oxide and α 1-antitrypsin in scorpion envenomed children. Toxicon 36: 1851–1859.CrossRefPubMed Meki, A.-R., and Z.M. El-Dean. 1998. Serum interleukin-1β, interleukin-6, nitric oxide and α 1-antitrypsin in scorpion envenomed children. Toxicon 36: 1851–1859.CrossRefPubMed
7.
Zurück zum Zitat Hammoudi-Triki, D., E. Ferquel, A. Robbe-Vincent, C. Bon, V. Choumet, and F. Laraba-Djebari. 2004. Epidemiological data, clinical admission gradation and biological quantification by ELISA of scorpion envenomations in Algeria: effect of immunotherapy. Transactions of the Royal Society of Tropical Medicine and Hygiene 98: 240–250.CrossRefPubMed Hammoudi-Triki, D., E. Ferquel, A. Robbe-Vincent, C. Bon, V. Choumet, and F. Laraba-Djebari. 2004. Epidemiological data, clinical admission gradation and biological quantification by ELISA of scorpion envenomations in Algeria: effect of immunotherapy. Transactions of the Royal Society of Tropical Medicine and Hygiene 98: 240–250.CrossRefPubMed
8.
Zurück zum Zitat Taibi-Djennah, Z., and F. Laraba-Djebari. 2015. Effect of cytokine antibodies in the immunomodulation of inflammatory response and metabolic disorders induced by scorpion venom. International Immunopharmacology 27: 122–129.CrossRefPubMed Taibi-Djennah, Z., and F. Laraba-Djebari. 2015. Effect of cytokine antibodies in the immunomodulation of inflammatory response and metabolic disorders induced by scorpion venom. International Immunopharmacology 27: 122–129.CrossRefPubMed
9.
Zurück zum Zitat Zoccal, K.F., C.A. Sorgi, J.I. Hori, F.W. Paula-Silva, E.C. Arantes, C.H. Serezani, D.S. Zamboni, L.H. Faccioli. 2016. Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality. Nature Communications. 7. Zoccal, K.F., C.A. Sorgi, J.I. Hori, F.W. Paula-Silva, E.C. Arantes, C.H. Serezani, D.S. Zamboni, L.H. Faccioli. 2016. Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality. Nature Communications. 7.
10.
Zurück zum Zitat Christofidou-Solomidou, M., and V.R. Muzykantov. 2006. Antioxidant strategies in respiratory medicine. Treatments in respiratory medicine 5: 47–78.CrossRefPubMed Christofidou-Solomidou, M., and V.R. Muzykantov. 2006. Antioxidant strategies in respiratory medicine. Treatments in respiratory medicine 5: 47–78.CrossRefPubMed
11.
Zurück zum Zitat Kobayashi, H., M. Kobayashi, T.A. Heming, A. Bidani, R.B. Pollard, and F. Suzuki. 1999. Cytokine production by rabbit alveolar macrophages. Differences between activated and suppressor cell phenotypes. Immunology letters 69: 339–346.CrossRefPubMed Kobayashi, H., M. Kobayashi, T.A. Heming, A. Bidani, R.B. Pollard, and F. Suzuki. 1999. Cytokine production by rabbit alveolar macrophages. Differences between activated and suppressor cell phenotypes. Immunology letters 69: 339–346.CrossRefPubMed
12.
Zurück zum Zitat Matsunaga, K., T.W. Klein, H. Friedman, and Y. Yamamoto. 2001. Alveolar macrophage cell line MH-S is valuable as an in vitro model for Legionella pneumophila infection. American journal of respiratory cell and molecular biology 24: 326–331.CrossRefPubMed Matsunaga, K., T.W. Klein, H. Friedman, and Y. Yamamoto. 2001. Alveolar macrophage cell line MH-S is valuable as an in vitro model for Legionella pneumophila infection. American journal of respiratory cell and molecular biology 24: 326–331.CrossRefPubMed
13.
Zurück zum Zitat Wright, J.R. 2004. Host defense functions of pulmonary surfactant. Neonatology 85: 326–332.CrossRef Wright, J.R. 2004. Host defense functions of pulmonary surfactant. Neonatology 85: 326–332.CrossRef
14.
Zurück zum Zitat Oberdörster, G., J. Ferin, R. Gelein, S.C. Soderholm, and J. Finkelstein. 1992. Role of the alveolar macrophage in lung injury: studies with ultrafine particles. Environmental Health Perspectives 97: 193.CrossRefPubMedPubMedCentral Oberdörster, G., J. Ferin, R. Gelein, S.C. Soderholm, and J. Finkelstein. 1992. Role of the alveolar macrophage in lung injury: studies with ultrafine particles. Environmental Health Perspectives 97: 193.CrossRefPubMedPubMedCentral
15.
Zurück zum Zitat Marshall, B.G., A. Wangoo, H.T. Cook, and R.J. Shaw. 1996. Increased inflammatory cytokines and new collagen formation in cutaneous tuberculosis and sarcoidosis. Thorax 51: 1253–1261.CrossRefPubMedPubMedCentral Marshall, B.G., A. Wangoo, H.T. Cook, and R.J. Shaw. 1996. Increased inflammatory cytokines and new collagen formation in cutaneous tuberculosis and sarcoidosis. Thorax 51: 1253–1261.CrossRefPubMedPubMedCentral
16.
Zurück zum Zitat Ware, L.B. 2006. Pathophysiology of acute lung injury and the acute respiratory distress syndrome. In Seminars in respiratory and critical care medicine. Copyright© by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.; 2006: 337–349. Ware, L.B. 2006. Pathophysiology of acute lung injury and the acute respiratory distress syndrome. In Seminars in respiratory and critical care medicine. Copyright© by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.; 2006: 337–349.
17.
Zurück zum Zitat Kaddache, A., M. Hassan, F. Laraba-Djebari, and D. Hammoudi-Triki. 2017. Switch of steady-state to an accelerated granulopoiesis in response to Androctonus australis hector venom. Inflammation 40: 871–883.CrossRefPubMed Kaddache, A., M. Hassan, F. Laraba-Djebari, and D. Hammoudi-Triki. 2017. Switch of steady-state to an accelerated granulopoiesis in response to Androctonus australis hector venom. Inflammation 40: 871–883.CrossRefPubMed
18.
Zurück zum Zitat Petricevich, V.L., A.H. Cruz, F.I. Coronas, and L.D. Possani. 2007. Toxin gamma from Tityus serrulatus scorpion venom plays an essential role in immunomodulation of macrophages. Toxicon 50: 666–675.CrossRefPubMed Petricevich, V.L., A.H. Cruz, F.I. Coronas, and L.D. Possani. 2007. Toxin gamma from Tityus serrulatus scorpion venom plays an essential role in immunomodulation of macrophages. Toxicon 50: 666–675.CrossRefPubMed
19.
Zurück zum Zitat Zoccal, K.F., C. da Silva Bitencourt, F.W.G. Paula-Silva, C.A. Sorgi, Kd.C.F. Bordon, E.C. Arantes, and L.H. Faccioli. 2014. TLR2, TLR4 and CD14 recognize venom-associated molecular patterns from Tityus serrulatus to induce macrophage-derived inflammatory mediators. PLoS One 9: e88174.CrossRefPubMedPubMedCentral Zoccal, K.F., C. da Silva Bitencourt, F.W.G. Paula-Silva, C.A. Sorgi, Kd.C.F. Bordon, E.C. Arantes, and L.H. Faccioli. 2014. TLR2, TLR4 and CD14 recognize venom-associated molecular patterns from Tityus serrulatus to induce macrophage-derived inflammatory mediators. PLoS One 9: e88174.CrossRefPubMedPubMedCentral
20.
Zurück zum Zitat Zoccal, K.F., C. da Silva Bitencourt, A. Secatto, C.A. Sorgi, Karla de Castro Figueiredo Bordon, S.V. Sampaio, E.C. Arantes, and L.H. Faccioli. 2011. Tityus serrulatus venom and toxins Ts1, Ts2 and Ts6 induce macrophage activation and production of immune mediators. Toxicon 57: 1101–1108.CrossRefPubMed Zoccal, K.F., C. da Silva Bitencourt, A. Secatto, C.A. Sorgi, Karla de Castro Figueiredo Bordon, S.V. Sampaio, E.C. Arantes, and L.H. Faccioli. 2011. Tityus serrulatus venom and toxins Ts1, Ts2 and Ts6 induce macrophage activation and production of immune mediators. Toxicon 57: 1101–1108.CrossRefPubMed
21.
22.
Zurück zum Zitat New, D.C., and Y.H. Wong. 2007. Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression. Journal of molecular signaling 2: 2.CrossRefPubMedPubMedCentral New, D.C., and Y.H. Wong. 2007. Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression. Journal of molecular signaling 2: 2.CrossRefPubMedPubMedCentral
23.
Zurück zum Zitat Kang, Y.J., J. Chen, M. Otsuka, J. Mols, S. Ren, Y. Wang, and J. Han. 2008. Macrophage deletion of p38α partially impairs lipopolysaccharide-induced cellular activation. The Journal of Immunology 180: 5075–5082.CrossRefPubMed Kang, Y.J., J. Chen, M. Otsuka, J. Mols, S. Ren, Y. Wang, and J. Han. 2008. Macrophage deletion of p38α partially impairs lipopolysaccharide-induced cellular activation. The Journal of Immunology 180: 5075–5082.CrossRefPubMed
24.
Zurück zum Zitat Barton, G.M., and R. Medzhitov. 2003. Toll-like receptor signaling pathways. Science 300: 1524–1525.CrossRefPubMed Barton, G.M., and R. Medzhitov. 2003. Toll-like receptor signaling pathways. Science 300: 1524–1525.CrossRefPubMed
25.
Zurück zum Zitat Senger, K., V.C. Pham, E. Varfolomeev, J.A. Hackney, C.A. Corzo, J. Collier, V.W. Lau, Z. Huang, K. Hamidzhadeh, and P. Caplazi. 2017. The kinase TPL2 activates ERK and p38 signaling to promote neutrophilic inflammation. Science Signaling 10: eaah4273.CrossRefPubMed Senger, K., V.C. Pham, E. Varfolomeev, J.A. Hackney, C.A. Corzo, J. Collier, V.W. Lau, Z. Huang, K. Hamidzhadeh, and P. Caplazi. 2017. The kinase TPL2 activates ERK and p38 signaling to promote neutrophilic inflammation. Science Signaling 10: eaah4273.CrossRefPubMed
26.
Zurück zum Zitat Zhang, Q., J. Huang, J. Yu, Z. Xu, L. Liu, Y. Song, X. Sun, A. Zhang, M. Jin. 2017. HP1330 contributes to Streptococcus suis virulence by inducing toll-like receptor 2-and ERK1/2-dependent pro-inflammatory responses and influencing in vivo S. suis loads. Frontiers in Immunology. 8. Zhang, Q., J. Huang, J. Yu, Z. Xu, L. Liu, Y. Song, X. Sun, A. Zhang, M. Jin. 2017. HP1330 contributes to Streptococcus suis virulence by inducing toll-like receptor 2-and ERK1/2-dependent pro-inflammatory responses and influencing in vivo S. suis loads. Frontiers in Immunology. 8.
27.
Zurück zum Zitat Bradley, P.P., D.A. Priebat, R.D. Christensen, and G. Rothstein. 1982. Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. Journal of Investigative Dermatology 78: 206–209.CrossRefPubMed Bradley, P.P., D.A. Priebat, R.D. Christensen, and G. Rothstein. 1982. Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. Journal of Investigative Dermatology 78: 206–209.CrossRefPubMed
28.
Zurück zum Zitat Bradford, M.M. 1976. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Analytical Biochemistry 72: 248–254.CrossRefPubMed Bradford, M.M. 1976. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Analytical Biochemistry 72: 248–254.CrossRefPubMed
29.
Zurück zum Zitat Green, L.C., D.A. Wagner, J. Glogowski, P.L. Skipper, J.S. Wishnok, and S.R. Tannenbaum. 1982. Analysis of nitrate, nitrite, and [15N] nitrate in biological fluids. Analytical Biochemistry 126: 131–138.CrossRefPubMed Green, L.C., D.A. Wagner, J. Glogowski, P.L. Skipper, J.S. Wishnok, and S.R. Tannenbaum. 1982. Analysis of nitrate, nitrite, and [15N] nitrate in biological fluids. Analytical Biochemistry 126: 131–138.CrossRefPubMed
31.
Zurück zum Zitat Scherle, P.A., E.A. Jones, M.F. Favata, A.J. Daulerio, M.B. Covington, S.A. Nurnberg, R.L. Magolda, and J.M. Trzaskos. 1998. Inhibition of MAP kinase kinase prevents cytokine and prostaglandin E2 production in lipopolysaccharide-stimulated monocytes. The Journal of Immunology 161: 5681–5686.PubMed Scherle, P.A., E.A. Jones, M.F. Favata, A.J. Daulerio, M.B. Covington, S.A. Nurnberg, R.L. Magolda, and J.M. Trzaskos. 1998. Inhibition of MAP kinase kinase prevents cytokine and prostaglandin E2 production in lipopolysaccharide-stimulated monocytes. The Journal of Immunology 161: 5681–5686.PubMed
32.
Zurück zum Zitat Dumitru, C.D., J.D. Ceci, C. Tsatsanis, D. Kontoyiannis, K. Stamatakis, J.-H. Lin, C. Patriotis, N.A. Jenkins, N.G. Copeland, and G. Kollias. 2000. TNF-α induction by LPS is regulated posttranscriptionally via a Tpl2/ERK-dependent pathway. Cell 103: 1071–1083.CrossRefPubMed Dumitru, C.D., J.D. Ceci, C. Tsatsanis, D. Kontoyiannis, K. Stamatakis, J.-H. Lin, C. Patriotis, N.A. Jenkins, N.G. Copeland, and G. Kollias. 2000. TNF-α induction by LPS is regulated posttranscriptionally via a Tpl2/ERK-dependent pathway. Cell 103: 1071–1083.CrossRefPubMed
33.
Zurück zum Zitat Martel, G., J. Bérubé, and S. Rousseau. 2013. The protein kinase TPL2 is essential for ERK1/ERK2 activation and cytokine gene expression in airway epithelial cells exposed to pathogen-associated molecular patterns (PAMPs). PLoS One 8: e59116.CrossRefPubMedPubMedCentral Martel, G., J. Bérubé, and S. Rousseau. 2013. The protein kinase TPL2 is essential for ERK1/ERK2 activation and cytokine gene expression in airway epithelial cells exposed to pathogen-associated molecular patterns (PAMPs). PLoS One 8: e59116.CrossRefPubMedPubMedCentral
34.
Zurück zum Zitat Valenca, S.S., F.S. Bezerra, A.A. Lopes, B. Romana-Souza, M.C.M. Cavalcante, A.B. Lima, V.L.G. Koatz, and L.C. Porto. 2008. Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide. Environmental research 108: 199–204.CrossRefPubMed Valenca, S.S., F.S. Bezerra, A.A. Lopes, B. Romana-Souza, M.C.M. Cavalcante, A.B. Lima, V.L.G. Koatz, and L.C. Porto. 2008. Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide. Environmental research 108: 199–204.CrossRefPubMed
35.
Zurück zum Zitat Skerrett, S.J., H.D. Liggitt, A.M. Hajjar, R.K. Ernst, S.I. Miller, and C.B. Wilson. 2004. Respiratory epithelial cells regulate lung inflammation in response to inhaled endotoxin. American Journal of Physiology-Lung Cellular and Molecular Physiology 287: L143–L152.CrossRefPubMed Skerrett, S.J., H.D. Liggitt, A.M. Hajjar, R.K. Ernst, S.I. Miller, and C.B. Wilson. 2004. Respiratory epithelial cells regulate lung inflammation in response to inhaled endotoxin. American Journal of Physiology-Lung Cellular and Molecular Physiology 287: L143–L152.CrossRefPubMed
36.
Zurück zum Zitat Medjadba, W., M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2016. Involvement of kallikrein-kinin system on cardiopulmonary alterations and inflammatory response induced by purified Aah I toxin from scorpion venom. Inflammation 39: 290–302.CrossRefPubMed Medjadba, W., M.F. Martin-Eauclaire, and F. Laraba-Djebari. 2016. Involvement of kallikrein-kinin system on cardiopulmonary alterations and inflammatory response induced by purified Aah I toxin from scorpion venom. Inflammation 39: 290–302.CrossRefPubMed
37.
Zurück zum Zitat Chair-Yousfi, I., F. Laraba-Djebari, and D. Hammoudi-Triki. 2015. Androctonus australis hector venom contributes to the interaction between neuropeptides and mast cells in pulmonary hyperresponsiveness. International Immunopharmacology 25: 19–29.CrossRefPubMed Chair-Yousfi, I., F. Laraba-Djebari, and D. Hammoudi-Triki. 2015. Androctonus australis hector venom contributes to the interaction between neuropeptides and mast cells in pulmonary hyperresponsiveness. International Immunopharmacology 25: 19–29.CrossRefPubMed
38.
Zurück zum Zitat Murphy, K., P. Travers, and M. Walport. 2008. Janeway’s immunobiology. New York: Garland Science. Taylor & Francis Group. Murphy, K., P. Travers, and M. Walport. 2008. Janeway’s immunobiology. New York: Garland Science. Taylor & Francis Group.
39.
Zurück zum Zitat Driscoll, K.E. 2000. TNFα and MIP-2: role in particle-induced inflammation and regulation by oxidative stress. Toxicology letters 112: 177–183.CrossRefPubMed Driscoll, K.E. 2000. TNFα and MIP-2: role in particle-induced inflammation and regulation by oxidative stress. Toxicology letters 112: 177–183.CrossRefPubMed
40.
Zurück zum Zitat De Filippo, K., R.B. Henderson, M. Laschinger, and N. Hogg. 2008. Neutrophil chemokines KC and macrophage-inflammatory protein-2 are newly synthesized by tissue macrophages using distinct TLR signaling pathways. The Journal of Immunology. 180: 4308–4315.CrossRefPubMed De Filippo, K., R.B. Henderson, M. Laschinger, and N. Hogg. 2008. Neutrophil chemokines KC and macrophage-inflammatory protein-2 are newly synthesized by tissue macrophages using distinct TLR signaling pathways. The Journal of Immunology. 180: 4308–4315.CrossRefPubMed
41.
Zurück zum Zitat Eliopoulos, A.G., C.C. Wang, C.D. Dumitru, and P.N. Tsichlis. 2003. Tpl2 transduces CD40 and TNF signals that activate ERK and regulates IgE induction by CD40. The EMBO Journal 22: 3855–3864.CrossRefPubMedPubMedCentral Eliopoulos, A.G., C.C. Wang, C.D. Dumitru, and P.N. Tsichlis. 2003. Tpl2 transduces CD40 and TNF signals that activate ERK and regulates IgE induction by CD40. The EMBO Journal 22: 3855–3864.CrossRefPubMedPubMedCentral
42.
Zurück zum Zitat Waterfield, M.R., M. Zhang, L.P. Norman, and S.-C. Sun. 2003. NF-κB1/p105 regulates lipopolysaccharide-stimulated MAP kinase signaling by governing the stability and function of the Tpl2 kinase. Molecular cell 11: 685–694.CrossRefPubMed Waterfield, M.R., M. Zhang, L.P. Norman, and S.-C. Sun. 2003. NF-κB1/p105 regulates lipopolysaccharide-stimulated MAP kinase signaling by governing the stability and function of the Tpl2 kinase. Molecular cell 11: 685–694.CrossRefPubMed
43.
Zurück zum Zitat Papoutsopoulou, S., A. Symons, T. Tharmalingham, M.P. Belich, F. Kaiser, D. Kioussis, A. O’Garra, V. Tybulewicz, and S.C. Ley. 2006. ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses. Nature immunology 7: 606.CrossRefPubMed Papoutsopoulou, S., A. Symons, T. Tharmalingham, M.P. Belich, F. Kaiser, D. Kioussis, A. O’Garra, V. Tybulewicz, and S.C. Ley. 2006. ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses. Nature immunology 7: 606.CrossRefPubMed
44.
Zurück zum Zitat Cormet-Boyaka, E., K. Jolivette, A. Bonnegarde-Bernard, J. Rennolds, F. Hassan, P. Mehta, S. Tridandapani, J. Webster-Marketon, and P.N. Boyaka. 2011. An NF-κB–independent and Erk1/2-dependent mechanism controls CXCL8/IL-8 responses of airway epithelial cells to cadmium. Toxicological Sciences 125: 418–429.CrossRefPubMedPubMedCentral Cormet-Boyaka, E., K. Jolivette, A. Bonnegarde-Bernard, J. Rennolds, F. Hassan, P. Mehta, S. Tridandapani, J. Webster-Marketon, and P.N. Boyaka. 2011. An NF-κB–independent and Erk1/2-dependent mechanism controls CXCL8/IL-8 responses of airway epithelial cells to cadmium. Toxicological Sciences 125: 418–429.CrossRefPubMedPubMedCentral
45.
Zurück zum Zitat Sato, S., H. Sanjo, K. Takeda, J. Ninomiya-Tsuji, M. Yamamoto, T. Kawai, K. Matsumoto, O. Takeuchi, and S. Akira. 2005. Essential function for the kinase TAK1 in innate and adaptive immune responses. Nature Immunology 6: 1087.CrossRefPubMed Sato, S., H. Sanjo, K. Takeda, J. Ninomiya-Tsuji, M. Yamamoto, T. Kawai, K. Matsumoto, O. Takeuchi, and S. Akira. 2005. Essential function for the kinase TAK1 in innate and adaptive immune responses. Nature Immunology 6: 1087.CrossRefPubMed
46.
Zurück zum Zitat Ninomiya-Tsuji, J., K. Kishimoto, A. Hiyama, J-i. Inoue, Z. Cao, and K. Matsumoto. 1999. The kinase TAK1 can activate the NIK-IκB as well as the MAP kinase cascade in the IL-1 signalling pathway. Nature 398: 252–256.CrossRefPubMed Ninomiya-Tsuji, J., K. Kishimoto, A. Hiyama, J-i. Inoue, Z. Cao, and K. Matsumoto. 1999. The kinase TAK1 can activate the NIK-IκB as well as the MAP kinase cascade in the IL-1 signalling pathway. Nature 398: 252–256.CrossRefPubMed
47.
Zurück zum Zitat McCubrey, J.A., L.S. Steelman, W.H. Chappell, S.L. Abrams, E.W. Wong, F. Chang, B. Lehmann, D.M. Terrian, M. Milella, and A. Tafuri. 2007. Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1773: 1263–1284.CrossRef McCubrey, J.A., L.S. Steelman, W.H. Chappell, S.L. Abrams, E.W. Wong, F. Chang, B. Lehmann, D.M. Terrian, M. Milella, and A. Tafuri. 2007. Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1773: 1263–1284.CrossRef
48.
Zurück zum Zitat Beinke, S., J. Deka, V. Lang, M. Belich, P. Walker, S. Howell, S. Smerdon, S. Gamblin, and S. Ley. 2003. NF-κB1 p105 negatively regulates TPL-2 MEK kinase activity. Molecular and Cellular Biology 23: 4739–4752.CrossRefPubMedPubMedCentral Beinke, S., J. Deka, V. Lang, M. Belich, P. Walker, S. Howell, S. Smerdon, S. Gamblin, and S. Ley. 2003. NF-κB1 p105 negatively regulates TPL-2 MEK kinase activity. Molecular and Cellular Biology 23: 4739–4752.CrossRefPubMedPubMedCentral
49.
Zurück zum Zitat Beinke, S., M. Robinson, M. Hugunin, and S. Ley. 2004. Lipopolysaccharide activation of the TPL-2/MEK/extracellular signal-regulated kinase mitogen-activated protein kinase cascade is regulated by IκB kinase-induced proteolysis of NF-κB1 p105. Molecular and Cellular Biology 24: 9658–9667.CrossRefPubMedPubMedCentral Beinke, S., M. Robinson, M. Hugunin, and S. Ley. 2004. Lipopolysaccharide activation of the TPL-2/MEK/extracellular signal-regulated kinase mitogen-activated protein kinase cascade is regulated by IκB kinase-induced proteolysis of NF-κB1 p105. Molecular and Cellular Biology 24: 9658–9667.CrossRefPubMedPubMedCentral
50.
Zurück zum Zitat Cho, J., M. Melnick, G.P. Solidakis, and P.N. Tsichlis. 2005. Tpl2 (tumor progression locus 2) phosphorylation at Thr290 is induced by lipopolysaccharide via an Iκ-B kinase-β-dependent pathway and is required for Tpl2 activation by external signals. Journal of Biological Chemistry 280: 20442–20448.CrossRefPubMed Cho, J., M. Melnick, G.P. Solidakis, and P.N. Tsichlis. 2005. Tpl2 (tumor progression locus 2) phosphorylation at Thr290 is induced by lipopolysaccharide via an Iκ-B kinase-β-dependent pathway and is required for Tpl2 activation by external signals. Journal of Biological Chemistry 280: 20442–20448.CrossRefPubMed
51.
Zurück zum Zitat Das, S., J. Cho, I. Lambertz, M.A. Kelliher, A.G. Eliopoulos, K. Du, and P.N. Tsichlis. 2005. Tpl2/cot signals activate ERK, JNK, and NF-κB in a cell-type and stimulus-specific manner. Journal of Biological Chemistry 280: 23748–23757.CrossRefPubMed Das, S., J. Cho, I. Lambertz, M.A. Kelliher, A.G. Eliopoulos, K. Du, and P.N. Tsichlis. 2005. Tpl2/cot signals activate ERK, JNK, and NF-κB in a cell-type and stimulus-specific manner. Journal of Biological Chemistry 280: 23748–23757.CrossRefPubMed
52.
Zurück zum Zitat Bowie, A., and L.A. O’Neill. 2000. Oxidative stress and nuclear factor-κB activation: A reassessment of the evidence in the light of recent discoveries. Biochemical Pharmacology 59: 13–23.CrossRefPubMed Bowie, A., and L.A. O’Neill. 2000. Oxidative stress and nuclear factor-κB activation: A reassessment of the evidence in the light of recent discoveries. Biochemical Pharmacology 59: 13–23.CrossRefPubMed
53.
54.
Zurück zum Zitat Alcamo, E., J.P. Mizgerd, B.H. Horwitz, R. Bronson, A.A. Beg, M. Scott, C.M. Doerschuk, R.O. Hynes, and D. Baltimore. 2001. Targeted mutation of TNF receptor I rescues the RelA-deficient mouse and reveals a critical role for NF-κB in leukocyte recruitment. The Journal of Immunology 167: 1592–1600.CrossRefPubMed Alcamo, E., J.P. Mizgerd, B.H. Horwitz, R. Bronson, A.A. Beg, M. Scott, C.M. Doerschuk, R.O. Hynes, and D. Baltimore. 2001. Targeted mutation of TNF receptor I rescues the RelA-deficient mouse and reveals a critical role for NF-κB in leukocyte recruitment. The Journal of Immunology 167: 1592–1600.CrossRefPubMed
55.
Zurück zum Zitat Delaney, J.R., and M. Mlodzik. 2006. TGFβ activated kinase-1: new insights into the diverse roles of TAK1 in development and immunity. Cell Cycle 5: 2852–2855.CrossRefPubMed Delaney, J.R., and M. Mlodzik. 2006. TGFβ activated kinase-1: new insights into the diverse roles of TAK1 in development and immunity. Cell Cycle 5: 2852–2855.CrossRefPubMed
56.
57.
Zurück zum Zitat Akira, S., and K. Takeda. 2004. Toll-like receptor signalling. Nature reviews immunology 4: 499–511.CrossRefPubMed Akira, S., and K. Takeda. 2004. Toll-like receptor signalling. Nature reviews immunology 4: 499–511.CrossRefPubMed
58.
Zurück zum Zitat Takeda, K., T. Kaisho, and S. Akira. 2003. Toll-like receptors. Annual review of immunology 21: 335–376.CrossRefPubMed Takeda, K., T. Kaisho, and S. Akira. 2003. Toll-like receptors. Annual review of immunology 21: 335–376.CrossRefPubMed
59.
Zurück zum Zitat Trinchieri, G., and A. Sher. 2007. Cooperation of Toll-like receptor signals in innate immune defence. Nature reviews Immunology 7: 179.CrossRefPubMed Trinchieri, G., and A. Sher. 2007. Cooperation of Toll-like receptor signals in innate immune defence. Nature reviews Immunology 7: 179.CrossRefPubMed
60.
Zurück zum Zitat Kaisho, T., and S. Akira. 2006. Toll-like receptor function and signaling. Journal of allergy and clinical immunology 117: 979–987.CrossRefPubMed Kaisho, T., and S. Akira. 2006. Toll-like receptor function and signaling. Journal of allergy and clinical immunology 117: 979–987.CrossRefPubMed
61.
Zurück zum Zitat Adachi, O., T. Kawai, K. Takeda, M. Matsumoto, H. Tsutsui, M. Sakagami, K. Nakanishi, and S. Akira. 1998. Targeted disruption of the MyD88 gene results in loss of IL-1-and IL-18-mediated function. Immunity 9: 143–150.CrossRefPubMed Adachi, O., T. Kawai, K. Takeda, M. Matsumoto, H. Tsutsui, M. Sakagami, K. Nakanishi, and S. Akira. 1998. Targeted disruption of the MyD88 gene results in loss of IL-1-and IL-18-mediated function. Immunity 9: 143–150.CrossRefPubMed
62.
Zurück zum Zitat Bhattacharyya, S., C.K. Ratajczak, S.K. Vogt, C. Kelley, M. Colonna, R.D. Schreiber, and L.J. Muglia. 2010. TAK1 targeting by glucocorticoids determines JNK and IκB regulation in Toll-like receptor–stimulated macrophages. Blood 115: 1921–1931.CrossRefPubMedPubMedCentral Bhattacharyya, S., C.K. Ratajczak, S.K. Vogt, C. Kelley, M. Colonna, R.D. Schreiber, and L.J. Muglia. 2010. TAK1 targeting by glucocorticoids determines JNK and IκB regulation in Toll-like receptor–stimulated macrophages. Blood 115: 1921–1931.CrossRefPubMedPubMedCentral
Metadaten
Titel
Involvement of Alveolar Macrophages and Neutrophils in Acute Lung Injury After Scorpion Envenomation: New Pharmacological Targets
verfasst von
Hadjer Saidi
Julie Bérubé
Fatima Laraba-Djebari
Djelila Hammoudi-Triki
Publikationsdatum
28.02.2018
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 3/2018
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-018-0731-9

Weitere Artikel der Ausgabe 3/2018

Inflammation 3/2018 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.