- About this Journal ·
- Abstracting and Indexing ·
- Advance Access ·
- Aims and Scope ·
- Annual Issues ·
- Article Processing Charges ·
- Articles in Press ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 867023, 9 pages
Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes
1Department of Endocrinology, The Shanghai Third People’s Hospital, Shanghai Jiao Tong University School of Medicine, 280 Mohe Road, Shanghai 201900, China
2State Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin No. 2 Road, Shanghai 200025, China
3Department of Ophthalmology, The Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai 200011, China
Received 17 March 2012; Revised 13 June 2012; Accepted 29 June 2012
Academic Editor: Soldano Ferrone
Copyright © 2012 Hui-Fang Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- J. M. Fernández-Real and J. C. Pickup, “Innate immunity, insulin resistance and type 2 diabetes,” Diabetologia, vol. 55, no. 2, pp. 273–278, 2012.
- G. H. Tesch, “Role of macrophages in complications of Type 2 diabetes,” Clinical and Experimental Pharmacology and Physiology, vol. 34, no. 10, pp. 1016–1019, 2007.
- C. N. Lumeng, J. B. Delproposto, D. J. Westcott, and A. R. Saltiel, “Phenotypic switching of adipose tissue macrophages with obesity is generated by spatiotemporal differences in macrophage subtypes,” Diabetes, vol. 57, no. 12, pp. 3239–3246, 2008.
- B. N. Lambrecht, “Alveolar macrophage in the driver's seat,” Immunity, vol. 24, no. 4, pp. 366–368, 2006.
- F. Y. Chang and M. F. Shaio, “Respiratory burst activity of monocytes from patients with non-insulin-dependent diabetes mellitus,” Diabetes Research and Clinical Practice, vol. 29, no. 2, pp. 121–127, 1995.
- R. Shurtz-Swirski, S. Sela, A. T. Herskovits et al., “Involvement of peripheral polymorphonuclear leukocytes in oxidative stress and inflammation in type 2 diabetic patients,” Diabetes Care, vol. 24, no. 1, pp. 104–110, 2001.
- A. Wykretowicz, B. Wierusz-Wysocka, J. Wysocki, A. Szczepanik, and H. Wysocki, “Impairment of the oxygen-dependent microbicidal mechanisms of polymorphonuclear neutrophils in patients with type 2 diabetes is not associated with increased susceptibility to infection,” Diabetes Research and Clinical Practice, vol. 19, no. 3, pp. 195–201, 1993.
- C. Romano-Carratelli, M. Galdiero, C. Bentivoglio, I. Nuzzo, D. Cozzolino, and R. Torella, “HLA class II antigens and interleukin-1 in patients affected by type-II diabetes mellitus and hyperlipemia,” Journal of Medicine, vol. 24, no. 1, pp. 28–34, 1993.
- Y. Ohno, N. Aoki, and A. Nishimura, “In vitro production of interleukin-1, interleukin-6, and tumor necrosis factor-α in insulin-dependent diabetes mellitus,” Journal of Clinical Endocrinology and Metabolism, vol. 77, no. 4, pp. 1072–1077, 1993.
- B. Kulseng, G. Skjåk-BræK, I. Følling, and T. Espevik, “TNF production from peripheral blood mononuclear cells in diabetic patients after stimulation with alginate and lipopolysaccharide,” Scandinavian Journal of Immunology, vol. 43, no. 3, pp. 335–340, 1996.
- L. Martinez-Pomares, D. M. Reid, G. D. Brown et al., “Analysis of mannose receptor regulation by IL-4, IL-10, and proteolytic processing using novel monoclonal antibodies,” Journal of Leukocyte Biology, vol. 73, no. 5, pp. 604–613, 2003.
- J. E. Volanakis, “The role of complement in innate and adaptive immunity,” Current Topics in Microbiology and Immunology, vol. 266, pp. 41–56, 2002.
- S. Gordon, “Alternative activation of macrophages,” Nature Reviews Immunology, vol. 3, no. 1, pp. 23–35, 2003.
- A. Mantovani, A. Sica, S. Sozzani, P. Allavena, A. Vecchi, and M. Locati, “The chemokine system in diverse forms of macrophage activation and polarization,” Trends in Immunology, vol. 25, no. 12, pp. 677–686, 2004.
- D. M. Mosser, “The many faces of macrophage activation,” Journal of Leukocyte Biology, vol. 73, no. 2, pp. 209–212, 2003.
- T. M. B. Rezende, D. L. Vargas, F. P. Cardoso, A. P. R. Sobrinho, and L. Q. Vieira, “Effect of mineral trioxide aggregate on cytokine production by peritoneal macrophages,” International Endodontic Journal, vol. 38, no. 12, pp. 896–903, 2005.
- A. Mantovani, A. Sica, and M. Locati, “Macrophage polarization comes of age,” Immunity, vol. 23, no. 4, pp. 344–346, 2005.
- R. M. Steinman and C. L. Moberg, “Zanvil Alexander Cohn 1926–1993,” Journal of Experimental Medicine, vol. 179, no. 1, pp. 1–30, 1994.
- L. R. Turchyn, T. J. Baginski, R. R. Renkiewicz, C. A. Lesch, and J. L. Mobley, “Phenotypic and functional analysis of murine resident and induced peritoneal macrophages,” Comparative Medicine, vol. 57, no. 6, pp. 574–580, 2007.
- H. Ma, G. Liu, W. Ding, Y. Wu, L. Cai, and Y. Zhao, “Diabetes-induced alteration of F4/80+ macrophages: a study in mice with streptozotocin-induced diabetes for a long term,” Journal of Molecular Medicine, vol. 86, no. 4, pp. 391–400, 2008.
- Z. A. Cohn and B. Benson, “The differentiation of mononuclear phagocytes. morphology, cytochemistry, and biochemistry,” The Journal of Experimental Medicine, vol. 121, pp. 153–170, 1965.
- W. Z. Ho, J. P. Lai, X. H. Zhu, M. Uvaydova, and S. D. Douglas, “Human monocytes and macrophages express substance P and neurokinin-1 receptor,” Journal of Immunology, vol. 159, no. 11, pp. 5654–5660, 1997.
- E. E. Bou Ghosn, A. A. Cassado, G. R. Govoni et al., “Two physically, functionally, and developmentally distinct peritoneal macrophage subsets,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 6, pp. 2568–2573, 2010.
- K. Imaizumi, T. Kawabe, S. Ichiyama et al., “Enhancement of tumoricidal activity of alveolar macrophages via CD40-CD40 ligand interaction,” The American Journal of Physiology, vol. 277, no. 1, part 1, pp. L49–L57, 1999.
- C. Yang, J. Y. Zhou, H. J. Zhong et al., “Exogenous norepinephrine correlates with macrophage endoplasmic reticulum stress response in association with XBP-1,” Journal of Surgical Research, vol. 168, no. 2, pp. 262–271, 2011.
- S. Fujisaka, I. Usui, A. Bukhari et al., “Regulatory mechanisms for adipose tissue M1 and M2 macrophages in diet-induced obese mice,” Diabetes, vol. 58, no. 11, pp. 2574–2582, 2009.
- B. R. Shah and J. E. Hux, “Quantifying the risk of infectious diseases for people with diabetes,” Diabetes Care, vol. 26, no. 2, pp. 510–513, 2003.
- T. Nikolic, M. Bunk, H. A. Drexhage, and P. J. M. Leenen, “Bone marrow precursors of nonobese diabetic mice develop into defective macrophage-like dendritic cells in vitro,” Journal of Immunology, vol. 173, no. 7, pp. 4342–4351, 2004.
- S. P. Weisberg, D. McCann, M. Desai, M. Rosenbaum, R. L. Leibel, and A. W. Ferrante, “Obesity is associated with macrophage accumulation in adipose tissue,” Journal of Clinical Investigation, vol. 112, no. 12, pp. 1796–1808, 2003.
- L. Monney, C. A. Sabatos, J. L. Gaglia et al., “Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease,” Nature, vol. 415, no. 6871, pp. 536–541, 2002.
- D. Chakraborty, S. Banerjee, A. Sen, K. K. Banerjee, P. Das, and S. Roy, “Leishmania donovani affects antigen presentation of macrophage by disrupting lipid rafts,” Journal of Immunology, vol. 175, no. 5, pp. 3214–3224, 2005.
- C. Sun, L. Sun, H. Ma et al., “The phenotype and functional alterations of macrophages in mice with hyperglycemia for long term,” Journal of Cellular Physiology, vol. 227, no. 4, pp. 1670–1679, 2012.
- M. Ferracini, J. O. Martins, M. R. M. Campos, D. B. C. Anger, and S. Jancar, “Impaired phagocytosis by alveolar macrophages from diabetic rats is related to the deficient coupling of LTs to the Fc γ R signaling cascade,” Molecular Immunology, vol. 47, no. 11-12, pp. 1974–1980, 2010.
- B. F. Liu, S. Miyata, H. Kojima et al., “Low phagocytic activity of resident peritoneal macrophages in diabetic mice: Relevance to the formation of advanced glycation end products,” Diabetes, vol. 48, no. 10, pp. 2074–2082, 1999.
- P. Sartipy and D. J. Loskutoff, “Monocyte chemoattractant protein 1 in obesity and insulin resistance,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 12, pp. 7265–7270, 2003.
- Y. Zhang, K. Y. Guo, P. A. Diaz, M. Heo, and R. L. Leibel, “Determinants of leptin gene expression in fat depots of lean mice,” The American Journal of Physiology, vol. 282, no. 1, pp. R226–R234, 2002.
- E. Tomas, T. S. Tsao, A. K. Saha et al., “Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation,” Proceedings of the National Academy of Sciences of the United States of America, vol. 99, no. 25, pp. 16309–16313, 2002.
- R. D. Stout and J. Suttles, “Functional plasticity of macrophages: reversible adaptation to changing microenvironments,” Journal of Leukocyte Biology, vol. 76, no. 3, pp. 509–513, 2004.
- J. K. Lee, M. H. Ryu, and J. A. Byun, “Immunotoxic effect of β-chlorolactic acid on murine splenocyte and peritoneal macrophage function in vitro,” Toxicology, vol. 210, no. 2-3, pp. 175–187, 2005.
- M. Benoit, B. Desnues, and J. L. Mege, “Macrophage polarization in bacterial infections,” Journal of Immunology, vol. 181, no. 6, pp. 3733–3739, 2008.
- P. J. Murray and T. A. Wynn, “Protective and pathogenic functions of macrophage subsets,” Nature Reviews Immunology, vol. 11, no. 11, pp. 723–737, 2011.
- J. C. O'Connor, C. L. Sherry, C. B. Guest, and G. G. Freund, “Type 2 diabetes impairs insulin receptor substrate-2-mediated phosphatidylinositol 3-kinase activity in primary macrophages to induce a state of cytokine resistance to IL-4 in association with overexpression of suppressor of cytokine signaling-3,” Journal of Immunology, vol. 178, no. 11, pp. 6886–6893, 2007.