期刊论文详细信息
BMC Research Notes
Infection of human monocytes by Chlamydia pneumoniae and Chlamydia trachomatis: an in vitro comparative study
Roberto Cevenini1  Claudio Foschi1  Paola Nardini1  Manuela Donati1  Claudia Cavallini2  Romana Fato3  Christian Bergamini3  Antonella Marangoni1 
[1]Microbiology, DIMES, University of Bologna, S.Orsola Hospital, via Massarenti 9, 40138 Bologna, Italy
[2]Laboratory of Molecular Biology and Stem Cell Engineering, DIMES, University of Bologna, Bologna, Italy
[3]FaBiT Department, University of Bologna, Bologna, Italy
关键词: Cytokines;    Reactive nitrogen species;    Reactive oxygen species;    Chlamydia trachomatis;    Chlamydia pneumoniae;    Human monocytes;   
Others  :  1133923
DOI  :  10.1186/1756-0500-7-230
 received in 2013-10-24, accepted in 2014-04-03,  发布年份 2014
PDF
【 摘 要 】

Background

An increasing number of studies suggest that chlamydiae can infect immune cells. The altered immune cell function could contribute to the progression of several chronic inflammatory diseases.

The aim of this study was to comparatively evaluate Chlamydia pneumoniae (CP) and Chlamydia trachomatis (CT) interactions with in vitro infected human blood monocytes.

Results

Fresh isolated monocytes were infected with viable CP and CT elementary bodies and infectivity was evaluated by recultivating disrupted monocytes in permissive epithelial cells.

The production of reactive oxygen and nitrogen species was studied in the presence of specific fluorescent probes. Moreover, TNF-α, INF-α, INF-β and INF-γ gene expression was determined.

CT clearance from monocytes was complete at any time points after infection, while CP was able to survive up to 48 hours after infection. When NADPH oxydase or nitric oxide synthase inhibitors were used, CT infectivity in monocytes was restored, even if at low level, and CT recovery’s rate was comparable to CP one.

CT-infected monocytes produced significantly higher levels of reactive species compared with CP-infected monocytes, at very early time points after infection. In the same meanwhile, TNF-α and INF-γ gene expression was significantly increased in CT-infected monocytes.

Conclusions

Our data confirm that CP, but not CT, is able to survive in infected monocytes up to 48 hours post-infection. The delay in reactive species and cytokines production by CP-infected monocytes seems to be crucial for CP survival.

【 授权许可】

   
2014 Marangoni et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150305020057237.pdf 1115KB PDF download
Figure 6. 88KB Image download
Figure 5. 51KB Image download
Figure 4. 50KB Image download
Figure 3. 68KB Image download
Figure 2. 86KB Image download
Figure 1. 42KB Image download
【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

Figure 5.

Figure 6.

【 参考文献 】
  • [1]Centers for Disease Control and Prevention: CDC grand rounds: Chlamydia prevention: challenges and strategies for reducing disease burden and sequelae. MMWR Morb Mortal Wkly Rep 2011, 60(Suppl 12):370-373.
  • [2]Stamm WE: Chlamydia trachomatis infections of the adult. In Sexually transmitted diseases. Edited by Holmes KK, Sparkling PF, Stamm WE, Wasserheit JN, Corey L, Cohen MS, Watts HD. New York: McGraw-Hill; 2008:575-594.
  • [3]Boman J, Hammerschlag MR: Chlamydia pneumoniae and atherosclerosis: critical assessment of diagnostic methods and relevance to treatment studies. Clin Microbiol Rev 2002, 15:1-20.
  • [4]Johnston SL, Martin RJ: Chlamydophila pneumoniae and Mycoplasma pneumoniae: a role in asthma pathogenesis? Am J Respir Crit Care Med 2005, 172:1078-1089.
  • [5]Gaydos CA, Summersgill JT, Sahney NN, Ramirez JA, Quinn TC: Replication of Chlamydia pneumoniae in vitro in human macrophages, endothelial cells and aortic artery smooth muscle cells. Infect Immun 1996, 64:1614-1620.
  • [6]Beagley KB, Houston WM, Hansbro PM, Timms P: Chlamydial infection of immune cells: altered function and implication for disease. Crit Rev Immunol 2009, 29:275-305.
  • [7]Kuo CC, Puolakkainen M, Lin TM, Witte M, Campbell LA: Mannose-receptor positive and negative mouse macrophages differ in their susceptibility to infection by Chlamydia species. Microb Pathog 2002, 32(Suppl 1):43-48.
  • [8]Yong EC, Chi EY, Kuo CC: Differential antimicrobial activity of human mononuclear phagocytes against the human biovars of Chlamydia trachomatis. J Immunol 1987, 139:1297-1302.
  • [9]Gerard HC, Kohler L, Branigan PJ, Zeidler H, Schumacher HR, Hudson AP: Viability and gene expression in Chlamydia trachomatis during persistent infection of cultured human monocytes. Med Microbiol Immunol 1998, 187:115-120.
  • [10]Poikonen K, Lajunen T, Silvennoinen-Kassinen S, Paldanius M, Leinonen M, Saikku P: Susceptibility of human monocyte-macrophages to Chlamydia pneumoniae infection in vitro is highly variable and associated with levels of soluble CD14 and C. pneumoniae IgA and human HSP-IgG antibodies in serum. Scand J Immunol 2008, 67:279-284.
  • [11]Kuo CC: Immediate cytotoxicity of Chlamydia trachomatis for mouse peritoneal macrophages. Infect Immun 1978, 20(Suppl 3):613-618.
  • [12]Kuo CC: Cultures of Chlamydia trachomatis in mouse peritoneal macrophages: factors affecting organism growth. Infect Immun 1978, 20(Suppl 2):439-445.
  • [13]Marangoni A, Accardo S, Aldini R, Guardigli M, Cavrini F, Sambri V, Montagnani M, Roda A, Cevenini R: Production of reactive oxygen species and expression of inducible nitric oxide synthase in rat isolated Kupffer cells stimulated by Leptospira interrogans and Borrelia burgdorferi. World J Gastroenterol 2006, 12:3077-3081.
  • [14]Roca FJ, Ramakrishnan L: TNF dually mediates resistance and susceptibility to mycobacteria via mitochondrial reactive oxygen species. Cell 2013, 153:521-534.
  • [15]Hu W, Ge Y, Ojcius DM, Sun D, Dong H, Yang XF, Yan J: p53 signalling controls cell cycle arrest and caspase-independent apoptosis in macrophages infected with pathogenic Leptospira species. Cell Microbiol 2013, 15(Suppl 10):1624-1659.
  • [16]Circu ML, Aw TY: Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010, 48(Suppl 6):749-762.
  • [17]Azenabor AA, Yang S, Job G, Adedokun OO: Elicitation of reactive oxygen species in Chlamydia pneumoniae-stimulated macrophages: a Ca2+ dependent process involving simultaneous activation of NADPH oxidase and cytochrome oxidase genes. Med Microbiol Immunol 2005, 194:91-103.
  • [18]Azenabor AA, York J: Chlamydia trachomatis evokes a relative anti-inflammatory response in a free Ca2+ dependent manner in human macrophages. Comp Immunol Microbiol Infect Dis 2010, 33:513-528.
  • [19]Azenabor AA, Cintrón-Cuevas J, Schmitt H, Bumah V: Chlamydia trachomatis induces anti-inflammatory effect in human macrophages by attenuation of immune mediators in Jurkat T-cells. Immunobiology 2011, 216:1248-1255.
  • [20]Azenabor AA, Muili K, Akoachere JF, Chaudhry A: Macrophage antioxidant enzymes regulate Chlamydia pneumoniae chronicity: evidence of the effect of redox balance on host-pathogen relationship. Immunobiology 2006, 211(Suppl 5):325-339.
  • [21]Michelini E, Donati M, Aldini R, Cevenini L, Mezzanotte L, Nardini P, Foschi C, Zvi IB, Cevenini M, Montagnani M, Marangoni A, Roda A, Cevenini R: Dual-color bioluminescent assay using infected HepG2 cells sheds new light on Chlamydia pneumoniae and human cytomegalovirus effects on human cholesterol 7α-hydroxylase (CYP7A1) transcription. Anal Biochem 2012, 430(Suppl 1):92-96.
  • [22]Donati M, Sambri V, Comanducci M, Di Leo K, Storni E, Giacani L, Ratti G, Cevenini R: DNA immunization with pgp3 gene of Chlamydia trachomatis inhibits the spread of chlamydial infection from the lower to the upper genital tract in C3H/HeN mice. Vaccine 2003, 21(Suppl 11–12):1089-1093.
  • [23]Storni E, Donati M, Marangoni A, Accardo S, Cevenini R: Comparative PCR-based restriction fragment length polymorphism analysis of the plasmid gene orf3 of Chlamydia trachomatis and Chlamydia psittaci. FEMS Immunol Med Microbiol 2006, 48:313-318.
  • [24]Cevenini R, Sarov I, Rumpianesi F, Donati M, Melega C, Varotti C, La Placa M: Serum specific IgA antibody to Chlamydia trachomatis in patients with chlamydial infections detected by ELISA and an immunofluorescence test. J Clin Pathol 1984, 37(Suppl 6):686-691.
  • [25]Marangoni A, Donati M, Cavrini F, Aldini R, Accardo S, Sambri V, Montagnani M, Cevenini R: Chlamydia pneumoniae replicates in Kupffer cells in mouse model of liver infection. World J Gastroenterol 2006, 12(Suppl 40):6453-6457.
  • [26]Farencena A, Comanducci M, Donati M, Ratti G, Cevenini R: Characterization of a new isolate of Chlamydia trachomatis which lacks the common plasmid and has properties of biovar trachoma. Infect Immun 1997, 65(Suppl 7):2965-2969.
  • [27]Lim MH, Xu D, Lippard SJ: Visualization of nitric oxide in living cells by a copper-based fluorescent probes. Nat Chem Biol 2006, 2:375-380.
  • [28]Fato R, Bergamini C, Bortolus M, Maniero AL, Leoni S, Ohnishi T, Lenaz G: Differential effects of mitochondrial Complex I inhibitors on production of reactive oxygen species. Biochim Biophys Acta 2009, 1787(Suppl 5):384-392.
  • [29]Wolf K, Fischer E, Hackstadt T: Degradation of Chlamydia pneumoniae by peripheral blood monocytic cells. Infect Immun 2005, 73(Suppl 8):4560-4570.
  • [30]Ieven MM, Hoymans VY: Involvement of Chlamydia pneumoniae and atherosclerosis: more evidence for lack of evidence. J Clin Microbiol 2005, 43:19-24.
  • [31]Shima K, Kuhlenbaumer G, Rupp J: Chlamydia pneumoniae infection and Alzheimer’s diseases: a connection to remember? Med Microbiol Immunol 2010, 199:283-289.
  • [32]Rizzo A, Domenico MD, Carratelli CR, Paolillo R: The role of Chlamydia and Chlamydophila infections in reactive arthritis. Intern Med 2012, 51:113-117.
  • [33]Mannonen L, Markkula E, Puolakkainen M: Analysis of Chlamydia pneumoniae infection in mononuclear cells by reverse transcription-PCR targeted to chlamydial gene transcripts. Med Microbiol Immunol 2011, 200(Suppl 3):143-154.
  • [34]Gieffers J, van Zandbergen G, Rupp J, Sayk F, Kruger S, Ehlers S, Solbach W, Maass M: Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature. Eur Respir J 2004, 23(Suppl 4):506-510.
  • [35]Azenabor AA, Chaudhry AU: Effective macrophage redox defense against Chlamydia pneumoniae depends on L-type Ca2+ channel activation. Med Microbiol Immunol 2003, 192(Suppl 2):99-106.
  • [36]Ramsey KH, Miranpuri GS, Sigar IM, Ouellette S, Byrne GI: Chlamydia trachomatis persistence in the female mouse genital tract: inducible nitric oxide synthase and infection outcome. Infect Immun 2001, 69:5131-5137.
  • [37]Rothfuchs AG, Gigliotti D, Palmblad K, Andersson U, Wigzell H, Rottenberg ME: IFN-alpha beta-dependent, IFN-gamma secretion by bone marrow-derived macrophages controls an intracellular bacterial infection. J Immunol 2001, 167:6453-6461.
  • [38]Ismail N, Olano JP, Feng HM, Walker DH: Current status of immune mechanisms of killing of intracellular microorganisms. FEMS Microbiol Lett 2002, 207:111-120.
  • [39]Herbst S, Schaible UE, Schneider BE: Interferon gamma activated macrophages kill mycobacteria by nitric oxide induced apoptosis. PLoS One 2011, 6:e19105. doi:10.1371/journal.pone.0019105
  • [40]Redecke V, Dalhoff K, Bohnet S, Braun J, Maass M: Interaction of Chlamydia pneumoniae and human alveolar macrophages: infection and inflammatory response. Am J Respir Cell Mol Biol 1998, 19:721-727.
  • [41]Mamata Y, Hakki A, Newton C, Burdash N, Klein TW, Friedman H: Differential effects of Chlamydia pneumoniae infection on cytokine levels in human T-lymphocyte- and monocyte-derived cell cultures. Int J Med Microbiol 2007, 297:109-115.
  • [42]Evani SJ, Murthy AK, Mareedu N, Montgomery RK, Arulanandam BP, Ramasubramanian AK: Hydrodynamic regulation of monocyte inflammatory response to an intracellular pathogen. PLoS One 2011, 6:e14492. doi: 10.1371/journal.pone.0014492
  • [43]Benagiano M, Munari F, Ciervo A, Amedei A, Paccani SR, Mancini F, Ferrari M, Della Bella C, Ulivi C, D’Elios S, Baldari CT, Prisco D, de Bernard M, D’Elios MM: Chlamydophila pneumoniae phospholipase D (CpPLD) drives Th17 inflammation in human atherosclerosis. Proc Natl Acad Sci U S A 2012, 109:1222-1227.
  文献评价指标  
  下载次数:31次 浏览次数:11次