cAMP levels within Mycobacterium tuberculosis and Mycobacterium bovis BCG increase upon infection of macrophages

被引:60
作者
Bai, Guangchun [1 ]
Schaak, Damen D. [1 ]
McDonough, Kathleen A. [1 ,2 ]
机构
[1] New York State Dept Hlth, Wadsworth Ctr, Albany, NY 12201 USA
[2] SUNY Albany, Dept Biomed Sci, Albany, NY USA
来源
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY | 2009年 / 55卷 / 01期
基金
美国国家卫生研究院;
关键词
Mycobacterium tuberculosis; Mycobacterium bovis BCG; cAMP; macrophage; albumin; DNA-BINDING PROTEIN; CYCLIC-AMP; IN-VITRO; CELLS; ADENOSINE-3'; 5'-MONOPHOSPHATE; IDENTIFICATION; NUCLEOTIDES; EXPRESSION; PHAGOSOMES; REGULATOR;
D O I
10.1111/j.1574-695X.2008.00500.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Adenosine 3',5'-cyclic monophosphate (cAMP)-mediated signal transduction is common in both prokaryotes and eukaryotes, and several bacterial pathogens modulate cAMP signaling pathways of their mammalian hosts during infection. In this study, cAMP levels associated with Mycobacterium tuberculosis and Mycobacterium bovis BCG were measured during macrophage infection. cAMP levels within both bacteria increased c. 50-fold during infection of J774.16 macrophages, relative to the cAMP levels within bacteria incubated in tissue culture media alone. cAMP levels also increased within the macrophage cytoplasm upon uptake of live, but not dead, mycobacteria. The presence of albumin in the absence of oleic acid significantly decreased cAMP secretion and production by both M. tuberculosis and M. bovis BCG. These results suggest that cAMP signaling plays a role in the interaction of tuberculosis-complex mycobacteria with macrophages during infection, and that albumin may be a physiological indicator differentiating host environments during infection.
引用
收藏
页码:68 / 73
页数:6
相关论文
共 32 条
[21]   PATHOGENESIS OF TUBERCULOSIS - INTERACTION OF MYCOBACTERIUM-TUBERCULOSIS WITH MACROPHAGES [J].
MCDONOUGH, KA ;
KRESS, Y ;
BLOOM, BR .
INFECTION AND IMMUNITY, 1993, 61 (07) :2763-2773
[22]   Fatty acid regulation of adenylyl cyclase Rv2212 from Mycobacterium tuberculosis H37Rv [J].
Motaal, Amira Abdel ;
Tews, Ivo ;
Schultz, Joachim E. ;
Linder, Juergen U. .
FEBS JOURNAL, 2006, 273 (18) :4219-4228
[23]  
PADH H, 1976, INDIAN J BIOCHEM BIO, V13, P413
[24]  
PADH H, 1976, MICROBIOS, V16, P183
[25]   A member of the cAMP receptor protein family of transcription regulators in Mycobacterium tuberculosis is required for virulence in mice and controls transcription of the rpfA gene coding for a resuscitation promoting factor [J].
Rickman, L ;
Scott, C ;
Hunt, DM ;
Hutchinson, T ;
Menéndez, MC ;
Whalan, R ;
Hinds, J ;
Colston, MJ ;
Green, J ;
Buxton, RS .
MOLECULAR MICROBIOLOGY, 2005, 56 (05) :1274-1286
[26]  
Sardesai V.M., 2003, INTRO CLIN NUTR, V2nd
[27]   New messages from old messengers: cAMP and mycobacteria [J].
Shenoy, Avinash R. ;
Visweswariah, Sandhya S. .
TRENDS IN MICROBIOLOGY, 2006, 14 (12) :543-550
[28]   Point mutations in the DNA- and cNMP-binding domains of the homologue of the cAMP receptor protein (CRP) in Mycobacterium bovis BCG:: implications for the inactivation of a global regulator and strain attenuation [J].
Spreadbury, CL ;
Pallen, MJ ;
Overton, T ;
Behr, MA ;
Mostowy, S ;
Spiro, S ;
Busby, SJW ;
Cole, JA .
MICROBIOLOGY-SGM, 2005, 151 :547-556
[29]  
STEINER AL, 1972, J BIOL CHEM, V247, P1106
[30]   STIMULATION OF POLYAMIN BIOSYNTHESIS BY FOLLICLE-STIMULATING-HORMONE IN SERUM-FREE CULTURES OF RAT SERTOLI CELLS [J].
SWIFT, TA ;
DIAS, JA .
ENDOCRINOLOGY, 1987, 120 (01) :394-400