The pilus and porin of Neisseria gonorrhoeae cooperatively induce Ca2+ transients in infected epithelial cells

被引:21
作者
Ayala, P [1 ]
Wilbur, JS
Wetzler, LM
Tainer, JA
Snyder, A
So, M
机构
[1] Oregon Hlth & Sci Univ, Dept Mol Microbiol & Immunol, Microscopy Core Facil, Portland, OR 97239 USA
[2] Boston Univ, Sch Med, Div Infect Dis, Boston, MA 02118 USA
[3] Evans Biomed Res Ctr, Boston, MA 02118 USA
[4] Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA
关键词
D O I
10.1111/j.1462-5822.2005.00586.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Purified pili and porin from Neisseria quickly mobilize calcium (Ca2+) stores in monocytes and epithelial cells, ultimately influencing host cell viability as well as bacterial intracellular survival. Here, we examined the Ca2+ transients induced in human epithelial cells during infection by live, piliated N. gonorrhoeae. Porin induced an influx of Ca2+ from the extracellular medium less than 60 s post infection. The porin-induced transient is followed by a pilus-induced release of Ca2+ from intracellular stores. The timing of these events is similar to that observed using purified proteins. Interestingly, the porin-induced Ca2+ flux is required for the pilus-induced transient, indicating that the pilus-induced Ca2+ release is, itself, Ca2+ dependent. Several lines of evidence indicate that porin is present on pili. Moreover, pilus retraction strongly influences the porin- and pilus-induced Ca2+ fluxes. These and other results strongly suggest that the pilus and porin cooperate to modulate calcium signalling in epithelial cells, and propose a model to explain how N. gonorrhoeae triggers Ca2+ transients in the initial stages of pilus-mediated attachment.
引用
收藏
页码:1736 / 1748
页数:13
相关论文
共 68 条
[42]   Type IV pili of pathogenic Neisseriae elicit cortical plaque formation in epithelial cells [J].
Merz, AJ ;
Enns, CA ;
So, M .
MOLECULAR MICROBIOLOGY, 1999, 32 (06) :1316-1332
[43]   Chromaffin-cell stimulation triggers fast millimolar mitochondrial Ca2+ transients that modulate secretion [J].
Montero, M ;
Alonso, MT ;
Carnicero, E ;
Cuchillo-Ibáñez, I ;
Albillos, A ;
García, AG ;
García-Sancho, J ;
Alvarez, J .
NATURE CELL BIOLOGY, 2000, 2 (02) :57-61
[44]   SEROVARS AND SERUM RESISTANCE OF NEISSERIA-GONORRHOEAE FROM DISSEMINATED AND UNCOMPLICATED INFECTIONS [J].
MORELLO, JA ;
BOHNHOFF, M .
JOURNAL OF INFECTIOUS DISEASES, 1989, 160 (06) :1012-1017
[45]   Neisserial porin (PorB) causes rapid calcium influx in target cells and induces apoptosis by the activation of cysteine proteases [J].
Müller, A ;
Günther, D ;
Düx, F ;
Naumann, M ;
Meyer, TF ;
Rudel, T .
EMBO JOURNAL, 1999, 18 (02) :339-352
[46]   ANTIGENIC VARIATION OF PILIN REGULATES ADHESION OF NEISSERIA-MENINGITIDIS TO HUMAN EPITHELIAL-CELLS [J].
NASSIF, X ;
LOWY, J ;
STENBERG, P ;
OGAORA, P ;
GANJI, A ;
SO, M .
MOLECULAR MICROBIOLOGY, 1993, 8 (04) :719-725
[47]  
PARGE HE, 1990, J BIOL CHEM, V265, P2278
[48]   STRUCTURE OF THE FIBER-FORMING PROTEIN PILIN AT 2.6-ANGSTROM RESOLUTION [J].
PARGE, HE ;
FOREST, KT ;
HICKEY, MJ ;
CHRISTENSEN, DA ;
GETZOFF, ED ;
TAINER, JA .
NATURE, 1995, 378 (6552) :32-38
[49]   Ca2+ responses in Chinese hamster ovary-K1 cells demonstrate an atypical pattern of ligand-induced 5-HT1A receptor activation [J].
Pauwels, PJ ;
Colpaert, FC .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2003, 307 (02) :608-614
[50]   Listeriolysin of Listeria monocytogenes forms Ca2+-permeable pores leading to intracellular Ca2+ oscillations [J].
Repp, H ;
Pamukçi, Z ;
Koschinski, A ;
Domann, E ;
Darji, A ;
Birringer, J ;
Brockmeier, D ;
Chakraborty, T ;
Dreyer, F .
CELLULAR MICROBIOLOGY, 2002, 4 (08) :483-491