Sticky interactions
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《细胞学杂志》
Upon infection with Neisseria gonorrhoeae, human epithelial cells typically float off the underlying extracellular matrix, reducing the bacterial burden for the host. Now, Muenzner et al. (page 825) show that variants of N. gonorrhoeae and other bacterial pathogens that bind to certain cell–cell adhesion molecules can inhibit this shedding, thus increasing the bacteria's ability to colonize their hosts.
The adhesion molecules under study are carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), which are thought to be involved in microbial infection. CEACAM engagement by the bacteria triggered expression of CD105, a TGF?-like receptor that helps organize focal adhesions. In turn, CD105 expression increased host cell adhesion by activating integrins.No physical association was detected between CEACAMs and CD105 or between CD105 and integrins, so the molecular mechanisms of the pathway are unclear. However, it is apparent that CEACAMs induce CD105 transcription without direct cytoplasmic signaling. CEACAM-6 naturally lacks a cytoplasmic domain and can trigger the response, as can a CEACAM-1 mutant lacking its cytoplasmic tail.
N. gonorrhoeae isolated from patient samples often contain a disproportionate fraction of bacteria that bind CEACAMs, even in controlled experiments where the infection started with bacterial cells that did not bind CEACAMs. The next question is whether bacteria that are beneficial to humans hosts also use CEACAMs. If not, blocking the reaction may be a viable antibacterial strategy.(Neisseria gonorrhoeae that bind CEACAMs )
The adhesion molecules under study are carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), which are thought to be involved in microbial infection. CEACAM engagement by the bacteria triggered expression of CD105, a TGF?-like receptor that helps organize focal adhesions. In turn, CD105 expression increased host cell adhesion by activating integrins.No physical association was detected between CEACAMs and CD105 or between CD105 and integrins, so the molecular mechanisms of the pathway are unclear. However, it is apparent that CEACAMs induce CD105 transcription without direct cytoplasmic signaling. CEACAM-6 naturally lacks a cytoplasmic domain and can trigger the response, as can a CEACAM-1 mutant lacking its cytoplasmic tail.
N. gonorrhoeae isolated from patient samples often contain a disproportionate fraction of bacteria that bind CEACAMs, even in controlled experiments where the infection started with bacterial cells that did not bind CEACAMs. The next question is whether bacteria that are beneficial to humans hosts also use CEACAMs. If not, blocking the reaction may be a viable antibacterial strategy.(Neisseria gonorrhoeae that bind CEACAMs )