Mycobacterium avium infection of epithelial cells results in inhibition ordelay in the release of interleukin-8 and RANTES

Citation
Fj. Sangari et al., Mycobacterium avium infection of epithelial cells results in inhibition ordelay in the release of interleukin-8 and RANTES, INFEC IMMUN, 67(10), 1999, pp. 5069-5075
Citations number
28
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
67
Issue
10
Year of publication
1999
Pages
5069 - 5075
Database
ISI
SICI code
0019-9567(199910)67:10<5069:MAIOEC>2.0.ZU;2-N
Abstract
Mycobacterium avium is an opportunistic pathogen in AIDS patients, who acqu ire the infection mainly through the gastrointestinal tract. Previous studi es in vitro have shown that M, avium invades epithelial cells of both intes tinal and laryngeal origin. In addition, M, avium enters the intestinal muc osa of healthy mice. Because M. avium invasion of the intestinal mucosa in vivo initially is not accompanied by significant influx of inflammatory cel ls, we sought to determine whether M. avium would trigger chemokine release upon entry into epithelial cells by using HT-29 intestinal and HEp-2 laryn geal epithelial cell lines, Chemokine synthesis was measured both by the pr esence of specific mRNA and protein secretion in the cell culture supernata nt as determined by enzyme-linked immunosorbent assay. Infection of HT-29 i ntestinal cells with M. avium did not induce the release of interleukin-8 ( IL-8) or RANTES for up to 7 days postinfection. However, infection of HEp-2 cells resulted in the release of IL-8 and RANTES at 72 h, Similar findings were observed,vith other AIDS M. avium isolates belonging to different ser ovars, Secretion of IL-8 by HEp-2 cells was dependent upon bacterial uptake . In addition, prior infection with M. avium suppressed IL-8 production by HT-29 cells infected with Salmonella typhimurium, Our results suggest that M. avium infection of epithelial cells is associated with a delay in IL-8 a nd RANTES production which, in the case of HT-29, is prolonged up to 1 week , These findings may explain the weak inflammatory response after intestina l mucosa invasion in mice and are probably related with the ability of the bacterium to evade the host's immune response.