Very interesting. Thanks for posting. I think someone once posted about indications that ibuprofen use is also liked to NTMs.
Here is a bunch of text from an older study. The first paragraph notes that zithro in CFers might lead to zithro-resistant NTMs. So that's kinda tangential info to the link you posted. The second paragraph notes a possible link between the ibuprofen and NTMs. I guess the key being: We need antiinflammatories to prevent lung damage from our raging immune systems, yet dampening the immune fight can result in bacterias getting a foothold.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570835/
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Azithromycin has a potential immunomodulatory effect in the treatment of CF, mainly for chronic P. aeruginosa respiratory tract infection (32). In our population, azithromycin was administered chiefly for its immunomodulatory properties and not to treat NTM pulmonary disease. Our study patients with NTM were treated more often with azithromycin (71.5% of case-patients vs. 51.4% of controls). Because macrolides are the treatment of choice for infections caused by MAC and M. abscessus, subtherapeutic doses of macrolides can induce selection of macrolide-resistant mycobacteria. The effect of long-term treatment with azithromycin on the antibimicrobial selection of NTM in CF patients remains undefined.
High doses of ibuprofen inhibit the inflammatory response to chronic infection, which contributes to lung destruction in patients with cystic fibrosis (33), and our patients with NTM were treated more frequently with ibuprofen. Furthermore, prostaglandin E inhibitors up-regulate the Th1 function with increasing levels of tumor necrosis factor, ?-interferon, and interleukin-2, which are necessary for the control of mycobacterial infections (34). The effect of prostaglandin inhibitors on mycobacterial infection has not been assessed in depth.
We did not find any correlation between the gene mutation profile and NTM infection. By contrast, others have demonstrated that 60.7% of patients with emerging bacteria were homozygous for the Delta F508 mutation in comparison to only 23.8% of the isolates from the control group (4).
