07/24/2014: Zark from Emerald City: "Not just Klebsiella.. also H. Pylori infection may play a major role in AS.
I have posted research abstracts regarding pathogens and AS here:
There are too many abstracts to post here, but I will post some of the most interesting below:
"90% AS patients suffer from Hp infection"
Arthritis Res Ther. 2012; 14(Suppl 1): P74.
Published online Feb 9,2012. doi: 10.1186/ar3675
Helicobacter pylori infection in rheumatic diseases
[... snip ...]
Patients of rheumatic diseases were significantly more likely to be Hp infection than health control (89 vs 42%, P < 0.01). The study revealed that 88% of RA patients and 90% AS patients suffer from Hp infection. RA patients carried a diagnosis of Hp, a higher prevalence of the value of CRP was associated with the DAS28(Disease Activity Scor-28) (r = 0.287, P = 0.034). AS patients carried a diagnosis of Hp, a higher prevalence of the value of MMP-3(matrix metalloproteinase-3, MMP-3) was associated with the BASDI(Bath AS Disease Activity Index) (r = 0.435, P = 0.009).
Patients of RA and AS are associated with a high prevalence of Hp infection rate. Hp infection may be play an important role in RA and AS.[... snip ...]
"H. pylori showed the highest percentage of positivity in all 3 patient groups (66.7% in the AAU, 73.3% in the SpA and 80% in the AAU+SpA group)"
"H. pylori affected GI permeability in both SpA and EndG patients...SpA patients taking chronic NSAID had increased gastroduodenal permeability only when H. pylori-positive ...Eradication therapy may help to maintain epithelial barrier function and possibly influence clinical improvement in patients with SpA."
This study showed Klebsiella having a "modifying factor" reacting with HLA-B27 lymphocytes and other cells. "Pronase and papain destroyed the modifying factor activity whereas trypsin and alpha-chymotrypsin degraded the factor into smaller fragments without destroying its ability to modify B27 AS- lymphocytes."
Hum Immunol 1986 Nov;17(3):224-38
Upfold LI, Sullivan JS, Geczy AF.
Biochemical studies on a factor isolated from Klebsiella K43-BTS1 that cross-reacts with cells from HLA-B27 positive patients with ankylosing spondylitis.
A component of the cell walls of certain enteric bacteria has been identified that cross-reacts with an HLA-B27-associated cell-surface structure on lymphocytes and other cell types from patients with ankylosing spondylitis. This component, or "modifying factor, " from one particular organism, Klebsiella K43-BTS1, has been studied in detail. [... snip ...]. Pronase and papain destroyed the modifying factor activity whereas trypsin and alpha-chymotrypsin degraded the factor into smaller fragments without destroying its ability to modify B27 AS- lymphocytes. Neuraminidase did not affect the modifying factor itself but did affect B27 AS- lymphocytes such that they became unresponsive to modification. Sugar inhibition studies suggested that sugar groups are probably not involved in the function of the modifying factor. The availability of purified modifying factor should permit more detailed chemical analyses as well as functional studies to determine the significance of this molecule to the pathogenesis of ankylosing spondylitis.
PMID: 3539895 [PubMed - indexed for MEDLINE]