Ankylosing spondylitis and Klebsiella [electronic resource] / by Alan Ebringer.

Ankylosing spondylitis as a scientific problem -- History of the origin of ankylosing spondylitis -- The discovery of HLA-B27 in ankylosing spondylitis and related disorders -- Molecular mimicry between  HLA-B27 and Klebsiella bacteria investigated by using rabbit antisera -- Molecular mimicry between HLA-B27 and Klebsiella bacteria investigated by using human tissue typing sera -- Muscle changes in ankylosing spondylitis -- Raised serum IgA is present in ankylosing spondylitis patients -- Faecal cultures in ankylosing spondylitis and uveitis -- Biochemical parameters and Klebsiella in ankylosing spondylitis -- Binding of Klebsiella antisera to HLA-B27 cells -- IgA antibodies to Klebsiella  and other Gram-negative bacteria in ankylosing spondylitis -- IgA antibodies to Klebsiella  measured by immunoblotting -- Antibodies to Klebsiella in ankylosing spondylitis measured by bacterial agglutination and ELISA against lipopolysaccharides -- Dutch and German patients with ankylosing  spondylitis have antibodies to Klebsiella -- Spanish, Finnish and Swedish patients with ankylosing  spondylitis have antibodies to Klebsiella -- Molecular mimicry between Klebsiella pullulanase enzyme, HLA-B27 and collagens I and IV -- Antibodies to Klebsiella and HLA-B27 peptides in ankylosing spondylitis patients from southern Japan -- Ankylosing spondylitis sera are cytotoxic to cells bearing HLA-B27 sequences -- Pathogenesis of ankylosing spondylitis and Klebsiella substrates -- Ankylosing spondylitis and the “low starch  diet” -- The problem of Crohn’s disease and Klebsiella -- Ankylosing spondylitis and “Popper sequences”.

Ankylosing spondylitis and Klebsiella is a comprehensive and informative text on the cause of Ankylosing spondylitis. Ankylosing spondylitis (AS) is a condition which affects 20 million people worldwide and is likely caused or initiated by a bowel infection from Klebsiella bacteria.   When a patient is infected by Klebsiella bacteria, his or her immune system will make antibodies against all the antigens or molecules found in the microbe. Because some of the bacterial antigens resemble self tissues, the anti-bacterial antibodies will attack not only the bacteria but also the self tissues such as the joints and the cells having the same HLA molecules, which is how the disease AS starts.  This is the concept of molecular similarity or “molecular mimicry” which previously has been found to work in two other autoimmune diseases; rheumatic fever and rheumatoid arthritis.   The first paper on this subject was published in 1976 and since then over 100 papers on rheumatological topics have been published, from Prof Ebringer’s group, at the Division of Life Sciences, King’s College in London, UK.   The relevant information from these papers is extracted and presented in this book format making it accessible to health professionals, research institutions, pharmaceutical companies and universities and the general public.  .