The concomitant role of Helicobacter pylori in Sjogren's syndrome (IL-8, TNF-alpha and HCl)

The diagram I wish to build that will ultimately help design a bridge to understanding the concomitant role of H. pylori in Sjogren's syndrome knows today an enhancement. But let me summarise a bit of what was revealed on my last post:

• Chronic gastric inflammation with high prevalence of serum titers of H. pylori causing mucosal atrophy is seen in ~ 80% of patients with Sjogren's syndrome;
• Patients with other connective tissue diseases do not reveal this anti-H. pylori antibodies relationship;
• However, biopsy results do not present an etiological link between H. pylori and Sjogren's patients; nevertheless, there might be genetic/infection differences from country to country;
• Correlation between H. pylori infection of the gastric mucosa and anti-H. pylori IgG serum titers has been revealed;
• Infection by H. pylori and disturbance of immunological mechanisms in Sjogren's syndrome patients may trigger a network of local and systemic reactions.

What else is there available in the literature that can support the concomitant role of H. pylori in the perturbed chain of responses typical of Sjogren's syndrome? 

The quite old discovery by Freimark et al (1989) that shows high serum levels of IL-8 (small signalling protein secreted by epithelial cells, macrophages, smooth muscle cells or even endothelial cells) [1] responding to alterations in the body system. The same pattern is also seen with increased levels of TNF-alpha, another signalling protein present in systemic inflammation and secreted by, for example, activated macrophages [1]. The elevated serum levels of both IL-8 and TNF-alpha reported by Freimark et al (1989) takes place in asymptomatic H. pylori patients who also show signs of increased gastrin (a peptide hormone that stimulates production of HCl in the stomach, duodenum and pancreas. 

As Miedany et al (2005) so well states, this direct relationship can help explain, in the future, if this bacteria is responsible for inducing Sjogren's or maintaining typical Sjogren's responses in the autoimmune scenario of the disease.

On the other hand we have a very interesting link between H. pylori infection and how long the disease actually lasts. The really curious fact is that presented by Fiocca et al (1994) disclosing that H. pylori antigens might be acting as antigen presenting cells recognised by lymphocytes [2]. Hence and in very simple terms, if H. pylori is still present, the organism still maintains an immunological response and the systemic inflammation is pursued. A vicious cycle indeed!

Most importantly, what I take from all this is that eradication of H. pylori might be adequate to alleviate Sjogren's or simply reduce the inflammatory response levels. Especially in avoiding lymphomas [3], a trait somewhat common in Sjogren's patients. 

See you soon in another interesting building of my diagram up there on the concomitant role of H. pylori in sjogren's syndrome. Please contribute with your findings, comments and own experiences.

[1] Freimark, B., Fantozzi, R., Bone, R., Bordin, G., Fox, R. (1989). "Detection of clonally expanded salivary gland lymphocytes in Sjogren's syndrome". Arthritis Rheumatology, 32(7), pp. 859-869.

[2] Fiocca, R., Luinetti, O, Villani, L., Chiaravalli, A., Capella, C., Solcia, E. (1994). "Epithelial cytotoxicity, immune response and inflammatory components of H. pylori gastritis". Scandinavian Journal of Gastroenterology, 205, pp. 11-16.

[3] Nardone, G (2000). "Risk Factor of Cancer Development in Helicobacter pylori". Digestive Liver Diseases, 32(suppl 3), pp. S190-S192.