Distribution of IkappaB proteins in gastric mucosa and other organs of mouse and gerbil.

Abstract

The NF-kappaB/IkappaB complex is a major transcription regulator of inflammatory and immune responses. Helicobacter pylori infection causes chronic inflammation in gastric mucosa by inducing dissociation of the inhibitory IkappaB protein from the complex with a resulting increased expression of interleukin (IL)-8. To clarify which of several known IkappaB proteins could be involved in this inflammatory response, we undertook immunohistochemical examination of normal mouse stomach as well as other murine tissues for comparison, using polyclonal antibodies specific for alpha-, beta-, gamma-, and in-isoforms of IkappaB. The results showed strong immunoreactivity for the alpha-isoform in parietal cells and for the beta-isoform in pit cells of the stomach, along with the presence of these proteins in various other sites. Comparative staining revealed a similar but not identical distribution of IkappaB proteins in the Mongolian gerbil, a rodent model for H. pylori infection. The findings suggest that the alpha- and beta-isoforms are dominant IkappaB proteins in gastric parietal and foveolar cells, respectively, and point to a role for these transcription regulators in modulating pathological responses in stomach and other organs. (J Histochem Cytochem 48:191-199, 2000)