Mast cells and histamine are present throughout the rat gastrointestinal system. Typical mast cells, differentiated from atypical mast cells by morphology, staining characteristics, and response to Compound 48/80, were the only mast cell type identified by histology in the cheek, tongue, esophagus, and nonglandular stomach. Atypical mast cells were found in large numbers in the glandular stomach, small and large intestine, and cecum, where they outnumbered typical mast cells by up to 20:1. Gastrointestinal histamine levels varied from 2.6 to 19.3 ng/mg in all tissues surveyed except for the glandular stomach, which contained 26 ng/mg. The amount of histamine per typical mast cell was estimated to be approximately 1.29 picograms; atypical mast cells contained less than 0.15 picograms per cell. Parenteral administration of Compound 48/80 resulted in the degranulation of typical mast cells, but not atypical mast cells, as determined by a fall both in typical mast cell number and a decrease in tissue histamine in areas rich in typical mast cells. These results indicate that striking regional differences in mast cell distribution and tissue histamine levels exist in the rat gastrointestinal system.

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Synovial biopsy specimens from 20 patients with rheumatoid arthritis were subjected to quantitative analysis for several parameters of inflammation and for enumeration of synovial tissue mast cells. Strong positive correlations were found between numbers of mast cells per cubic millimeter of synovial tissue and the following synovial tissue parameters: inflammatory index (a quantification of lymphocytic infiltration), Leu‐3a grade (T helper/inducer lymphocytes), Leu‐1 grade (T lymphocyte), and plasma cell grade. A strong negative correlation was found between the synovial mast cell count and the extent of sublining layer fibrin deposition. Correlations between synovial mast cell count and Leu‐2a grade, ratio of Leu‐3a grade:Leu‐2a grade, OKM1 grade, HLA–DR grade, and lining layer thickness grade did not reach statistical significance. In addition, we obtained synovial specimens from 6 of the patients both before and after long‐term therapy with oral methotrexate and from 3 of the patients before, and 1 week after, an intraarticular injection of steroid. The 3 patients who had an intraarticular steroid injection showed a 67–96% decrease in the number of synovial tissue mast cells; there was no significant change in the number of synovial mast cells in the tissues of the 6 patients who received oral methotrexate. These observations are the first documentation of a quantitative relationship between the number of mast cells and the number and phenotypic profile of infiltrating lymphocytes in an inflamed tissue, which in this case, is human synovium. Our findings suggest that mast cells are involved in the pathologic interactions in rheumatoid arthritis and might play a role in the early phases of exacerbations of disease activity.