Suppression of delayed cutaneous hypersensitivity and inflammatory cell delivery by sterile barium peritonitis

We have previously shown that experimental peritonitis secondary to fecal bacteria plus barium sulfate suppresses delayed cutaneous hypersensitivity (DCH) in rats. We examined herein the role of barium sulfate. In a series of experiments presensitized rats were simultaneously skin tested with intradermal keyhole limpet hemocyanin and given an intraperitoneal injection of either (1) a mixture of four fecal bacteria in their nutrient broths, (2) bacteria and broths plus barium sulfate, (3) sterile broths plus barium, (4) sterile barium alone, (5) nutrient broths, or (6) saline. In rats given sterile barium we measured phagocyte delivery to subcutaneous polyvinyl alcohol sponges. We found that (1) the coadministration of barium sulfate was necessary for rats given bacteria to die (P = 0.03) or develop abdominal abscesses (P less than 0.005), (2) suppression of DCH occurred in 70% of rats receiving sterile barium sulfate vs 0% in saline controls (P = 0.0001), (3) early suppression of DCH was associated with subsequent death and abscess formation in rats given bacteria plus barium (P = 0.00002) and with intraabdominal barium collections in rats given barium alone (P less than 0.02), (4) barium sulfate administration caused suppression of phagocyte delivery to subcutaneous sponges: 23.2 X 10(6) cells/site vs 43.1 X 10(6) cells/site in saline controls (P less than 0.005). We conclude that barium sulfate itself has profound systemic effects in the rat model of intraabdominal sepsis. Early suppression of DCH is associated with a poor outcome in septic rats.