Search

Appendicitis due to foreign bodies is rare. Foreign bodies leading to appendicitis or perforation are usually sharp, pointed objects. Lead shot can become lodged in the appendix. Few prior cases have shown a causal relationship between the presence of pellets in the appendix and acute appendicitis. We present the case of a 9-year-old white boy who presented to the emergency room with a 36-hour history of right lower quadrant pain over McBurney's point accompanied by anorexia. The patient's history was significant for consumption of pheasant meat 4 days before onset of symptoms. The pheasant had been shot with a shotgun. X-ray of the child's abdomen revealed a metallic foreign body in the right lower quadrant. Appendectomy was performed. Bird shot was found obstructing the lumen of the grossly inflamed appendix. Pathology was consistent with acute appendicitis. This case is presented as an interesting consequence of bird shot ingestion.

These studies examined the cellular targets of benzo[a]pyrene (BaP)-induced immunomodulation. The immunocompetence of murine mononuclear leukocytes was evaluated following in vivo exposure to BaP. In vitro cell separation and reconstitution techniques were used to evaluate T-dependent antibody (TDAb) production and delineate the immunomodulatory events. Reconstitution of cultures using combinations of adherent and nonadherent cell populations from BaP- and vehicle-treated mice demonstrated that both of these populations were sensitive to the immunomodulatory effects of BaP. Examination of the adherent cell population demonstrated that low numbers of BaP-exposed accessory cells enhanced in vitro TDAb responses. These responses were greater than those observed for analogous cultures containing vehicle-exposed accessory cells. Recombination of separated B cells and T cells from vehicle- or BaP-treated mice in cultures containing normal adherent cells demonstrated that both B cells and T cells were sensitive to the effects of BaP. Cultures containing BaP-exposed cell populations were incapable of supporting control level antibody responses. The results indicate that in vivo BaP exposure induces immunomodulation through effects on macrophages, B cells, and T cells.

Several functionally defined in vitro antibody generating systems were used to assess the immunomodulating mechanisms of the benzopyrenes. When benzo(a)pyrene (BaP) or benzo(e)pyrene (BeP) was incorporated into a T-dependent antibody (TDAb)-producing spleen cell culture system, dose- and time-dependent inhibition of plaque-forming cell responses was observed. Addition of BaP at concentrations as low as 0.002 microgram/ml (7.93 nM) resulted in suppression of the TDAb plaque-forming cell response. BeP-induced suppression was seen at the 2-microgram level (7.93 microM). Time course evaluations demonstrated an early requirement for either chemical in culture in order to induce significant suppression. In vitro incorporation of BaP and BeP into polyclonal antibody-generating cultures also resulted in a dose-related inhibition. Inhibition of these antibody responses was also noted following in vivo exposure of mice to BaP or BeP. Fourteen-day exposure of mice to BaP (40 mg/kg) resulted in 98% suppression of the TDAb response. Polyclonal antibody responses were reduced 50 to 66% following 7 days of chemical exposure. BeP caused 51% suppression of the TDAb response following 14-day exposure of animals. These studies indicate that the suppressive effects of the benzopyrenes are multicellular in origin, occur apart from the carcinogenic effects of the chemicals, and cannot be attributed merely to cellular toxicity.

B6C3F1 mice were exposed to the environmental carcinogen benzo(a)pyrene, a well known immunosuppressant. The ability of isolated splenocytes to produce and respond to the immunoregulatory molecules interleukin-2 (IL-2) and interleukin-3 (IL-3) was measured. Significant suppression by BaP of IL-2, but not IL-3, production following BaP exposure was observed. Further, exogenous recombinant IL-2 reconstituted the ability of splenocytes from benzo(a)pyrene treated mice to generate IgM antibody producing cells to the T-dependent antigens of sheep red blood cells. These results indicate that one of the cellular target(s) of BaP induced immunosuppression may be the mechanism(s) responsible for lymphokine production and regulation by activated T cells.

The capacity of lymphocytes from C57Bl/6 X C3H/HeN F1 (B6C3F1) mice to proliferate in vitro following exposure to benzo(a)pyrene (BaP) in vivo or in vitro was examined. Using two assay systems designed to examine the expression of IL-2 receptors without the production of IL-2, a dose-dependent inhibition in IL-2 dependent proliferation was observed in cultures of lymphocytes from animals exposed to BaP in vivo. A similar decrease was seen when lymphocytes were exposed to BaP in vitro. Admixing BaP-exposed and untreated macrophages and T-cells in culture demonstrated that the defect in IL-2 responsiveness resided exclusively within the macrophage compartment. Splenocytes from mice exposed in vivo to BaP showed a marked decrease in the percentage of cells expressing IL-2 receptor following three days of culture. No alterations were seen in the percentage of the Thy 1.2+ and L3T4+ cells. These results suggest that BaP causes an alteration in the macrophage signal(s) needed for the expression of IL-2 responsiveness. The resulting defect in IL-2 dependent proliferation may play a central role in BaP modulation of humoral immunity.