Polymorphonuclear leukocyte chemiluminescence and chemotaxis assays were performed on cells obtained from normal individuals and patients with defined defects in chemotaxis or chemiluminescence. After in-vitro pre-incubation with trimethoprim/sulphamethoxazole, its separate components, clindamycin and cefotaxime, normal cells showed some enhancement in chemotaxis and significant increase in chemiluminescence. There was an even more marked increase in chemotaxis when these antibiotics were incubated with cells from patients with leukocyte chemotaxic defects. When the cells from patients with chemiluminescence defects were pre-incubated with these antibiotics, there was also substantial enhancement in chemiluminescence.

Ribosomes, organelles that carry out protein synthesis, are composed of ribosomal RNA and proteins and are divided into two subunits. The small subunit decodes genetic information while the large subunit helps form the peptide bonds of the newly created proteins. Ribosomes are the target for some antibiotics; if the ribosome cannot function, the bacteria cannot make proteins. Ribosomal mutations can cause antibiotic resistance that decreases the drug's activity. Antibiotics have been overused, and bacteria are becoming resistant to them. Two antibiotics, chloramphemicol and erythromycin, inhibit protein synthesis. Chloramphemicol inhibits peptide bond formation while erythromycin can block the tunnel of the large ribosomal subunit preventing the new proteins from exiting the ribosome. Mutations in ribosomal proteins can cause cells to be resistant to the effects of these drugs. The Patterson SMART (Students Modeling a Research Topic) Team, in collaboration with UMBC and MSOE, designed and built a 3‐D physical model of the ribosome using 3D printing technology to show how the ribosome interacts with antibiotics. Supported by a HHMI Precollege Science Education grant.