The effects of indomethacin and interleukin-2 on the proliferation of lymphocytes from patients with lung cancer

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Abstract
The effects of the addition of indomethacin and interleukin-2 (IL-2) to phytohemagglutinin (PHA)-stimulated lymphocytes from patients with untreated squamous-cell carcinoma of the lung and with chronic obstructive pulmonary disease and from normal individuals were studied. In 13 of 21 patients with lung carcinoma, the response of lymphocytes to PHA stimulation was significantly augmented by indomethacin. In these 13 patients, the nonaugmented PHA response was also significantly depressed, with only 1 patient falling in the normal range. In the other 8 patients, the average PHA reactivity was normal, as was the degree of augmentation by indomethacin. In additional studies, IL-2 was added to PHA-stimulated lymphocytes with and without the addition of indomethacin. In the normal group, IL-2 further increased PHA reactivity by an average of 46.0%. The addition of indomethacin to these cultures increased the PHA reactivity by only 8.8%, which is similar to the indomethacin effect for the PHA-stimulated cells without the addition of IL-2. In the cancer group, the PHA reactivity of 13 of 19 patients was significantly increased by the addition of IL-2. When indomethacin was added simultaneously with IL-2, the proliferative response for 12 of 19 patients was increased significantly more than for the normal controls. Thus, this study indicates that the PHA reactivity of lymphocytes from many lung carcinoma patients is augmented to a greater extent than for normal individuals by inhibiting prostaglandin synthesis. Also, the addition of IL-2 to these PHA-stimulated cultures did not mimic the addition of indomethacin, but instead the effects were usually additive. These findings may have clinical implications with regard to designing new clinical trials in patients with lung carcinoma.