Filtration deformability of rabbit pulmonary macrophage.
Rabbit PAM deformability was evaluated by positive-pressure filtration through Nucleopore membranes of well-specified pore diameter. The PAM filtration method was standardized and was influenced by apparatus variations (pore size, flow rate, cell concentration), environment (temperature, pH, divalent cations, protein concentration), and differences in PAM cell volume. The influence of phagocyte function on filtration deformability was evaluated by exposing PAMs to pharmacologic and physiologic agents with somewhat exclusive influences on phagocyte physiology. Agents that interact with microfilament contractile protein (N-ethylmaleimide, cytochalasin B) altered deformability profoundly, but no effect was observed with agents interacting with microtubules (vinblastine, colchicine). Agents that cause general PAM activation (phorbol myristate acetate) or stimulate chemotaxis (F-Met-Leu-Phe) increased deformability. On the contrary, PAM deformability was not changed by phagocytosis of Staphylococcus aureus or latex beads. Pharmacologic agents that alter PAM adhesion (aspirin, indomethacin, physiologic dose hydrocortisone) or inhibit glycolysis (2-deoxyglucose) had no influence on filtration deformability. Filtration PAM deformability reflects passive whole cell rigidity, which appears to be determined by the state of polymerization of the actin-myosin microfilament complex.
D000818:Animals; D003571:Cytochalasin B / Q000494:pharmacology; D003584:Cytological Techniques; D005033:Ethylmaleimide / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D008851:Micropore Filters; D008855:Microscopy, Electron, Scanning; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000166:cytology; D011817:Rabbits; D014160:Transducers, Pressure; D014462:Ultrafiltration / Q000295:instrumentation / Q000379:methods
D003571:Cytochalasin B; D005033:Ethylmaleimide