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Notes: Abstract The ability to respond metabolically to stimulation with both soluble and paniculate substances was investigated in human polymorphonuclear leukocytes (PMNLs) isolated from an aseptic inflammatory reaction. Exudate PMNLs isolated from skin chambers (E-PMNLs) and blood PMNLs isolated from the peripheral blood (B-PMNLs) of the same individual were investigated in parallel. E-PMNLs were primed, resulting in an increased chemiluminescence (CL) response to subsequent stimulation with the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) (334%) and serum-opsonized yeast particles (C3 yeast) (201%), as compared to B-PMNLs. Phorbol myristate acetate (PMA) on the other hand, induced a CL response in E-PMNLs that was only 70% of the response obtained in B-PMNLs. A similar primed state resulting in enhancement of the CL response to FMLP and C3 yeast could be induced in B-PMNLs by pretreatment with a bacterial culture filtrate. Pretreatment of E-PMNLs with the bacterial culture filtrate, however, did not increase the CL response to FMLPs any further. The enhanced functional response to FMLPs in E-PMNLs was accompanied by an increased binding of the peptide, demonstrated by a doubling of the amount of bound f-Met-Leu-[3H]Phe (209%), as compared to B-PMNLs. The increased C3-yeast-induced CL generation in E-PMNLs was accompanied by an increased ingestion and attachment of C3-opsonized yeast particles. The enhancement of phagocytosis in E-PMNLs was, however, dependent upon the opsonin used, since IgG-opsonized yeast particles were phagocytosed to the same extent by E-PMNLs and B-PMNLs, thereby indicating that selective receptor modulation is also involved in the priming of E-PMNLs for an enhanced response to C3-yeast. These results show that exudate cells isolated from skin chambers are modulated with respect to receptor-mediated functions resulting in an increased metabolic response to FMLP coupled with an increased binding of the peptide and an increased phagocytosis of C3-coated yeast particles. Receptor modulation during exudation may be an important mechanism in regulating the inflammatory response by PMNLs.