title: IL-1beta stimulation induces paracrine regulation of PMN function and apoptosis.
abstract: Polymorphonuclear leukocytes (PMN) play a crucial role in the primary immunological defense against infectious agents. PMN activation and function is influenced in a paracrine manner by cytokines and bacterial products. While cell-cell communication has been demonstrated between PMN and other cell types, little data is available addressing PMN-PMN communication. Therefore, the aim of this study was to determine whether PMN were able to affect PMN function in vitro in a cell-contact independent manner, and whether IL-1beta influenced this effect. Conditioned medias (CM) were prepared by incubating PMN in HBSS +/- IL-1beta for 1-4 h. Incubation of fresh PMN in these conditioned medias had little or no effect on the expression of cell surface FcgammaR expression or oxidative metabolism. However, incubation of PMN in CM-IL1beta, but not control CM, increased phagocytotic activity and suppressed apoptosis. Additionally, CM-IL1beta, but not control CM, slowed the changes in Mac-1 and CR1 cell surface expression that occurred in HBSS within 2 h of incubation. Finally, control CM down-regulated the cell surface expression of PSGL-1; an effect that was not observed with CM-IL1beta. In conclusion, we demonstrate that PMN are able to communicate with and influence the immunological function of other PMN independent of cell-cell contact, and that this influence is regulated by cytokines such as IL-1beta. The major impact of this paracrine regulation is to down-regulate PMN apoptosis with the potential for an upregulated inflammatory response.
authors.affiliation: Rhode Island Hospital, Division of Surgical Research, Providence 02903, USA.
authors.forename: P S
authors.initials: PS
authors.lastname: Grutkoski
authors.forename: R
authors.initials: R
authors.lastname: D'Amico
authors.forename: A
authors.initials: A
authors.lastname: Ayala
authors.forename: H H
authors.initials: HH
authors.lastname: Simms
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D018821:CD18 Antigens / Q000187:drug effects / Q000378:metabolism; D015687:Cell Hypoxia / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects; D017077:Culture Media, Conditioned / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D005452:Fluoresceins / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism* / Q000494:pharmacology; D019041:L-Selectin / Q000187:drug effects / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000187:drug effects / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D010587:Phagocytosis / Q000187:drug effects; D017463:Receptors, Complement 3b / Q000187:drug effects / Q000378:metabolism; D017452:Receptors, IgG / Q000378:metabolism
chemical_list: D018821:CD18 Antigens; D017077:Culture Media, Conditioned; D005452:Fluoresceins; D007375:Interleukin-1; D016177:Macrophage-1 Antigen; D008562:Membrane Glycoproteins; C084882:P-selectin ligand protein; D017463:Receptors, Complement 3b; D017452:Receptors, IgG; D019041:L-Selectin; C029569:diacetyldichlorofluorescein