@article{881d9ee201d14e4da8c9b3db036a9e49,
title = "Polymorphonuclear leukocyte function in psoriasis: Chemotaxis, chemokinesis, beta-adrenergic receptors, and proteolytic enzymes of polymorphonuclear leukocytes in the peripheral blood from psoriatic patients",
abstract = "Psoriatic patients, particularly those with psoriatic arthritis, have neutrophilic and eosinophilic leukocytosis. Isolated polymorphonuclear leukocytes (PMNLs) from psoriatic patients have normal concentrations of proteolytic enzymes and they have beta-adrenergic receptors of normal density and affinity. PMNLs from psoriatic patients responded normally to the synthetic chemotactic peptide, f-Met-Leu-Phe (formyl-methionine-leucine-phenylalanine). The chemotactic activities of sera from psoriatic patients were similar to those of normal sera. Sera from psoriatic patients enhanced chemokinesis of PMNLs more than normal control sera at a final concentration of 1%; no difference in chemokinetic response between psoriatic and normal sera was found at serum concentrations greater than 2.5%. This study suggests that the peripheral PMNLs from psoriatic patients are normal, but the sera of psoriatic patients has more chemokinetic activity for PMNLs than does normal serum.",
author = "Fraki, {J. E.} and L. Jakoi and Davies, {A. O.} and Lefkowitz, {R. J.} and R. Snyderman and Lazarus, {G. S.}",
note = "Funding Information: One of the histologic findings in psoriasis is the accumulation of polymorphonuclear leukocytes (PMNLs) in the stratum corneum of psoriatic epidermis. This phenomenon may be an early histologic change in the development of the psoriatic plaque [1], although some investigators suggest that mononuclear leukocytes infiltrate the skin before PMNLs [2,3]. A number of mechanisms have been postulated to explain the localization of PMNLs in psoriatic epidermis. These include: epidermal localization of chemotactic components of complement [4), epidermal proteinase activation [5), deposition of immune complexes in the stratum corneum [6], production of chemoattractant arachidonic acid metabolites [7), and the Manuscript received August 10, 1981; accepted for publication December 22, 1982. Publication #116 from the Dermatological Research Laboratories, Duke University Medical Center. This work was supported by NIH Grant 5 R01 AM19067, NIH Fogarty International Fellowship 5F05-TW-02774-02, and by grants from the National Psoriasis Foundation. • NIH Fogarty International Fellow and Psoriasis Foundation Fellow. Present address: Department of Dermatology, University of Kuopio, SF-70101 Kuopio 10, Finland. t Present address: Department of Dermatology, University of Penn{"} sylvania, Philadelphia, Pennsylvania 19104. Reprint requests to: Gerald Lazarus, M.D., Department of Dermatology, University of Pennsylvania, 329 Medical Education Building, 36th & Hamilton Walk, Philadelphia, Pennsylvania 19104. Abbreviations: · Bz-Phe-0-Nap: benzoyl-DL-phenylalanine-2-naphthol ester f-Met-Leu-Phe: formylmethionine-leucine-phenylalanine PMNL: polymorphonuclear leukocyte Suc-(Alah-NA: succinyl-L-alanine-L-alanine-L-alanine-parani-troanilide presence of bacterial products [8]. There are a number of recent studies suggesting that PMNLs are activated in the peripheral blood of psoriatic patients. Wahba et a! [9,10) suggest that PMNLs from psoriatic patients have enhanced chemotaxis to activated serum and they have increased capacity to engulf 125llabeled Shigella flexneri. Sedgwick et a! [11] report that blood from psoriatic patients has increased numbers ofPMNLs which adhere more avidly to glass wool columns; these investigators correlate elevated PMNL counts and increased PMNL adherence with severity of psoriasis, and with the presence of psoriatic arthritis. Other investigators report enhanced PMNL chemotaxis and chemokinesis [12], which were most marked when studies of psoriatic PMNL function were performed in autologous sera [13]. Glinski et al [14] report that PMNLs from patients with psoriasis have increased levels of proteinases. Other investigators have not been able to confirm abnormalities of PMNL chemotaxis in vitro [15,16] or in vivo [16-18]; normal or even decreased phagocytic function of PMNLs in psoriasis has been reported [15,19,20]. Beta-adrenergic receptor dysfunction has been implicated in the pathogenesis of psoriasis [21,22]. Decreased cyclic AMP levels or alteration in the cyclic AMP/cyclic GMP ratio has been observed in association with increased PMNL mobility and function [23]. Enhanced chemotaxis of peripheral PMNLs in psoriasis reverted to normal upon administration of the phosphodiesterase inhibitor, diphylline [9]. These observations may indicate an abnormality in functions of beta-adrenergic receptors in psoriatic PMNLs. In this study, we report our investigations of a number of pertinent parameters of PMNL function in psoriasis.",
year = "1983",
doi = "10.1111/1523-1747.ep12518273",
language = "English (US)",
volume = "81",
pages = "254--257",
journal = "Unknown Journal",
issn = "0309-1708",
publisher = "Elsevier Limited",
number = "3",
}