Leukocyte inhibitory factor stimulates neutrophil-endothelial cell adhesion.

We investigated the ability of the human lymphokine leukocyte inhibitory factor (LIF) to modulate neutrophil-endothelial cell (EC) adherence. EC were cultured from collagenase-treated human umbilical cord veins and grown in complete medium supplemented with EC growth factor. Adherence was measured as the percent of 51Cr-labeled neutrophils remaining adherent to the EC after gentle lavage. Polymorphonuclear neutrophils (PMN) were pretreated with LIF (0.5 to 8 U/ml), extensively washed, and allowed to interact with the EC monolayers. LIF was demonstrated to induce an increase in the capacity of PMN to bind EC in a dose-dependent fashion (from 30.9 +/- 2.1% adherence with control-treated PMN to 68.6 +/- 3.0% at 4 U LIF; p less than 0.001). In subsequent experiments we demonstrated that 10 min was a sufficient preincubation time for LIF to modulate the capacity of the PMN to adhere to EC. LIF has previously been observed to up-regulate expression of C receptor type 3 on PMN, a receptor which has been shown to be involved in PMN-EC binding. Exposure of PMN to anti-C receptor type 3 antibody before their incubation with LIF abrogated its effect as did inactivation of LIF by an esterase inhibitor. We also investigated the ability of LIF to stimulate EC to bind untreated PMN. EC were pretreated with LIF (0.25 to 4 U/ml), extensively washed, and adherence measured as before. LIF was shown to induce a dose-dependent increase in the capacity of the EC to bind PMN (from 28.8 +/- 3.1% for untreated EC to 91.1 +/- 4.0% at 4 U LIF; p less than 0.001). Modulation of EC function required a minimum of 30 min and was inhibited in the presence of cycloheximide or actinomycin D. Neither anti-TNF-alpha or -beta antibodies nor polymixin B abrogated the augmentation by LIF. However, anti-IL-1 antibody partially inhibited the stimulation of EC adhesiveness by LIF, suggesting the possible involvement of this cytokine. These studies provide further evidence that LIF may mediate an important pro-inflammatory role in vivo.

Potentiation of neutrophil aggregation by human leukocyte inhibitory factor.

The current studies were designed to extend our investigations on the ability of the lymphokine leukocyte inhibitory factor (LIF) to function as a neutrophil activator. Specifically, we investigated whether LIF could modulate neutrophil (PMN) aggregation. Aggregation was measured as the increase in light transmission using a Payton aggregometer. We found that up to 16 units of LIF was not able to directly induce PMN clumping. However, when preincubated with 0.5-16 units LIF for 10 min, PMN aggregation was significantly enhanced in a dose-dependent manner after stimulation with 10(-7) M FMLP (94.5 +/- 3.1%), 20 nM leukotriene B4 (183.1 +/- 8.2%), and 100 micrograms guinea pig serum-opsonized zymosan (29.8 +/- 8.6%). While the LIF preparation used in these studies was highly purified, specificity for the LIF effect was demonstrated by the ability of several treatments to prevent augmentation of aggregation including: (1) the competitive binding of LIF to one of its substrates: benzoyl-arginine-ethyl-ester; (2) the blocking of PMN LIF receptors with N-acetyl-D-glucosamine; and (3) phenylmethylsulfonylfluoride treatment of the LIF preparation. As aggregation is thought to represent the in vitro correlate to adherence, these studies provide further evidence for a proinflammatory role for LIF in vivo.

Helper (OKT4)/suppressor (OKT8) ratios in the peripheral blood and synovial fluid of patients with rheumatoid arthritis.

Lymphocyte subsets in the peripheral blood of 10 patients with RA were studied using monoclonal antibodies. The mean percentages of total T, T helper, T suppressor and TAR in the peripheral blood of RA patients were not different from those observed in normal controls. In the synovial fluid the mean percentages of T suppressor cells were present in increased numbers associated with a decreased number of autorosette T cells. We conclude that patients with rheumatoid arthritis present distinct immunoregulatory abnormalities in the synovial fluid not present in the peripheral blood. These changes may be related to the immune abnormalities present and related to the etiology of RA.

Subpopulacoes linfocitarias em pacientes com artrite reumatoide.I. Valores distintos no sangue periferico e liquido sinovial. / Lymphocytic subpopulations in patients with rheumatoid arthritis. I. Different values in the peripheral blood and synovial fluid

Este estudo mostra que pacientes com artrite reumatoide somente em uso de antiinflamatorios nao hormonais apresentam disturbios na relacao T4/T8 do liquido sinovial com niveis normais no sangue periferico associados com baixos numeros de rosetas autologas no liquido sinovial, sugerindo pontos adicionais de disturbios imunologicos em pacientes com artrite reumatoide

Sindrome de Cogan. Relato de um caso e revisao de literatura. / Cogan's syndrome. Report of a case and review of the literature

A sindrome de Cogan e uma enfermidade de etiologia desconhecia cuja incidencia e maior em adultos jovens do sexo feminino.Evolui episodicamente com periodos de crise alterados com periodos de remissao. A apresentacao de episodios agudos de ceratite intersticial difusa nao sifilitica acompanhada de uma disfuncao vestibulo-auditiva caracteriza clinicamente esta doenca. Tendo esta enfermidade caracteristicas peculiares e sendo de apresentacao sumamente rara, julgamos interessante descrever este caso, contribuindo desta forma a um maior conhecimento desta patologia que muitas vezes e confundida e tratada como outras de caracteristicas clinicas semelhantes