Psoriasis is a common papulosquamous skin disease. The histopathology is characterized by epidermal hyperplasia and inflammation. Recent studies suggest that keratinocyte proliferation and inflammation in psoriasis are manifestations of the same underlying pathological process.

To evaluate whether IL-6 participates in the host response to intrauterine infection, we studied IL-6 bioactivity and isoforms in amniotic fluid (AF). Two different assays for IL-6 were used: the hepatocyte stimulating factor assay (in Hep3B2 cells) and the SDS-PAGE/immunoblot assay. IL-6 determinations were performed in 205 AF samples. Samples were obtained from patients in the midtrimester of pregnancy (n = 25), at term with no labor (n = 31), at term in active labor (n = 40), and from patients in preterm labor (n = 109). Higher AF IL-6 levels were observed in women in preterm labor with intraamniotic infection than in women in preterm labor without intraamniotic infection (median = 375 ng/ml, range = 30-5000 ng/ml vs. median = 1.5 ng/ml, range = 0-500, respectively, P < 0.0001). The 23-25-and 28-30-kD IL-6 species could be readily detected in SDS-PAGE immunoblots performed directly on 10-,ul aliquots of AF from patients with intraamniotic infection. Among women in preterm labor with culture-negative AF, those who failed to respond to subsequent tocolytic treatment had higher AF IL-6 concentrations than those who responded to therapy (median = 50 ng/ml vs. median = 1.2 ng/ml, respectively, P < 0.05). Only low levels of IL-6 were detected in AF obtained from normal women in the midtrimester and third trimester of pregnancy. Decidual tissue explants obtained from the placentas of women undergoing elective cesarean section at term without labor (n = 11) produced IL-6 in response to bacterial endotoxin. In a pilot study, AF IL-6 was determined in 56 consecutive women admitted with preterm labor. All patients (n = 10) with elevated AF IL-6 (cutoff = 46 ng/ml) delivered a premature neonate. 4 of these 10 patients had positive AF cultures for microorganisms. These studies implicate IL-6 in the host response to intrauterine infection and suggest that evaluation of AF IL-6 levels may have diagnostic and prognostic value in the management of women in preterm labor. (J. Clin. Invest. 1990Invest. . 85:1392Invest. -1400.) prematurity -parturition-decidua * cytokines -bacterial endotoxins

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Intranasal inoculation of type 5 adenovirus (AdS) produced pneumonia in mice even though the virus did not replicate. To induce the pneumonia, however, a large viral infectious dose was required-i.e., 1010 plaque-forming units.Four strains of inbred mouse were studied (C57BL/6N, C57BL/1OScN, CBA/N, and C3H/N): all showed similar inflammatory responses, although the greatest infiltration occurred in the C57BL/6N mice. The pathological response to AdS infection resembled that previously described in cotton rats: it consisted of overlapping early and late phases, and the infiltration contained primarily lymphocytes and monocytes/macrophages with a scattering of polymorphonuclear leukocytes. The prominent early phase and the presence of polymorphonuclear leukocytes suggested that induction of cytokines may play an important role in the pathogenesis ofthis pneumonia. Assays showed the appearance of tumor necrosis factor a (TNF-a), interleukin 1 (IL-1), and IL-6 in the infected mouse lungs concomitant with the developing early-phase infiltration. Only IL-6 was found in the peripheral blood. IL-6 reached maximum titers 6-24 hr after infection, whereas maximum levels of TNF-a and IL-1 were attained 2-3 days after infection. Specific RNAs for each of these cytokines were demonstrated in the infected lungs. To test the hypothesis that a cytotoxic T-cell response was responsible for the second phase, which primarily consisted of a perivascular and peribronchial infiltration of lymphocytes, AdS was used to infect C57BL/lOScN Nu/Nu and parent mice. The nude mice showed a normal early-phase response, but essentially no peribronchial and only minimal perivascular infiltrations occurred.Intranasal inoculation of type 5 adenovirus (Ad5) into the cotton rat Sigmodon hispidus initiates the development of a pneumonia that closely resembles that produced in humans (1, 2). This model was then used to investigate the viral genes required to produce the pathogenesis of the disease, which for these studies is termed "molecular pathogenesis." The results obtained, using mutants that contained defects in a 19-kDa glycoprotein, implied that the inflammatory response resulted from both the. production of cytokines and the infiltration of cytotoxic T cells (3). Thus, it was hypothesized that the first phase of the pneumonia, which consists of a lymphocyte and monocyte/macrophage intraalveolar and interstitial infiltration as well as a scattering of polymorphonuclear leukocytes (PMNs), resulted from a local elaboration of cytokines. It was further hypothesized that the second phase, which is composed of a lymphocytic perivascular and bronchiolar infiltration, was due to a virus-specific cytotoxic T-cell response.It was not readily possible to test these hypotheses in cotton rats since reagents are not available either to assay their cytokines or to identify the species of lymphocytes present in the pneumonic infiltration. It appeared possible to overcome these experimental barriers, however, when we demonstrated that H5ts125 (4), a co...

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