Objective: To compare concentrations of interleukin-5 (IL-5), immunoglobulin E (IgE), eosinophilic cationic protein (ECP), and soluble intercellular adhesion molecule-1 (sICAM-1) in nasal secretion and serum of patients with chronic nonallergic sinusitis, allergic rhinitis, and nonallergic nasal polyposis to obtain information about the pathogenesis of these diseases. Methods: Nasal secretion and serum were analyzed by routine enzyme-linked immunosorbent assay techniques. Nineteen patients with chronic nonallergic sinusitis, 24 patients with seasonal allergic rhinitis, and 18 patients with nonallergic nasal polyposis were included in the study. Eight healthy, nonallergic probands served as control subjects. Results: Significantly elevated concentrations of IL-5 (5-fold, P < .05) and IgE (15-fold, P < .01) were detected in nasal secretion of patients with allergic rhinitis (IL-5, 51.8 ؎ 13.2 pg/mL; IgE, 41.9 ؎ 20.9 kU/L) or nonallergic nasal polyposis (IL-5, 57.9 ؎ 36.9 pg/mL; IgE, 40.5 ؎ 20.2 kU/L) compared with controls (IL-5, 10.6 ؎ 7.8 pg/mL; IgE, 2.8 ؎ 0.5 kU/L) or with patients with chronic nonallergic sinusitis (IL-5, 16.5 ؎ 13.2 pg/mL; IgE, 5.4 ؎ 3.1 kU/L). There were no significant differences between patients with allergic rhinitis and those with nonallergic nasal polyposis. Concentrations of ECP were significantly elevated (sixfold, P < .01) in patients with allergic rhinitis (297.8 ng/mL ؎ 173.1) compared with controls (52.4 ؎ 28.0 ng/mL) or patients with chronic nonallergic sinusitis (44.8 ؎ 40.1 ng/mL), whereas twofold higher concentrations (not significant) of ECP were observed in patients with nonallergic nasal polyposis (107.1 ؎ 26.6 ng/mL). Significantly elevated concentrations of sICAM-1 in nasal secretion (threefold, P < .05) were detected only in patients with chronic nonallergic sinusitis (79.4 ؎ 45.6 ng/mL). The elevated sICAM-1 nasal secretion values in this group correlated significantly (P < .05) to the serum values. Conclusions: Equally elevated concentrations of IL-5 and IgE in patients with allergic rhinitis and nonallergic nasal polyposis implicated similar pathogenic processes in both diseases. Whereas the pathogenesis of allergic rhinitis is IgE-specific, the pathogenesis of nasal polyps is not as clear. IL-5 was suggested to play a pivotal role in tissue eosinophilia, which was confirmed by data in the present study. Elevated concentrations of ECP were suggested to result from tissue eosinophilia-a characteristic of both diseases. Elevated concentrations of sICAM-1 in patients with chronic nonallergic sinusitis pointed to its key role in the recruitment of neutrophils into the inflamed tissue, whereas an important role in eosinophil recruitment was ruled out.

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Late-phase response in allergic rhinitis is characterized by tissue eosinophilia and influx of CD4+ T-cells. IL-16 and MIP-1 alpha are highly chemotactic on T-cells and on eosinophils. Both IL-16 and MIP-1 alpha have been demonstrated to be up-regulated after challenge in the late-phase response in various atopic conditions other than allergic rhinitis. The aim of our study was to determine the expression of IL-16 and MIP-1 alpha in nasal secretions following allergen challenge in allergic rhinitis, and to compare these with characteristic late-phase mediators such as IL-5 and ECP. Nasal secretions of 14 allergic volunteers challenged intranasally by their specific allergen were studied from 20 minutes to 8 hours after allergen challenge. Nasal secretions were analyzed by routine ELISA for IL-16, MIP-1 alpha, IL-5, and ECP. IL-16 and MIP-1 alpha increased significantly in nasal secretions of challenged allergic patients in the late-phase response. IL-16 revealed highest amounts 5 hours after challenge, whereas MIP-1 alpha peaked at 7 hours. Both correlated significantly (r = 0.917, p < 0.05) at 6 hours. IL-5 and ECP peaked between 6 and 8 hours and correlated significantly (r = 0.951, p < 0.01) at 6 hours as well. Our data demonstrate that IL-16 and MIP-1 alpha are expressed in the late-phase response in allergic rhinitis in a more or less similar kinetic like IL-5 and ECP. They are suggested to be responsible for the observed influx of eosinophils (IL-5, IL-16, and MIP-1 alpha) and CD4+ T-cells (IL-16 and MIP-1 alpha) into the challenged allergic mucosa.

In patients with polytrauma or major surgery, severe bacterial infections leading to septic shock and multiorgan failure are still a major cause of death. Prevention of septic shock in patients at risk would be an alternative to treatment of patients with overt septic shock. We therefore conducted a trial with the monocyte activator muramyl tripeptide phosphatidylethanolamine (MTP-PE) in an experimental pig model. Liposome encapsulated MTP-PE (50 g/kg of body weight) or liposomes alone were given intravenously at 72 or 24 h before endotoxemia was induced by lipopolysaccharide (LPS), simultaneously with the induction of endotoxin shock, or 1 h thereafter. Pretreatment with MTP-PE at 72 and 24 h before endotoxemia was induced resulted in a reduction of endotoxin shock-induced mortality from 81.8% (9 of 11 animals) in the control group to 8.3% (1 of 12 animals) of the MTP-PE-pretreated animals (P < 0.001). The administration of MTP-PE 24 h before the induction of endotoxin shock was more effective (P < 0.01) than administration of MTP-PE 72 h before endotoxemia was induced (P ‫؍‬ 0.05). The pretreated animals did not develop fever or cardiovascular complications, and pulmonary function was significantly improved. Furthermore, the ␣-form of the soluble CD14 LPS receptor in pig serum showed a marked decrease in LPS-treated animals, and this decrease was reduced by MTP-PE pretreatment at 24 h before endotoxemia was induced. When MTP-PE was given simultaneously with the induction of septic shock or 1 h thereafter, it did not influence either mortality or morbidity. In conclusion, pretreatment of pigs with MTP-PE improves several parameters of endotoxin shock and it reduces mortality. Patients with high risk of developing septic complications might benefit from a pretreatment with this monocyte-activating substance.

Epidemiological and clinical data are discussed dealing with a possible influence of inflammatory changes of the nasal and especially the paranasal tissue on lower airway disease like asthma, the so-called "sinobronchial syndrome". Even though there is clear evidence of an association of the upper with the lower airway diseases, a causal relationship and a possible work of action are still up for discussion. The literature has been reviewed, and different theories are discussed. Generally speaking, a branch of differently accentuated mechanisms seems to play a role.