Influenza-derived peptides cross-react with allergens and provide asthma protection.

Background: The hygiene hypothesis is the leading concept to explain the current asthma epidemic, which is built on the observation that a lack of bacterial contact early in life induces allergic T2 immune responses.

Objective: Because little is known about the contribution of respiratory tract viruses in this context, we evaluated the effect of prior influenza infection on the development of allergic asthma.

Methods: Mice were infected with influenza and, once recovered, subjected to an ovalbumin- or house dust mite-induced experimental asthma protocol.

Phenotypical and functional characterization of alveolar macrophage subpopulations in the lungs of NO2-exposed rats.

Background: Alveolar macrophages (AM) are known to play an important role in the regulation of inflammatory reactions in the lung, e.g. during the development of chronic lung diseases.

CD14 is required for influenza A virus-induced cytokine and chemokine production.

Infection of monocytes and macrophages by influenza A virus leads to proinflammatory and chemotactic cytokine production. The signalling pathways linking innate immune virus recognition to cytokine expression are little understood. Here, we report that blocking of CD14 on human monocytes by specific antibody or use of CD14-deficient murine macrophages abolished influenza A virus-induced cytokine production.

Impaired superoxide radical production by bronchoalveolar lavage cells from NO(2)-exposed rats.

Production of superoxide radicals is a central property of professional phagocytes used to combat invading microorganisms. Even though the number of macrophages and neutrophils is often increased in the lungs of patients with chronic lung diseases, these patients frequently suffer from bacterially induced exacerbations. To understand the underlying mechanisms, we investigated the production of superoxide radicals by bronchoalveolar lavage (BAL) cells in a rat NO(2) exposure model (10 ppm NO(2) for 1, 3, or 20 days).

Smooth and rough lipopolysaccharide phenotypes of Brucella induce different intracellular trafficking and cytokine/chemokine release in human monocytes.

Virulence of the intracellular pathogen Brucella for humans is mainly associated with its lipopolysaccharide (LPS) phenotype, with smooth LPS phenotypes generally being virulent and rough ones not. The reason for this association is not quite understood. We now demonstrate by flow cytometry, electron microscopy, and ELISA that human peripheral blood monocytes interact both quantitatively and qualitatively different with smooth and rough Brucella organisms in vitro.

Chemokine receptor expression and chemotactic responsiveness of human monocytes after influenza A virus infection.

Chemokines and their receptors play an important role in site-directed migration and activation of leukocytes. To understand how viral infections may impair this function, we analyzed chemokine receptor expression and responsiveness of human monocytes after infection with influenza A virus. Whereas treatment with infectious virus induced a rapid down-regulation of the CCL2/monocyte chemoattractant protein-1 (MCP-1)-specific receptor CCR2, inactivated virus did not significantly alter CCR2 surface expression.

Induction of epidermal fatty acid binding protein in intravascular monocytes of renal allografts.

During acute rejection of rat renal allografts, numerous activated monocytes accumulate in the vasculature of the graft. These monocytes seem to be involved in allograft destruction. Proinflammatory and effector functions of monocytes and macrophages can be down-regulated by peroxisome proliferators, which are probably transported in the cytoplasm by fatty acid binding proteins (FABPs).

Shift toward an alternatively activated macrophage response in lungs of NO2-exposed rats.

Inflammatory mechanisms are thought to play an important role in the pathogenesis of acute and chronic obstructive pulmonary diseases. In a rat inhalation model using continuous exposure to 10 ppm nitrogen dioxide for 1, 3, and 20 d, we investigated the inflammatory response with particular focus on the activation state of alveolar macrophages. Whereas the number of inflammatory cells and total protein concentration were increased in the bronchoalveolar lavage (BAL), the amount of the proinflammatory cytokine tumor necrosis factor-alpha was markedly reduced with increasing exposure time.

Up-regulation of macrophage migration inhibitory factor gene and protein expression in glial tumor cells during hypoxic and hypoglycemic stress indicates a critical role for angiogenesis in glioblastoma multiforme.

Glioblastoma multiforme (GBM) is the most malignant variant of human glial tumors. A prominent feature of this tumor is the occurrence of necrosis and vascular proliferation. The regulation of glial neovascularization is still poorly understood and the characterization of factors involved in this process is of major clinical interest.

Release of macrophage migration inhibitory factor and CXCL8/interleukin-8 from lung epithelial cells rendered necrotic by influenza A virus infection.

Bronchiolar epithelial cells are the prime targets for influenza A virus infection. It still remains to be clarified which signals are generated from these cells to initiate an immune response. Among chemokines, viral infection of primary lung epithelial cells triggered exclusively the release of CXCL8/interleukin-8 (IL-8), which contrasts with our previous observation that influenza A virus induced in monocytes the expression of mononuclear-leukocyte-attracting chemokines and even suppressed the production of neutrophil-attracting chemokines.

IL-24 is expressed by rat and human macrophages.

Recently, a number of interleukin-10 (IL-10) homologues, among them IL-24 formerly known as melanocyte differentiation factor-7 (mda-7), has been described. Since IL-10 is released by macrophages and plays an important role in the resolution of inflammatory processes, we hypothesized that IL-24 might also be expressed in cells of the monocyte/macrophage lineage. We analyzed IL-24 expression on the mRNA and protein level in stimulated rat and human macrophages.

Long term iNOS expression in thoracic lymph nodes of silicotic rats.

Beside the lung, thoracic lymph nodes are most affected during silicosis. The mechanisms leading to enlargement of the lymph nodes and partial activation of lymph node cells are still unclear. The present study demonstrates an increase in iNOS mRNA expression in the lung draining lymph nodes of rats at 1, 2, and 8 months following silica exposure.

Human cytomegalovirus-mediated induction of MIF in fibroblasts.

Human cytomegalovirus (HCMV) infection of fibroblasts induces the proinflammatory mediator macrophage migration inhibitory factor (MIF). Our in vitro experiments show that active HCMV infection alone is required to induce an early and sustained induction of MIF mRNA and protein production. Unlike in other infection models, in which MIF has been described to be released from preformed stores, our data conclusively show that HCMV infection triggers de novo synthesis and subsequent secretion of MIF.

Borna disease virus-induced accumulation of macrophage migration inhibitory factor in rat brain astrocytes is associated with inhibition of macrophage infiltration.

To test the hypothesis that macrophage migration inhibitory factor (MIF) plays a role in macrophage invasion during virus-induced encephalitis, we analyzed the expression and cellular localization of MIF in the Borna disease virus (BDV)-infected rat brain, monitored monocyte/macrophage infiltration, and evaluated the influence of anti-inflammatory treatment with dexamethasone. MIF mRNA expression was restricted to neurons and remained unchanged after BDV infection or after dexamethasone treatment of either BDV-infected or uninfected control rats. In contrast, MIF protein immunoreactivity (ir) was not only seen in neurons but also in glia.