Mutualisms are often viewed as reciprocal exploitations that nonetheless provide net benefits to each partner. While the benefits of symbiosis with dinoflagellates of the genus Symbiodinium (zooxanthellae) for corals are well understood, the costs of the association, particularly when under stress, remain a focus of much research. One of the primary impediments to exploring the costs of symbiosis in zooxanthellate corals is that it is impossible to examine the animal host in isolation. Evidence for a cost of symbiosis with zooxanthellae includes the fact that direct transmission of zooxanthellae between generations is rare, particularly in broadcast spawning corals. Fortuitously, the absence of zooxanthellae in oocytes of many species and the ability to readily infect larvae with zooxanthellae provide an opportunity to compare individuals with and without these symbionts. Here, we use this larval model to show that individuals with zooxanthellae have lower survival than those lacking zooxanthellae when exposed to high temperature. Higher activity of anti-oxidant defenses and higher levels of oxidative cellular damage in larvae with zooxanthellae suggest that oxidative stress originating in the symbionts is a cause of tissue damage in the host under heat stress. We hypothesize that this may be one reason for the absence of direct transmission of zooxanthellae in most broadcast spawning corals whose propagules must spend at least 1 d on the ocean surface.
Chronic rhinosinusitis (CRS) is presently classified into two subgroups: CRS without and CRS with nasal polyps. A variety of inflammatory mediators, including cytokines and chemokines, as well as adhesion molecules and matrix metalloproteinases, are upregulated in both subgroups of CRS; remodeling is also observed in both. However, there are also characteristic differences. Whereas CRS without nasal polyps has more neutrophilic infiltration, in CRS with nasal polyps (especially when associated with allergy/asthma) eosinophil infiltration is strikingly increased. Although several features of remodeling (eg, squamous metaplasia, basement membrane thickening, collagen deposition, hyperplasia of mucous glands, and goblet cells) are features seen in both subgroups of CRS, epithelial shedding as observed in asthma is not seen in either subgroup. Furthermore, pseudocyst formation seen in CRS with nasal polyps is not seen in CRS without nasal polyps.
Systemic lupus erythematosus (SLE) is associated with the presence of complement proteins and immune complexes in affected organs. Since complement proteins are synthesized in hepatic and extrahepatic sites, we studied a murine model of SLE to ascertain the relative importance of local and humoral (liver) synthesis of complement. C3, C4, and C2 mRNA increase in kidney coincident with the development of nephritis in the MRL lpr/lpr mouse, a strain that spontaneously develops SLE. Two factor B messenger RNA transcripts are expressed in kidney and intestine; SLE nephritis is associated with decrease in the long factor B mKNA and increase in the short form. Increased local synthesis of C3 and I1 protein and a concomitant glomerular and renal interstitial macrophage infiltrate paralleled the increase in mRNA content in the (lpr/ lpr) mice. In addition to kidney, an increase in C3, C4, C2 and factor B mRNA was noted in the lung, heart and intestine and to a lesser extent in liver of (Ipr/lpr) in comparison to the MRL (+/+) animals.These results suggest that in SLE local expression of complement genes plays a role in the pathogenesis of chronic glomerulonephritis and in the autoimmune arteritis of other organs.
PurposeNasal polyposis is a chronic inflammatory disease of the upper airways often associated with asthma and characterized by markedly increased numbers of eosinophils, Th2 type lymphocytes, fibroblasts, goblet cells and mast cells. Previous studies have shown elevated levels of thymic stromal lymphopoietin (TSLP) in atopic diseases like asthma, atopic dermatitis and mainly in animal models of allergic rhinitis (AR). Here, we investigated the expression of TSLP in nasal polyps from atopics and non-atopics in comparison with the nasal mucosa and its potential role in nasal polyposis.MethodsMessenger RNA expression for TSLP, thymus and activation-regulated chemokine (TARC) and macrophage derived chemokine (MDC) in nasal polyps and nasal mucosa of atopics and non-atopics was analyzed by real time PCR. Immunoreactivity for TSLP in nasal polyps and in the nasal mucosa of patients with AR and non-allergic rhinitis (NAR) was analyzed by immunohistochemistry. Eosinophil counts was analyzed by Wright-Giemsa staining and nasal polyp tissue IgE, by ELISA.ResultsMessenger RNA expression for TSLP,TARC and MDC was markedly higher in nasal polyps as compared to the allergic nasal mucosa. Immunoreactivity for TSLP was detected in epithelial cells, endothelial cells, fibroblasts and inflammatory cells of the nasal mucosa and nasal polyps. The number of TSLP+ cells was significantly greater in the nasal mucosa of AR than NAR patients. The number of TSLP+ cells in nasal polyps from atopics was significantly greater than that of non-atopics and that in the allergic nasal mucosa. The number of TSLP+ cells correlated well with the number of eosinophils and the levels of IgE in nasal polyps.ConclusionsThe high expression of TSLP in nasal polyps and its strong correlation to eosinophils and IgE suggest a potential role for TSLP in the pathogenesis of nasal polyps by regulating the Th2 type and eosinophilic inflammation.
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