Safeguarding marine life: conservation of biodiversity and ecosystems

Reviews in Fish Biology and Fisheries - Marine ecosystems and their associated biodiversity sustain life on Earth and hold intrinsic value. Critical marine ecosystem services include maintenance of...     

Phytophthora himalsilva sp. nov. an unusually phenotypically variable species from a remote forest in Nepal

The Himalaya have received little investigation for Phytophthora species. In a remote forest in Western Nepal ten isolates of an unknown Phytophthora were recovered from the rhizosphere of Quercus, Castanopsis, Carpinus and Cupressus spp. The Phytophthora, formally named here as a P. himalsilva sp. nov., is homothallic with either amphigynous or paragynous antheridia and papillate, highly variable sporangia which may also be facultatively caducous. Based on ITS, β-tubulin, and cox I sequences Phytophthora himalsilva falls within Phytophthora Clade 2c together with Phytophthora citrophthora, Phytophthora meadii, Phytophthora colocasiae, and Phytophthora botryosa. It is suggested that Clade 2c has radiated within Asia. Molecular and sporangial characters indicate that P. himalsilva and P. citrophthora may share a recent common ancestor although they have diverged in their breeding systems. Although highly local the P. himalsilva isolates exhibited significant variation in growth rates and optimum temperatures for growth. This may reflect adaptation to different niches within a heterogeneous sub-tropical to temperate forest environment. Their cox I polymorphisms were also rather variable, including possible clustering for subsite. The occurrence of a previously unknown Phytophthora in a remote forest in Nepal highlights once again the plant health risk associated with moving rooted plants and soil between different bio-geographical regions of the world and the need for rapid pathological screening of potential risk organisms.     

Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells: An NF-κB Dependent Mechanism of Th2 Differentiation?

Background

A series of epidemiologic studies have identified the fungus Alternaria as a major risk factor for asthma. The airway epithelium plays a critical role in the pathogenesis of allergic asthma. These reports suggest that activated airway epithelial cells can produce cytokines such as IL-25, TSLP and IL-33 that induce Th2 phenotype. However the epithelium-derived products that mediate the pro-asthma effects of Alternaria are not well characterized. We hypothesized that exposure of the airway epithelium to Alternaria releasing cytokines that can induce Th2 differentiation.

Methodology/Principal Finding

We used ELISA to measure human and mouse cytokines. Alternaria extract (ALT-E) induced rapid release of IL-18, but not IL-4, IL-9, IL-13, IL-25, IL-33, or TSLP from cultured normal human bronchial epithelial cells; and in the BAL fluids of naïve mice after challenge with ALT-E. Both microscopic and FACS indicated that this release was associated with necrosis of epithelial cells. ALT-E induced much greater IL-18 release compared to 19 major outdoor allergens. Culture of naïve CD4 cells with rmIL-18 induced Th2 differentiation in the absence of IL-4 and STAT6, and this effect was abrogated by disrupting NF- κB p50 or with a NEMO binding peptide inhibitor.

Conclusion/Significance

Rapid and specific release of IL-18 from Alternaria-exposed damaged airway epithelial cells can directly initiate Th2 differentiation of naïve CD4⁺ T-cells via a unique NF-κB dependent pathway.     

Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner

Junín virus (JUNV), an arenavirus, is the causative agent of Argentine hemorrhagic fever, an infectious human disease with 15-30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of interferon and cytokines are reported in AHF patients, which might be correlated to the severity of the disease. However the innate immune response to JUNV infection has not been well evaluated. Previous studies have suggested that the virulent strain of JUNV does not induce IFN in human macrophages and monocytes, whereas the attenuated strain of JUNV was found to induce IFN response in murine macrophages via the TLR-2 signaling pathway. In this study, we investigated the interaction between JUNV and IFN pathway in human epithelial cells highly permissive to JUNV infection. We have determined the expression pattern of interferon-stimulated genes (ISGs) and IFN-β at both mRNA and protein levels during JUNV infection. Our results clearly indicate that JUNV infection activates the type I IFN response. STAT1 phosphorylation, a downstream marker of activation of IFN signaling pathway, was readily detected in JUNV infected IFN-competent cells. Our studies also demonstrated for the first time that RIG-I was required for IFN production during JUNV infection. IFN activation was detected during infection by either the virulent or attenuated vaccine strain of JUNV. Curiously, both virus strains were relatively insensitive to human IFN treatment. Our studies collectively indicated that JUNV infection could induce host type I IFN response and provided new insights into the interaction between JUNV and host innate immune system, which might be important in future studies on vaccine development and antiviral treatment.