Marine Tourism Development in the Arkhangelsk Region, Russian Arctic : Stakeholder’s Perspectives

Author's accepted version (postprint).This is an Accepted Manuscript of an article published by Springer in Springer Polar Sciences on (07/03/2020).Available online: https://link.springer.com/chapter/10.1007%2F978-3-030-28404-6_17acceptedVersio

REGULATION OF IMMUNE RESPONSE AGAINST MYCOBACTERIUM TUBERCULOSIS BY THE POPULATION OF REGULATORY DENDRITIC CELLS

On the background of a high level of genetic susceptibility to tuberculosis infection (TB), granulomatous reactions in the lung  tissue fail to effectively isolate infection foci and rather result in  diffuse pathology, confluence of granulomata and  formation of  necrotic zones. Uncontrolled inflammation severely affect breathing  function of the lung. Thus, effective disease control requires a good  balance between protective and pathogenic immune responses.  Immature regulatory dendritic cells (DCreg) and regulatory T  lymphocytes (Treg) represent a pool of important cellular regulators  of inflammation. Earlier we have demonstrated that stromal lung  cells support development of CD11b+CD11clowCD103– DCreg from  their bone marrowderived precursors in in vitro cultures. In addition,  significantly larger population size and more rapid  development of the lung CD4+Foxp3+ Treg cells characterize TB- resistant B6 mice compare to their TB-susceptible I/St counterparts.  Here, we report that adoptive transfer of DCreg cells into TB-infected I/St mice is capable to enlarge the population of Treg cells in the  lungs. This, in turn, attenuates lung pathology, decreases  mycobacterial multiplication and diminishes lung infiltration with  neutrophils, i.e., selectively restricts the population of cell largely  responsible for TB pathogenesis. The key difference in lung  pathology between DCreg recipients and control animals was the  lack of tissue-destructive foci and necrotic zones in the former  group. Meanwhile, the groups of mice did not differ in production of  regulatory (IL-10 and TGF-β) and key inflammatory (IFNγ and IL-6)  cytokines by lung cells. The latter result suggests that contact rather  than secretory mechanisms underlie moderate attenuation of  the TB process in the lungs of mice with an elevated lung Treg level,  given that plethora of such mechanisms were described for Treg  functioning. Although therapeutic effects were relatively weak, our  results indicate that cell therapy approaches are applicable to  regulation of lung tissue inflammation during TB course

A role for the pattern recognition receptor Nod2 in promoting recruitment of CD103+ dendritic cells in the colon in response to Trichuis muris infection

The ability of the colon to generate an immune response to pathogens, such as the model pathogen Trichuris muris, is a fundamental and critical defense mechanism. Resistance to T. muris infection is associated with the rapid recruitment of dendritic cells (DCs) to the colonic epithelium via epithelial chemokine production. However, the epithelial–pathogen interactions that drive chemokine production are not known. We addressed the role of the cytosolic pattern recognition receptor Nod2. In response to infection, there was a rapid influx of CD103+CD11c+ DCs into the colonic epithelium in wild-type(WT)mice, where as this was absent in Nod2−/− animals. In vitro chemotaxis assays and in vivo experiments using bone marrow chimeras of WT mice reconstituted with Nod2−/− bone marrow and infected with T. muris demonstrated that the migratory function of Nod2−/− DCs was normal. Investigation of colonic epithelial cell (CEC) innate responses revealed a significant reduction in epithelial production of the chemokines CCL2 and CCL5 but not CCL20 by Nod2-deficient CECs. Collectively, these data demonstrate the importance of Nod2 in CEC responses to infection and the requirement for functional Nod2 in initiating host epithelial chemokine-mediated responses and subsequent DC recruitment and T-cell responses following infection