Showing papers by "Anna Krasnodembskaya published in 2014"
TL;DR: The study showed that arenicins are found in different body compartments responsible for providing a first line of defense against infections, which implies their important role as key components of both epithelial and systemic branches of host defense.
Abstract: Immune responses of invertebrate animals are mediated through innate mechanisms, among which production of antimicrobial peptides play an important role. Although evolutionary Polychaetes represent an interesting group closely related to a putative common ancestor of other coelomates, their immune mechanisms still remain scarcely investigated. Previously our group has identified arenicins - new antimicrobial peptides of the lugworm Arenicola marina, since then these peptides were thoroughly characterized in terms of their structure and inhibitory potential. In the present study we addressed the question of the physiological functions of arenicins in the lugworm body. Using molecular and immunocytochemical methods we demonstrated that arencins are expressed in the wide range of the lugworm tissues - coelomocytes, body wall, extravasal tissue and the gut. The expression of arenicins is constitutive and does not depend on stimulation of various infectious stimuli. Most intensively arenicins are produced by mature coelomocytes where they function as killing agents inside the phagolysosome. In the gut and the body wall epithelia arenicins are released from producing cells via secretion as they are found both inside the epithelial cells and in the contents of the cuticle. Collectively our study showed that arenicins are found in different body compartments responsible for providing a first line of defence against infections, which implies their important role as key components of both epithelial and systemic branches of host defence.
24 citations
Journal Article•
TL;DR: Bone marrow-derived hMSCs transform the phenotype and functional properties of alveolar macrophages towards a less inflammatory state and simultaneously enhance bacterial phagocytosis as mentioned in this paper.
Abstract: Background: Acute Respiratory Distress Syndrome (ARDS) is characterized by dysregulated pulmonary inflammation. Macrophages are key cellular mediators of the lung immune response. Macrophages can be polarized towards an M1 (implicated in driving inflammation) or an M2 (responsible for the resolution) phenotype. We have previously reported that MSC treatment is protective in several models of ARDS. Aims: The current studies were undertaken to test if human bone-marrow derived MSCs have a role in polarizing alveolar macrophages (AM) towards an M2 phenotype in vivo and in vitro . Methods : In vivo studies were performed using mouse model of E.coli pneumonia. For in vitro studies MSC and AM were co-cultured without cell contact. Cytokine levels were measured by ELISA. Expression of cell surface markers and phagocytic activity were assessed by Flow Cytometry. Results: In the in vivo model of E.coli pneumonia, hMSC treatment demonstrated reduction in the severity of lung injury, improved bacterial clearance and reduced TNF-α levels in the BAL 24 h after infection, compare to non-treated animals. hMSC administration was associated with significant up-regulation of CD206 and CD71 (markers of M2) on AM. In addition, in vitro co-culture with hMSC markedly decreased LPS-induced TNF-α secretion by mouse AM, up-regulated their expression of CD206 and enhanced their phagocytic activity towards bacteria. Conclusions: Bone marrow-derived hMSCs transform the phenotype and functional properties of AM. hMSCs drive the polarization of macrophages towards a less inflammatory state and simultaneously enhance bacterial phagocytosis. These data provide further rationale for clinical trials of hMSC in ARDS.
6 citations
Journal Article•
1 citations
TL;DR: Patients on aspirin therapy prior to hospital admission had a reduced incidence of ARDS and by acetylating cyclooxygenase, aspirin inhibits platelet aggregation and generates anti-inflammatory molecules which modulate neutrophilic inflammation.
Abstract: Acute respiratory distress syndrome (ARDS) is characterized by damage to the alveolar epithelial-endothelial barrier resulting in neutrophil influx and pulmonary oedema. The activation of platelet and secondary capture of neutrophils may play an important role in propagation of inflammation in ARDS [1]. Various animal studies have shown that aspirin therapy reduces pulmonary oedema and development of lung injury [2]. In observational studies, patients on aspirin therapy prior to hospital admission had a reduced incidence of ARDS [3]. By acetylating cyclooxygenase, aspirin inhibits platelet aggregation and generates anti-inflammatory molecules which modulate neutrophilic inflammation [4].