Extracts of different pollen species and their effect on human tear fluid and an epithelial cell line

Purpose: Hazelnut and birch pollen are known to destroy tear film components and attack ocular surface cells. We investigated further pollen species from different plant families, whether they show similar effects on human tear fluid and an epithelial cell line in vitro, to provide a broad basis for further research on pollen reactions affecting the tear film and ocular surface.

Materials and methods: Regional pollen species from different plant families (Adoxaceae, Betulaceae, Fagaceae, Juglandaceae, Malvaceae, Oleaceae, Pinaceae, Plantaginaceae, Poaceae, Salicaceae, Sapindaceae) were collected. Their proteolytic activity was evaluated by Zymography. Human tear fluid and cells of an epithelial cell line were incubated with pollen extracts. Tear fluid was analyzed by Polyacrylamide gel electrophoresis (PAGE). Cytomorphology was assessed microscopically and cell viability by proliferation (MTS), water-soluble tetrazolium (WST-1) assay and the impedance-based xCELLigence real-time analysis (RTCA).

Results: Zymography revealed significant protease activity and PAGE showed the degradation of tear proteins by different pollen species. Cells incubated with pollen extracts presented dose- and time-dependent cytomorphological changes. MTS, WST-1, and RTCA revealed cytostatic as well as cytotoxic effects of pollen extracts.

Conclusions: Pollen species from different plant families exert proteolytic activity and degrade human tear fluid as well as epithelial cells, which may play a crucial role in the pathogenesis of allergic and non-allergic reactions affecting the ocular surface.     

The awareness of the scared - context dependent influence of oxytocin on brain function

Brain Imaging and Behavior - Oxytocin is both a hormone and a neurotransmitter and has been originally recognized for its role in childbirth and lactation. Later, it became widely known as a...     

Reconstruction of the temporal contour for traumatic tissue loss using a CAD/CAM-prefabricated titanium implant-case report

INTRODUCTION: A 16-year-old Arab boy had suffered from a severe head injury including an intracranial haematoma. Despite replantation of the bone flap later on, the cosmetic result was very unfavourable due to partial resorption of the reinserted bone and atrophy of the right temporalis muscle. AIM: For contour reconstruction of both soft and hard tissues the boy was transferred from Saudi Arabia. METHOD: A spiral CT was obtained and the contour was reconstructed using a new algorithm for surface generation. RESULT: The resulting titanium implant was inserted without complications or the need for revision. The cosmetic result was good and corresponded to the preoperative digital planning. CONCLUSION: Techniques of computer-assisted implant prefabrication and surgery may include special algorithms for considering soft tissues including contour deficits of the temporalis muscle.     

IL-1β induces expression of costimulatory molecules and cytokines but not immune feedback regulators in dendritic cells

Dendritic cells play an important role in the initiation of immune reactions. Due to their high capacity to prime T-cell responses, the activation of dendritic cells must be tightly controlled. Because Interleukin-1β (IL-1β) is a key player in autoinflammatory diseases, we compared the ability of IL-1β to activate human dendritic cells and induce immune-regulatory molecules versus the effects induced by pathogen-derived stimuli.Upon activation with either IL-1β or microbial stimuli, monocyte-derived dendritic cells showed enhanced expression of costimulatory molecules, increased secretion of chemokines and cytokines, and the ability to activate T cells. In contrast, immune-feedback molecules, including PD-L1, IL-1RA, IL-10 and SOCS1, were exclusively upregulated in response to microbial stimuli, whereas IL-1β treatment had no inducing effect on them. Thus, the limited capacity of IL-1β to induce potential feedback inhibitors may support its key etiologic role in chronic inflammation and autoinflammatory responses.