β-glucans are well-known modulators of the immune system in mammals but little is known about β-glucan triggered immunity in planta. Here we show by isothermal titration calorimetry, circular dichroism spectroscopy and nuclear magnetic resonance spectroscopy that the FGB1 gene from the root endophyte Piriformospora indica encodes for a secreted fungal-specific β-glucan-binding lectin with dual function. This lectin has the potential to both alter fungal cell wall composition and properties, and to efficiently suppress β-glucan-triggered immunity in different plant hosts, such as Arabidopsis, barley and Nicotiana benthamiana. Our results hint at the existence of fungal effectors that deregulate innate sensing of β-glucan in plants.

Summary In the root endophyte Serendipita indica, several lectin‐like members of the expanded multigene family of WSC proteins are transcriptionally induced in planta and are potentially involved in β‐glucan remodeling at the fungal cell wall. Using biochemical and cytological approaches we show that one of these lectins, SiWSC3 with three WSC domains, is an integral fungal cell wall component that binds to long‐chain β1‐3‐glucan but has no affinity for shorter β1‐3‐ or β1‐6‐linked glucose oligomers. Comparative analysis with the previously identified β‐glucan‐binding lectin SiFGB1 demonstrated that whereas SiWSC3 does not require β1‐6‐linked glucose for efficient binding to branched β1‐3‐glucan, SiFGB1 does. In contrast to SiFGB1, the multivalent SiWSC3 lectin can efficiently agglutinate fungal cells and is additionally induced during fungus–fungus confrontation, suggesting different functions for these two β‐glucan‐binding lectins. Our results highlight the importance of the β‐glucan cell wall component in plant–fungus interactions and the potential of β‐glucan‐binding lectins as specific detection tools for fungi in vivo.

Since the bacterial ability to develop resistance against various factors of their surroundings is a well-known phenomenon, resistance against iodine and specifically against povidone-iodine (PVP-I) has been widely investigated. Yet there is little known about bacterial resistance in long-term daily use of disinfectants in continuous ambulatory peritoneal dialysis (CAPD) patients. The aim of our study was to investigate whether on daily use of PVP-I over a period of at least 6 months coagulase-negative staphylococci (CNS) – the predominant infective organisms of peritonitis – developed resistance against PVP-I. At the catheter exit site of 40 CAPD patients we isolated 36 CNS. 23 CNS (CNS + PVP) orginate from patients using PVP-I, 13 CNS (CNS + Cl) from patients using sodium hypochlorite (NaOC1) as disinfectant. The strains were biotyped, antibiotic resistance patterns were determined and resistance against PVP-I or NaOC1 was calculated as reduction factor using the quantitative suspension test combined with a turbidimetric standardization. Resistance against PVP-I 0.01% and against NaOC1 0.005% was determined at two contact times (30 and 300 s) for each patient group. In addition, we investigated the effects of plasmid loss on sensitivity to PVP-I. Out of 5 multiple-antibiotic-resistant CNS, 3 strains showed no difference in reduction factor against PVP-I before and after curing. There was no significant difference in reduction factor against NaOC1. CNS + PVP were even significantly more sensitive to PVP-I than CNS + C1. Taken together, our results demonstrate that long-term use of PVP-I does not cause any bacterial resistance in CNS of CAPD patients.