Biological Functions of the Novel Collectins CL-L1, CL-K1, and CL-P1

Collectins are characterized by a collagen-like sequence and a carbohydrate recognition domain and are members of the vertebrate C-type lectin superfamily. Recently, “novel collectins”, different from “classical collectins” consisting of mannan-binding lectin (MBL) and surfactant proteins A and D (SP-A and SP-D), have been found by reverse genetics. These “novel collectins” consist of collectin liver 1 (CL-L1), collectin kidney 1 (CL-K1), and collectin placenta 1 (CL-P1) and are encoded by three separate genes. Experimental findings on human and animal collectins have shown that both novel collectins and classical collectins play an important role in innate immunity. Based on our recent results and those of others, in this paper, we summarize the new biological functions of these novel collectins in embryonic morphogenesis and development

Quinolone Resistance in Non-typhoidal Salmonella

Non‐typhoidal Salmonella is the primary foodborne zoonotic agent of salmonellosis in many countries. Non‐typhoidal Salmonella infections are transmitted to humans primarily through consumption of contaminated foods from animal origin, whereas S. Typhi and Paratyphi infections are spread directly or indirectly by contact with an infected person. Quinolones exhibit potent antibacterial activity against Salmonella and are usually the first choice of treatment for life‐threatening salmonellosis due to multidrug‐resistant strains. However, by the early 1990s, quinolones have been approved for use in food‐producing animals. The increased use of this group of antimicrobials in animal has led to the concomitant emergence of quinolone‐resistant non‐typhoidal Salmonella strains. However, in some countries, there are no legal provisions, which apply to veterinary drugs. This situation provides favorable conditions for spread and persistence of quinolone‐resistant bacteria in food‐producing animals. The objective of this chapter is to review the current regulatory controls for the use of quinolones in food‐producing animals, its effect on development of quinolone resistance, and the potential impact on human and animal health. Moreover, this chapter reviews the current knowledge of quinolone resistance mechanisms and the future directions of research with particular attention to the strategies to control the emergence of quinolone‐resistant Salmonella

Different Pathological Roles of Toll-Like Receptor 9 on Mucosal B Cells and Dendritic Cells in Murine IgA Nephropathy

Although pathogenesis of IgA nephropathy (IgAN) is still obscure, pathological contribution of mucosal immunity including production of nephritogenic IgA and IgA immune complex (IC) has been discussed. We have reported that mucosal toll-like receptor (TLR)-9 is involved in the pathogenesis of human and murine IgAN. However, cell-type expressing TLR9 in mucosa remains unclear. To address this, we nasally challenged cell-specific CpG DNA ((i): dendritic cell: (DC), (ii): B cell, (iii): both), known as ligand for TLR9, to IgAN prone mice and analyzed disease phenotype of each group. After 8 times of the weekly administration, every group showed deterioration of glomerular damage. However, CpG-A-group showed clear extension of mesangial proliferative lesions with increase of serum IgA-IgG2a IC and its glomerular depositions, while CpG-B-group showed extent of glomerular sclerotic lesions with increase of serum and glomerular IgA and M2 macrophage infiltration. Present results indicate that mucosal TLR9 on B cells and DC may differently contribute to the progression of this disease via induction of nephritogenic IgA or IgA-IgG IC, respectively. This picture is suggestive for the pathological difference between child and adult IgAN

Analysis and Application of Decaying Turbulence with Initial Fractal Geometry

In this paper, we address high‐Schmidt‐number (Sc) scalar turbulent mixing that results from grid‐generated turbulence using the initial fractal geometry of the velocity profile. More specifically, as was proposed in our recent study, we adopt an initial flow field generated by a fractal grid and apply it to a water channel experiment based on a high‐Sc‐number scalar‐mixing layer in order to create grid‐generated turbulence, and thus solve our current research problem. The high‐Sc‐number scalar and velocity fields of the grid‐generated turbulence are then measured using planar laser‐induced fluorescence (PLIF) and particle image velocimetry (PIV), respectively. By means of fractal analysis, this study specifically addresses the turbulent mixing phenomena in which the fractal dimension of the mixing interface of an observed high‐Sc‐number scalar field is calculated. Additionally, we discuss the efficiency of using fractal grids as devices for enhancing high‐Sc‐number scalar turbulent mixing by observing turbulent intensities and dissipation by PIV

Pathological Role of Tonsillar B Cells in IgA Nephropathy

Although impaired immune regulation along the mucosa-bone marrow axis has been postulated to play an important role, the pathogenesis of IgA nephropathy (IgAN) is unknown; thus, no disease-specific therapy for this disease exists. The therapeutic efficacy of tonsillectomy or tonsillectomy in combination with steroid pulse therapy for IgAN has been discussed. Although randomized control trials for these therapies are ongoing in Japan, the scientific rationale for these therapies remains obscure. It is now widely accepted that abnormally glycosylated IgA1 and its related immune complex (IC) are probably key molecules for the pathogenesis, and are thus considered possible noninvasive biomarkers for this disease. Emerging evidence indicates that B cells in mucosal infections, particularly in tonsillitis, may produce the nephritogenic IgA. In this paper, we briefly summarize characteristics of the nephritogenic IgA/IgA IC, responsible B cells, and underlying mechanisms. This clinical and experimental information may provide important clues for a therapeutic rationale