Neutrophils and Visceral Leishmaniasis: Impact on innate immune response and cross-talks with macrophages and dendritic cells.

Neutrophils with their array of microbicidal activities are the first innate immune cells to guard against infection. They are also most crucial for the host's initial defense against Leishmania parasites which cause clinically diverse diseases ranging from self-healing cutaneous leishmaniasis (CL) to a more severe visceral form, visceral leishmaniasis (VL). Neutrophils are recruited in large numbers at the infection site after bite of sandfly, which is the vector for the disease. The initial interaction of neutrophils with the parasites may modulate the subsequent innate and adaptive immune responses and hence affect the disease outcome. The purpose of this review is to comprehensively appraise the role of neutrophils during the early stages of Leishmania infection with a focus on the visceral form of the disease. In the past decade, new insights regarding the role of neutrophils in VL have surfaced which have been extensively elaborated in the present review. In addition, since much of the information regarding neutrophil-Leishmania early interaction has accumulated through studies on mouse models of CL, these studies are also revisited. We begin by reviewing the factors which drive the recruitment of neutrophils at the site of injection by the sandfly. We then discuss the studies delineating the molecular mechanisms involved in the uptake of the Leishmania parasite by neutrophils and how the parasite subverts their microbicidal functions. In the end, the interaction of infected neutrophils with macrophages and dendritic cells is summarized.

Muller glia in retinal innate immunity: a perspective on their roles in endophthalmitis.

Muller cells are the predominant glial cell type in the retina and have a unique anatomy, with processes that span the entire retinal thickness. Although extensive morphological and physiological studies of Muller glia have been performed, much less is known about their role in retinal innate immunity, specifically in infectious endophthalmitis. They were found to express toll-like receptors (TLRs), a major family of pattern recognition receptors that mediate innate responses and provide an important mechanism by which Muller glia are able to sense both pathogen- and host-derived ligands in the vitreous and the retina. An increasing body of evidence suggests that TLR-signaling mediates beneficial effects in the retina via production of proinflammatory cytokines/chemokines, antimicrobial peptides, and neuroprotective growth factors to restore tissue homeostasis. In this review, we discussed retinal innate immunity in general with emphasis on the role of Muller glia in initiating retinal innate defense.

Targeting toll-like receptor signaling as a novel approach to prevent ocular infectious diseases.

Toll-like receptors (TLRs) play a key role in the innate immune response to invading pathogens. Thus, their discovery has opened up a wide range of therapeutic possibilities for various infectious and inflammatory diseases. In the last several years, extensive research efforts have provided a considerable wealth of information on the expression and function of TLRs in the eye, with significant implications for better understanding of pathogenesis of infectious eye diseases affecting the cornea, uvea, and the retina. In this review, by using bacterial keratitis and endophthalmitis as examples, we discuss the possibilities of targeting TLR signaling for the prevention or treatment of ocular infectious diseases.

APOB gene signal peptide deletion polymorphism is not associated with infertility in Indian men.

Apolipoprotein B (APOB) plays a key role in lipoprotein metabolism and plasma lipid transport. It has been shown that about two-thirds of male mice heterozygous for ApoB were infertile. Moreover, a 3-codon deletion polymorphism (rs11279109) in the signal peptide region of the APOB gene has been shown to be a risk factor for infertility in Slovenian men, but its association with infertility in Indian men has not been evaluated to date. Hence, in the present study, we have genotyped this polymorphism in 545 Indian men, including 294 infertile and 251 fertile men. Our results show that the distribution of this deletion polymorphism was consistent with the Hardy-Weinberg equilibrium in both infertile and fertile men. No statistically significant difference was observed in the distribution of the APOB signal peptide deletion polymorphism between infertile and fertile men (chi(2) = 0.156, P = .925 for genotypes; chi(2) = 0.015, P = .903 for alleles). Moreover, no significant difference was observed when infertile and fertile men were categorized on the basis of presence (D/D and D/W genotypes) or absence (W/W genotypes) of deletion (odds ratio, 0.955; 95% confidence interval, 0.644-01.418; P = .820). Our study concludes that the APOB gene deletion polymorphism is not a risk factor for the development of infertility in Indian men.