ABO blood group antigens may be associated with increased susceptibility to schistosomiasis: a systematic review and meta-analysis.

Schistosomiasis or bilharzia is a widespread parasitic disease caused by blood flukes of the genus Schistosoma. Some factors have been investigated previously regarding their effect on the pathophysiological mechanism of human schistosomiasis, but the possible influence of the ABO blood group on the severity of Schistosoma infection has been the most promising. Hence, we performed a systematic review and meta-analysis to further investigate the association of the ABO blood group with schistosomiasis susceptibility. Selected publications were retrieved from PubMed up to 21 August 2018, for related studies written in English. Number of cases (with schistosomiasis) and controls (without schistosomiasis) were extracted across all ABO blood types. Odds ratios (OR) and 95% confidence intervals (CI) were computed, pooled and interpreted. Subgroup analysis by the species of Schistosoma infecting the population and the participants' ethnicity was also performed. The overall analysis revealed heterogeneity in the outcomes, which warranted the identification of the cause using the Galbraith plot. Post-outlier outcomes of the pooled ORs show that individuals who are not blood type O are more susceptible (OR: 1.40; 95% CI: 1.17-1.67; PA < 0.001) to schistosomiasis than those who are blood type O (OR: 0.71; 95% CI: 0.60-0.85; PA < 0.001). Subgroup analysis yielded the same observations regardless of the species of schistosome and the ethnicity of the participants. Results of this meta-analysis suggest that individuals who are blood type B and A are more susceptible to schistosomiasis than those who are blood type O. However, more studies are needed to confirm our claims.

Expression of the innate defense receptor S5D-SRCRB in the urogenital tract.

S5D-SRCRB is a novel mouse secretory glycoprotein belonging to the ancient and highly conserved scavenger receptor cysteine-rich superfamily of protein receptors. Available evidence indicates that S5D-SRCRB interacts with conserved microbial cell wall components, as well as with some endogenous proteins, and presents a restricted tissue expression pattern. This study further analyzes the expression of S5D-SRCRB along the mouse urogenital tract. Immunohistochemical staining for S5D-SRCRB was observed in spermatocytes from seminiferous tubules and in the epithelial surface from urethra and bladder, as well as in kidney tubules, mainly from medulla and papilla. Double stainings showed that S5D-SRCRB is expressed in both principal (P) and intercalated (IC) cells from renal collecting ducts (CD). By using an in vitro cell model of IC cell differentiation, preferential expression of S5D-SRCRB was observed in the apical border of terminally differentiated IC. Colocalization of S5D-SRCRB with galectin-3 (Gal-3) was also observed in kidney and bladder, but not in testis, supporting concurrent biochemical studies demonstrating the carbohydrate-dependent interaction of Gal-3 and S5D-SRCRB. Furthermore, upregulation of S5D-SRCRB expression was observed in in vitro and in vivo models of bacterial aggression, reinforcing the emerging view that CD, and specially IC, are important players in innate defense of the urinary tract against infection. Taken together, the results indicate that S5D-SRCRB is an integral component of the urogenital tract involved in innate immune functions.

Neutrophil gelatinase-associated lipocalin: pathophysiology and clinical applications.

Neutrophil gelatinase-associated lipocalin (NGAL), a 25 kDa protein produced by injured nephron epithelia, is one of the most promising new markers of renal epithelial injury. In contrast to serum creatinine and urinary output, which are the measures of kidney function, NGAL is specifically induced in the damaged nephron and then released into blood and urine, where it can be readily measured. Careful proof-of-concept studies using defined animal models have uncovered the sources and trafficking of NGAL in acute kidney injury (AKI) and have addressed the contributions of renal and non-renal sources. Clinical studies indicate that NGAL, unlike creatinine, is a marker responsive to tissue stress and nephron injury, but less so to adaptive hemodynamic responses. In certain clinical settings, NGAL is an earlier marker compared with serum creatinine. In addition, clinical studies have shown that NGAL is a powerful predictor of poor clinical outcomes, which can be used to risk stratify patients when combined with serum creatinine. NGAL has important limitations, including its responsiveness in systemic inflammation, which is partially uncoupled from its response to kidney injury and which needs to be considered when interpreting NGAL results clinically. This review covers the biology and pathophysiology of NGAL and summarizes the results of the growing body of clinical studies that have addressed the utility of NGAL in the early diagnosis of AKI, in the distinction of intrinsic AKI and in the prognostic assessment of broad patient populations.