Mechanisms of Intracellular Chlamydiae Survival

Chlamydiae are Gram-negative, non-motile, obligate intracellular, and spherically shaped bacteria with a diameter of 0.2-1.5 μm. Chlamydiae are present in several different morphological forms: the elementary body, the reticular body, and in the last several years, there has been the observation of a third form known as the persistent or atypical form. The intracellular localization of Chlamydia provides a unique replication cycle that occurs inside a membrane-surrounded vacuole in the host cell cytoplasm and is significantly different from the method of multiplication of other microorganisms. Chlamydiae are capable of manipulating different signalling pathways inside the infected cell, thus avoiding the host immune response. This ensures intracellular multiplication, survival, and long-term persistence of Chlamydiae. There are two basic means of achieving this persistence: inhibition of apoptosis and manipulation of NF-κB (nuclear factor kappa B)-mediated signals in the host

Potential Hepatoprotective Role of Galectin-3 during HCV Infection in End-Stage Renal Disease Patients

Hepatitis C virus infection (HCV), one of the greatest causes of liver disease, is a frequent complication in patients with end-stage renal disease (ESRD) on dialysis. ESRD is defined as decreased glomerular filtration and also accompanied by impaired function of the immune system. Galectin-3 is a β-galactoside-binding lectin, involved in various biological processes including pathogenesis of chronic renal disease. The aim of our study was to estimate disease severity in ESRD HCV+ patients and analyze the serum concentrations of IL-1β, IL-4, IL-23, and IL-6; anti-HCV antibodies; and galectin-3. Also, we attempted to determine potential correlation between galectin-3 level and parameters of disease severity ALT and AST. Our results showed decreased levels of ALT and AST (p=0.00), demonstrating less liver destruction in ESRD HCV+ patients in comparison to HCV+ patients. Increased levels of IL-6 (p=0.03) implicate a hepatoprotective role of IL-6 in these patients. Also, level of galectin-3 (p=0.00) in the serum of ESRD HCV+ patients was higher than that of HCV+ patients. This alteration was accompanied with negative correlation between galectin-3 and AST and ALT, respectively (p=0.029; p=0.033). The presence of increased systemic levels of IL-6 and Gal-3 in ESRD HCV+ patients may be an attempt to counteract or limit ongoing proinflammatory processes and to downregulate chronic inflammation, suggesting the new aspects of HCV infection in ESRD patients