Bones are metabolically active organs. Their reconstruction is crucial for the proper functioning of the skeletal system during bone growth and remodeling, fracture healing, and maintaining calcium–phosphorus homeostasis. The bone metabolism and tissue properties are influenced by trace elements that may act either indirectly through the regulation of macromineral metabolism, or directly by affecting osteoblast and osteoclast proliferation or activity, or through becoming part of the bone mineral matrix. This study analyzes the skeletal impact of macroelements (calcium, magnesium, phosphorus), microelements (fluorine), and heavy metals (lead), and discusses the concentration of each of these elements in the various bone tissues.

The aim of the study was to investigate relationships between the concentrations of macroelements (Ca), microelements (Cr, Cu, Fe, Mn, Mo, Ni, Sn, Sr, V, Zn) and heavy metals (Ag, Cd, Pb) in the placenta, fetal membrane and umbilical cord. ‪Furthermore, we examined relationships between the concentrations of these metals in the studied afterbirths and maternal age, gestational age, placenta parameters (breadth, length, weight) and newborn parameters (length, weight and Apgar score). This study confirms previously reported Zn-Cd, Pb-Cd and Ni-Pb interactions in the placenta. New types of interactions in the placenta, fetal membrane and umbilical cord were also noted. Analysis of the correlations between metal elements in the afterbirths (placenta, fetal membrane and umbilical cord) and biological parameters showed the following relationships: maternal age and Mn (in the fetal membrane); gestational age and Cr, Fe, Zn (in the fetal membrane), Ag and Cu (in the umbilical cord); newborn’s length and Sr (in the placenta), Ag (in the umbilical cord); newborn’s weight and Sr (in the placenta), Cu (in the fetal membrane), Ag (in the umbilical cord); Apgar score and Ca, Cr and Ni (in the umbilical cord); placenta’s length and Cr and Sn (in the fetal membrane), Cu (in the umbilical cord); placenta’s width and Mo, Pb (in the placenta) and placenta weight and Sr (in the placenta), Ag, Fe, Mn (in the fetal membrane). The results show the influence of metals on the placenta, mother and newborn parameters, and the same point indicates the essential trace elements during the course of pregnancy.

Little is known about the pathomechanism of pulmonary infections caused by Acanthamoeba sp. Therefore, the aim of this study was to determine whether Acanthamoeba sp. may affect the expression and activity of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), resulting in the altered levels of their main products, prostaglandins (PGE2) and thromboxane B2 (TXB2), in lungs of immunocompetent or immunosuppressed hosts. Acanthamoeba sp. induced a strong expression of COX-1 and COX-2 proteins in the lungs of immunocompetent mice, which, however, did not result in significant differences in the expression of PGE2 and TXB2. Our immunohistochemical analysis showed that immunosuppression induced by glucocorticoids in Acanthamoeba sp.-infected mice caused a decrease in COX-1 and COX-2 (not at the beginning of infection) in lung tissue. These results suggest that similar to COX-2, COX-1 is an important mediator of the pathophysiology in experimental pulmonary acanthamoebiasis. We suggest that the signaling pathways important for Acanthamoeba sp. induction of lung infection might interact with each other and depend on the host immune status.

Free-living amoebas, including Acanthamoeba spp., are widely distributed in soil, water, and air. They are capable of causing granulomatous amebic encephalitis, Acanthamoeba pneumonia, Acanthamoeba keratitis, and disseminated acanthamoebiasis. Despite low occurrence worldwide, the mortality rate of Acanthamoeba spp. infections is very high, especially in immunosuppressed hosts. Acanthamoeba infections are a medical problem, owing to limited improvement in diagnostics and treatment, which is associated with incomplete knowledge of pathophysiology, pathogenesis, and the host immune response against Acanthamoeba spp. infection. The aim of this review is to present the biochemical and molecular mechanisms of Acanthamoeba spp.–host interactions, including the expression of Toll-like receptors, mechanisms of an immune response, the activity of metalloproteinases, the secretion of antioxidant enzymes, and the expression and activity of cyclooxygenases. We show the relationship between Acanthamoeba spp. and the host at the cellular level and host defense reactions that lead to changes in the selected host’s organs.

Toll-like receptors (TLRs) play a key role in the innate immune response to numerous pathogens, including Acanthamoeba spp. The aim of this study was to determine the expression of TLR2 and TLR4 in the eyes of mice following intranasal infection with Acanthamoeba spp. in relation to the host’s immunological status. Amoebae used in this study were isolated from the bronchial aspirate of a patient with acute myeloid leukemia (AML) and atypical symptoms of pneumonia. We found statistically significant differences in the expression of TLR2 and TLR4 in the eye of immunocompetent mice at 8, 16, and 24 days after Acanthamoeba spp. infection (dpi) compared to control group. Immunosuppressed mice showed significant differences in the expression of TLR2 at 16 and 24 dpi compared to uninfected animals. Our results indicate that TLR2 and TLR4 are upregulated in the eyes of mice in response to Acanthamoeba spp. We suggest that it is possible for trophozoites to migrate through the optic nerve from the brain to the eyes. The course of disseminated acanthamoebiasis may be influenced by the host’s immunological status, and the observed changes in expression of TLR2 and TLR4 in the host’s organs may indicate the role of these receptors in the pathomechanism of acanthamoebiasis.