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Infectious Pathogens (infectious + pathogen)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Mice with neonatally induced inactivation of the vascular cell adhesion molecule-1 fail to control the parasite in Toxoplasma encephalitis

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2003
Martina Deckert
Abstract Under various inflammatory conditions, cell adhesion molecules are up-regulated in the central nervous system (CNS) and may contribute to the recruitment of leukocytes to the brain. In the present study, the functional role of vascular cell adhesion molecule (VCAM)-1 in Toxoplasma encephalitis (TE) was addressed using VCAMflox/flox MxCre mice. Neonatal inactivation of the VCAM-1 gene resulted in a lack of induction of VCAM-1 on cerebral blood vessel endothelial cells, whereas the constitutive expression of VCAM-1 on choroid plexus epithelial cells and the ependymawas unaffected; in these animals, resistance to T.,gondii was abolished, and VCAMflox/flox MxCre mice died of chronic TE caused by a failure to control parasites in the CNS. Although leukocyte recruitment to the CNS was unimpaired, the B cell response was significantly reduced as evidenced by reduced serum levels of anti- T.,gondii -specific IgM and IgG antibodies. Furthermore, the frequency and activation state of intracerebral T.,gondii -specific T cells were decreased, and microglial activation was markedly reduced. Taken together, these data demonstrate the crucial requirement of VCAM-1-mediated immune reactions for the control of an intracerebral infectious pathogen, whereas other cell adhesion molecules can efficiently compensate for VCAM-1-mediated homing across cerebral blood vessels. [source]

A reversibly immortalized human hepatocyte cell line as a source of hepatocyte-based biological support

ADDICTION BIOLOGY, Issue 4 2001
Naoya Kobayashi
The application of hepatocyte transplantation (HTX) is increasingly envisioned for temporary metabolic support during acute liver failure and provision of specific liver functions in inherited liver-based metabolic diseases. Compared with whole liver transplantation, HTX is a technically simple procedure and hepatocytes can be cryopreserved for future use. A major limitation of this form of therapy in humans is the worldwide shortage of human livers for isolating an adequate number of transplantable human hepatocyes when needed. Furthermore, the numbers of donor livers available for hepatocyte isolation is limited by competition for their use in whole organ transplantation. Considering the cost of hepatocyte isolation and the need for immediate preparation of consistent and functional cells, it is unlikely that human hepatocytes can be obtained on such a scale to treat a large number of patients with falling liver functions. The utilization of xenogenic hepatocytes will result in additional concerns regarding transmission of infectious pathogens and immunological and physiological incompatibilities between animals and humans. An attractive alternative to primary human hepatocytes is the use of tightly regulated human hepatocyte cell lines. Such cell lines can provide the advantages of unlimited availability, sterility and uniformity. We describe here methods for creating transplantable human hepatocyte cell lines using currently available cell cultures and gene transfer technology. [source]

Detection of presence or absence of herpes simplex virus, Epstein Barr virus and human cytomegalovirus in infected pulp using a polymerase chain reaction

AUSTRALIAN ENDODONTIC JOURNAL, Issue 1 2009
Hannah Rosaline mds
Abstract The development of methods to amplify nucleic acids has provided a way of identifying and quantifying infectious pathogens in infected pulp and periapical region. Recent studies have detected human herpes virus in periapical pathosis and periodontitis. The aim of this study is to detect the presence or absence of herpes simplex virus, human cytomegalovirus and Epstein Barr virus in an infected pulp. Ten pulp tissue samples from teeth with irreversible pulpitis and eight control samples were subjected to polymerase chain reaction (Perkin , Elmer Gene Amplification System) for detection of human herpes virus. The results of this study did not reveal any human herpes virus in both the control and infected pulp tissue samples. According to this study, human herpes virus may not have an entry through the infected pulp to reach the periapical region and may not be a causative organism in the pulp. [source]

T cell-mediated immune responses in human newborns: ready to learn?

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2005
A. Marchant
Summary Infections with intracellular pathogens are often more severe or more prolonged in young infants suggesting that T cell-mediated immune responses are different in early life. Whereas neonatal immune responses have been quite extensively studied in murine models, studies of T cell-mediated immunity in human newborns and infants are scarce. Qualitative and quantitative differences when compared with adult immune responses have been observed but on the other hand mature responses to certain vaccines and infectious pathogens were demonstrated during the postnatal period and even during foetal life. Herein, we review the evidence suggesting that under appropriate conditions of stimulation, protective T cell-mediated immune responses could be induced by vaccines in early life. [source]

Infection and early atherosclerosis: Does the evidence support causation?

ACTA PAEDIATRICA, Issue 6 2005
Petru Liuba
Abstract Although clinical manifestations of atherosclerotic coronary heart disease occur in adult life, the initial stages of its development commence in childhood. Therefore, elucidating the pathogenesis of early atherosclerosis and identifying the network of risk factors have become fundamental priorities for both cardiovascular healthcare providers and scientists. There is mounting evidence from both human studies and animal experiments that infectious pathogens could be implicated in atherosclerosis development. The vulnerability of the arterial wall to the adverse effects of infection is probably augmented when additional risk factors and/or certain proatherogenic genetic profiles are also present. The precise mechanisms whereby infection, alone or in synergy with conventional cardiovascular risk factors, could contribute to atherosclerosis are not fully understood. Conclusion: Injury to the vascular endothelium, which could be elicited by infection through inflammatory, metabolic, autoimmune, and pathogen-related mechanisms, might be a central link between infection and early atherosclerosis. [source]