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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper is concerned with intracellular infections such as herpes virus, cytomegalovirus and Chlamydia pneumonia which may be implicated in the pathogenesis of atherosclerosis. These viral and bacterial pathogens are regarded as potential causative factors in the pathogenesis of atherosclerosis. The authors support the hypothesis that these infections may induce endothelial injury. The paper reviews both direct and indirect immune system-mediated effect of the viruses indicated on the disease process and the potential role of killer cells in endothelial injury.
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PMID:[The role of the immune system in the pathogenesis of atherosclerosis]. 1603 97

Chlamydia pneumoniae causes a range of respiratory infections including bronchitis, pharyngitis and pneumonia. Infection has also been implicated in exacerbation/initiation of asthma and chronic obstructive pulmonary disease (COPD) and may play a role in atherosclerosis and Alzheimer's disease. We have used a mouse model of Chlamydia respiratory infection to determine the effectiveness of intranasal (IN) and transcutaneous immunization (TCI) to prevent Chlamydia lung infection. Female BALB/c mice were immunized with chlamydial major outer membrane protein (MOMP) mixed with cholera toxin and CpG oligodeoxynucleotide adjuvants by either the IN or TCI routes. Serum and bronchoalveolar lavage (BAL) were collected for antibody analysis. Mononuclear cells from lung-draining lymph nodes were stimulated in vitro with MOMP and cytokine mRNA production determined by real time PCR. Animals were challenged with live Chlamydia and weighed daily following challenge. At day 10 (the peak of infection) animals were sacrificed and the numbers of recoverable Chlamydia in lungs determined by real time PCR. MOMP-specific antibody-secreting cells in lung tissues were also determined at day 10 post-infection. Both IN and TCI protected animals against weight loss compared to non-immunized controls with both immunized groups gaining weight by day 10-post challenge while controls had lost 6% of body weight. Both immunization protocols induced MOMP-specific IgG in serum and BAL while only IN immunization induced MOMP-specific IgA in BAL. Both immunization routes resulted in high numbers of MOMP-specific antibody-secreting cells in lung tissues (IN>TCI). Following in vitro re-stimulation of lung-draining lymph node cells with MOMP; IFNgamma mRNA increased 20-fold in cells from IN immunized animals (compared to non-immunized controls) while IFNgamma levels increased 6- to 7-fold in TCI animals. Ten days post challenge non-immunized animals had >7,000 IFU in their lungs, IN immunized animals <50 IFU and TCI immunized animals <1,500 IFU. Thus, both intranasal and transcutaneous immunization protected mice against respiratory challenge with Chlamydia. The best protection was obtained following IN immunization and correlated with IFNgamma production by mononuclear cells in lung-draining LN and MOMP-specific IgA in BAL.
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PMID:Comparison of intranasal and transcutaneous immunization for induction of protective immunity against Chlamydia muridarum respiratory tract infection. 1615 55

As a consequence of seminal laboratory and experimental work conducted in the 1970s, infections have recently been recognized among possible risk factors for atherosclerosis and its clinical cardiovascular disease manifestations. The infectious hypothesis also relates to modern atherogenesis theories that consider the crucial role of inflammation in the initial development as well as in the natural history of the atherosclerotic plaque. During the last 2 decades, numerous clinical and epidemiologic studies have explored the association between markers of chronic infections in relation to a variety of clinical and subclinical cardiovascular disease outcomes. These studies have focused on a variety of agents including herpesvirus (especially cytomegalovirus), Chlamydia pneumonia, Helicobacter pylori, and periodontal pathogens, and have produced inconsistent results. Some of the limitations and methodological issues in interpreting the existing epidemiologic evidence are discussed in this article. In addition, other supporting evidence is presented here, including pathology studies documenting the presence of infectious agents' DNA in atherosclerotic plaque tissue and experimental infection models in animal studies. Areas for future research are discussed in light of the strengths and limitations of the existing evidence.
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PMID:Infective agents and cardiovascular disease. 1622 30

The subjects of the study were 64 patients with coronary artery disease (CAD), and 38 healthy controls. The study included determination of Chlamydia pneumonia (CLPN), Toxoplasma gondii (TG), Herpes simplex virus (HSV) 1, 2, Epstein-Barr virus (EBV), and antibodies to these microorganisms. Diagnostically significant elevation of the serum levels of IgG antibodies to CLPN, HSV 1, 2, or TG was associated with CAD progression, and seropositivity to several of the agents strongly correlated with CAD progression. Moreover, the risk of future coronary events increased depending on the level of total pathogen burden. These results suggest that intracellular infectious agents are involved in the development of atherosclerosis and CAD.
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PMID:[Effect of respiratory infections on the clinical course of coronary artery disease]. 1640 34

Chlamydia pneumoniae, an obligate intracellular human pathogen, causes infections of the respiratory tract. It is a significant cause of both lower and upper acute respiratory illnesses, including pneumonia, bronchitis, pharyngitis and sinusitis. Most respiratory infections caused by C. pneumoniae are mild or asymptomatic. Some studies have suggested a possible association of C. pneumoniae infection and acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Seroepidemiological studies showing antibody prevalence rates in a range of 50 to 70% suggest that C. pneumoniae is widely distributed and that nearly everybody is infected with the agent at some time. C. pneumoniae can cause prolonged or chronic infections which may be due to persistence for months or years. These persistent infections have been implicated in the development of a number of chronic diseases including atherosclerosis, asthma and COPD. These persistent chlamydial infections can be established in vitro using several methods including cytokines, antibiotics and deprivation of certain nutrients. Despite differences in treatment, chlamydiae respond to form inclusions containing atypical reticulate bodies (RBs), which occasionally have been shown to be pleomorphic forms, termed aberrant form (AF). The AF is generally larger in diameter than typical RBs, and display a sparse densinometric appearance. In general, it is likely that this aberrant developmental step leads to the persistence of viable but nonculturable chlamydiae within infected cells over long periods. Removal of several stress factors described above results in the condensation of nuclei, the appearance of late proteins, and the production of viable, infectious elementary bodies (EBs). Most of the major sequelae of chlamydial disease are thought to arise from either repeated or persistent chlamydial infection of an individual. The persistence would allow constant presentation to the individual immune response of these potentially deleterious immune targets. Since repeated infection can certainly be documented in many clinical settings, persistence is thought to also play a role.
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PMID:[Chlamydia pneumoniae infections]. 1703 92

Chlamydophila pneumoniae is an obligate intracellular respiratory pathogen that has been associated with pneumonia and chronic bronchitis, atherosclerosis, asthma and other chronic diseases in humans. However, C. pneumoniae is not restricted to humans, as originally thought, and can cause infections in several animal hosts. C. pneumoniae was isolated in cell culture from nine Western barred bandicoots (Perameles bougainville) from Australia. The sequences of five genomic regions were determined, including full-length sequences of the 16S rRNA and ompA genes and the ygeD-urk intergenic spacer, and partial sequences of the 23S rRNA and rpoB genes. Sequence analysis of the entire 16S rRNA and ompA genes from bandicoot isolates demonstrated that they were 98.2-98.3% similar to human isolates, 94.6-99.3% similar to the equine biovar and almost identical, with 99.5-99.9% similarity, to the koala biovar. Comparative genotyping of the variable domain 4 region of the ompA gene demonstrated that bandicoot isolates seemed to be identical to the animal genotype that has been recently identified in human carotid plaque specimens. Minor sequence polymorphism observed in ompA, 16S rRNA and rpoB genes of animal isolates, indicating genomic diversity within C. pneumoniae, may have important implications for diagnostic PCR assays leading to false negative results. Forty percent of selected published species-specific PCR assays were found to have sequence variability in primer and/or probe that might affect their performance in detecting bandicoot isolates of C. pneumoniae, or possibly other animal and human strains where minor sequence polymorphisms may be present. The data from this study support the previous observations that C. pneumoniae is not restricted to humans and may be widespread in an animal reservoir with a potential risk of transmission to humans.
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PMID:Molecular characterization of Chlamydophila pneumoniae isolates from Western barred bandicoots. 1731 74

Infection with bacteria such as Chlamydia pneumonia, Helicobacter pylori or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK-293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to lipopolysaccharide (LPS) from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid raft-dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonize TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis.
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PMID:Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells. 1741 16

The presence of anti-heat shock protein 60 (Hsp60) antibodies in healthy individuals and the association of these antibodies with diseases such as arthritis and atherosclerosis are well documented. However, there is limited population-level data on interindividual variation in anti-Hsp60 levels. We investigated the influence of early-life factors on IgG reactivity to human Hsp60 at age 18 years. A population-based prospective birth cohort study included 5914 births in the city of Pelotas, Brazil, in 1982. Early-life exposures were documented during home visits in childhood. In 2000, 79% of all males in the cohort were traced. Sera from a systematic 20% sample (411 subjects) were analyzed. Anti-Hsp60 total IgG reactivity was determined by ELISA. Data were analyzed using analysis of variance and generalized linear models. Anti-Hsp60 reactivity was lognormally distributed and showed a significant direct correlation with low birthweight (p=0.039) and total duration of breastfeeding (p=0.018), of which only the latter remained significant after adjustment for potential confounders. Reactivity was not associated with asthma, pneumonia, diarrhea, or early-life malnutrition. Mother-child immunological interactions, rather than infection/disease factors seem to be associated with reactivity to Hsp60 later in life. This is in agreement with the hypothesis that maternal antibodies influence future antibody profile.
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PMID:Mother-child immunological interactions in early life affect long-term humoral autoreactivity to heat shock protein 60 at age 18 years. 1752 83

Chlamydophila (Chlamydia) pneumoniae is an intracellular respiratory pathogen known to cause community-acquired pneumonia. Infection with this organism has been associated with atherosclerosis, inflammatory arthritis, and other chronic diseases, many of which also have been associated with possession of the epsilon4 allele at the APOE locus on (human) chromosome 19. An earlier study from this laboratory suggested that some relationship exists between apolipoprotein E4 (apoE4), the product of the epsilon4 allele, and the pathobiology of C. pneumoniae. A standard attachment assay and real time PCR targeting a sequence on the C. pneumoniae chromosome were used to monitor host cell binding of elementary bodies (EB) of that organism. Our data indicate that 3-fold more EB of strain AR-39 attach to an epsilon3 homozygous human cell line transfected with a plasmid expressing the epsilon4 coding sequence than to the same cell line harboring empty vector, vector containing an irrelevant insert sequence, or vector containing the DNA sequence encoding apoE3. The quantitative real time data were confirmed by immunolabeling of chlamydial inclusions in parallel attachment and infection assays. Experiments using Chlamydophila trachomatis EB showed no enhancement of attachment in the presence of the epsilon4 allele in any assays. These observations indicate that apoE4 enhances attachment of C. pneumoniae EB, but not those of C. trachomatis, to target host cells.
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PMID:Apolipoprotein E4 enhances attachment of Chlamydophila (Chlamydia) pneumoniae elementary bodies to host cells. 1799 73

The paleopathological study of 31 Italian Renaissance mummies from the Basilica of S. Domenico Maggiore in Naples has allowed us to perform about 20 diagnoses, of which 5 concern infectious (smallpox, hepatitis, condyloma, syphilis and pneumonia), 3 metabolic (obesity, atherosclerosis, gallstones), I articular (DISH) and 2 neoplastic (colon adenocarcinoma and skin carcinoma) diseases. The mummy of an anonymous child, dated back to the 16th century (14C: 1569 +/- 60), presented a diffuse vesiculopustular exanthema. Macroscopic aspects and regional distribution suggested smallpox, while EM revealed many egg-shaped, virus-like particles (250 x 50 nm), with a central dense core. Following incubation with anti-smallpox virus antiserum and protein A-gold complex immunostaining, the particles resulted completely covered with protein A-gold. These results clearly show that this Neapolitan child died of a severe form of smallpox some four centuries ago. The mummy of Maria d'Aragona, Marquise of Vasto (1503-1568), revealed on the left arm an oval, cutaneous ulcer (15 x l0 mm) with linen dressing. Indirect immunofluorescence with anti-treponema pallidum antibody identified a large number of filaments with the morphological characteristics of fluorescent treponemes. Electron microscopy evidenced typical spirochetes, with axial fibril. These findings clearly demonstrate a treponemal, probably venereal, infection. Further examination of the mummy showed a large peduncolate arborescent neoformation (2 x 7 mm) of the right inguinal region, which was rehydrated and submitted to histology by hematoxylineosin, Van Gieson and Masson's trichromic staining. Light microscopy evidenced an exophytic, papillary skin lesion, with typical connective axis and pronounced parakeratosis. These macroscopic and histological aspects seemed peculiar of condyloma acuminatum, a papillomavirus-induced squamous lesion also called "venereal wart". Molecular study revealed the presence of HPV 18, a virus with high oncogenic potential. Automated sequencing of several clones revealed 100% similarity sequences of both HPV 18 and JC9813 DNA, a putative novel HPV with low oncogenic potential. This study represents the first molecular diagnosis of HPV in mummies and could pave the way for further research about the secular evolution of these viruses, very important in human oncology. The buccal surfaces of the teeth of Isabella d'Aragona, duchess of Milan ((1470-1524), covered by a black patina with high mercury levels, have been intensively and intentionally abraded. The black patina can be attributed to chronic mercury intoxication, used therapeutically in the treatment of syphilis. The mummy of Ferrante I d'Aragona, King of Naples (1431-1494), revealed an adenocarcinoma extensively infiltrating the muscles of the small pelvis. A molecular study of the neoplastic tissue evidenced a typical mutation of the K-ras gene codon 12: the normal sequence GGT (glycine) was altered into GAT (aspartic acid). At present this genetic change is the most frequent mutation of the K-ras gene in sporadic colorectal cancer. The alimentary "environment" of the Neapolitan court of the XV century, with its abundance of natural alimentary alkylating agents, well explains this acquired mutation. These and other diseases as, for example, a case of cirrhosis, some cases of anthracosis and other peculiar traumatic conditions, such as a mortal stab-wound, can elucidate the pathocenosis of this wealthy classes of the Italian Renaissance.
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PMID:[The Aragonese mummies of the Basilica of Saint Domenico Maggiore in Naples]. 1817 25


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