Molecular pathogenesis of chronic Chlamydia pneumoniae infection: a brief overview

Kern, Jan Marco; Maass, Viola; Maass, Matthias

doi:10.1111/j.1469-0691.2008.02631.x

Cited by 30 publications

(30 citation statements)

References 52 publications

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“…The inhibition of neutrophil apoptosis by C. pneumoniae appears to play a major role in the production of infection of these cells by C. pneumoniae [65].…”

Section: Chlamydophila Pneumoniaementioning

confidence: 99%

Community-acquired pneumonia related to intracellular pathogens

Cillóniz¹,

Niederman

Eerden

et al. 2016

Intensive Care Med

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Community-acquired pneumonia (CAP) is associated with high rates of morbidity and mortality worldwide; the annual incidence of CAP among adults in Europe has ranged from 1.5 to 1.7 per 1000 population. Intracellular bacteria are common causes of CAP. However, there is considerable variation in the reported incidence between countries and change over time. The intracellular pathogens that are well established as causes of pneumonia are Legionella pneumophila, Mycoplasma pneumoniae, Chlamydophila pneumoniae, Chlamydophila psittaci, and Coxiella burnetii. Since it is known that antibiotic treatment for severe CAP is empiric and includes coverage of typical and atypical pathogens, microbiological diagnosis bears an important relationship to prognosis of pneumonia. Factors such as adequacy of initial antibiotic or early de-escalation of therapy are important variables associated with outcomes, especially in severe cases. Intracellular pathogens sometimes appear to cause more severe disease with respiratory failure and multisystem dysfunction associated with fatal outcomes. The clinical relevance of intracellular pathogens in severe CAP has not been specifically investigated. We review the prevalence, general characteristics, and outcomes of severe CAP cases caused by intracellular pathogens.

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“…The inhibition of neutrophil apoptosis by C. pneumoniae appears to play a major role in the production of infection of these cells by C. pneumoniae [65].…”

Section: Chlamydophila Pneumoniaementioning

confidence: 99%

Community-acquired pneumonia related to intracellular pathogens

Cillóniz¹,

Niederman

Eerden

et al. 2016

Intensive Care Med

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“…In response to infection with C. pneumoniae, acute phase proteins enhance progression and destabilization of atherosclerotic plaques [76]. C. pneumoniae can induce proliferation of vascular smooth muscle cells (VSMCs) and stimulate production of numerous pro-inflammatory mediators and adhesion molecules in VSMCs and endothelial cells [76,78,79]. C. pneumoniae infection can also induce reactive oxygen species (ROS) in macrophages, platelets, endothelial cells and VSMCs, contributing to atherosclerotic lesion development [74].…”

Section: Chlamydia Pneumoniae: Respiratory Infections Coronary Artermentioning

confidence: 99%

Chronic Chlamydial Diseases: From Atherosclerosis to Urogenital Infections

Leonard

Borel

2014

Curr Clin Micro Rpt

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Chlamydiae cause a wide range of diseases in human and animal hosts. Chlamydia pneumoniae and Chlamydia trachomatis are important human pathogens with worldwide distribution that produce significant morbidity. Acute infections with C. pneumoniae cause respiratory tract infections, while chronic infection has been linked to chronic bronchitis, asthma and atherosclerosis. Ocular serovars of C. trachomatis induce trachoma, the leading cause of infectious blindness worldwide. C. trachomatis is the most common bacterial cause of sexually transmitted diseases (STDs) worldwide. Acute infections with genital serovars of C. trachomatis remain clinically silent in most women, but can progress to upper genital tract infection leading to pelvic inflammatory disease (PID), infertility and ectopic pregnancy. Chlamydiainduced, reactive arthritis can develop as a late-term condition after genital C. trachomatis or respiratory C. pneumoniae infection. In this review, we address recent information on pathogenesis, immune response, diagnosis and treatment of chronic diseases induced by C. trachomatis and C. pneumoniae. Abstract:Chlamydiae cause a wide range of diseases in human and animal hosts. Chlamydia pneumoniae and Chlamydia trachomatis are important human pathogens with worldwide distribution that produce significant morbidity. Acute infections with C. pneumoniae cause respiratory tract infections, while chronic infection has been linked to chronic bronchitis, asthma and atherosclerosis. Ocular serovars of C. trachomatis induce trachoma, the leading cause of blindness worldwide. C. trachomatis is the most common bacterial cause of sexually-transmitted diseases (STDs) worldwide. Acute infections with genital serovars of C. trachomatis remain clinically silent in most women but can progress to upper genital tract infection leading to pelvic inflammatory disease (PID), infertility and ectopic pregnancy. Chlamydia-induced, reactive arthritis can develop as a late-term condition after genital C. trachomatis or respiratory C. pneumoniae infection. In this review we address recent information on pathogenesis, immune

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“…Before detailed discussion of pathogen-induced cell death, the three main pathogens discussed in this review will be briefly introduced. For detailed description of the individual pathogens and the diseases they cause, the interested reader is kindly referred to related reviews [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Host cell death induced by the egress of intracellular Plasmodium parasites

2009

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Intracellular pathogens are known to inhibit host cell apoptosis efficiently to ensure their own survival. However, following replication within a cell, they typically need to egress in order to infect new cells. For a long time it was assumed that this happens by simply disrupting the host cell and in some cases, such as for Plasmodium-infected erythrocytes, this seems indeed to be true. However, recently it has been shown that in Plasmodium-infected hepatocytes, an ordered form of cell death is initiated. This cell death is parasite-dependent and can clearly be distinguished from apoptosis and necrosis. The key event, and point of no return, appears to be the rupture of the parasitophorous vacuole membrane (PVM). PVM disruption and host cell death depend on the activation of cysteine proteases. Whether these are of parasite or host cell origin seems to rely on the life cycle stage of the Plasmodium parasite and the corresponding host cell.

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Molecular pathogenesis of chronic Chlamydia pneumoniae infection: a brief overview

Cited by 30 publications

References 52 publications

Community-acquired pneumonia related to intracellular pathogens

Community-acquired pneumonia related to intracellular pathogens

Chronic Chlamydial Diseases: From Atherosclerosis to Urogenital Infections

Host cell death induced by the egress of intracellular Plasmodium parasites

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