Differential effects of Chlamydia pneumoniae infection on cytokine levels in human T lymphocyte- and monocyte-derived cell cultures

Mamata, Yukimitsu; Hakki, Amal; Newton, Catherine; Burdash, N M; Klein, Thomas; Friedman, Herman

doi:10.1016/j.ijmm.2006.11.004

Cited by 12 publications

(9 citation statements)

References 39 publications

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“…Microbial infection stimulates the innate immune system, resulting in enhanced expression of costimulatory molecules and proinflammatory cytokines 34 . H pylori infection has been shown to induce Th1- and Th17-type cytokine production,35 while C pneumoniae infection produces a predominantly Th1-type cytokine profile 20. We and others have shown that anti-AQP4 antibody positive OSMS and NMO patients develop a prominent Th17 and Th1 shift in CSF cytokine profiles16 17 and peripheral blood CD4 positive T cell cytokine profiles 18 19.…”

Section: Discussionmentioning

confidence: 93%

“…Therefore, in the present study, we aimed to clarify whether immunogenetic background and common infection profiles are the same or differ between anti-AQP4 antibody positive and negative NMO patients. Thus, in addition to H pylori infection, we studied Chlamydia pneumoniae infection as a representative other type of chronic bacterial infection because we and others have shown that anti-AQP4 antibody positive OSMS and NMO patients develop a prominent Th17 and Th1 shift in CSF cytokine profiles16 17 and peripheral blood CD4 positive T cell cytokine profiles,18 19 and C pneumoniae can induce a predominantly Th1-type cytokine profile 20. EBV and varicella zoster virus infections were also investigated as representative types of chronic viral infection.…”

Section: Introductionmentioning

confidence: 99%

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Distinct genetic and infectious profiles in Japanese neuromyelitis optica patients according to anti-aquaporin 4 antibody status

Yoshimura

Isobe

Matsushita

et al. 2012

J Neurol Neurosurg Psychiatry

119

107

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Distinct genetic and infectious profiles in Japanese neuromyelitis optica patients according to anti-aquaporin 4 antibody status

Yoshimura

Isobe

Matsushita

et al. 2012

J Neurol Neurosurg Psychiatry

119

107

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“…Stimulation of human PBMC with C. pneumoniae induces the production of chemokines IL-8, MIP-1α and MCP-1, and cytokines TNF-α, IL-1β and IL-6 [32]. C. pneumoniae induced the production of TNF-α, IL-10 and IL-12 in THP-1 monocytic cell line [39], and gene expression of a number of cytokines including IL-1β, TNF-α, MCP1, MIP-1α in a time-dependent fashion in U937 monocytic cell line [40]. Consistent with these reports, we observed a time-dependent increase in the expression of TNF-α, IL-1β, IL-6 and IL-8.…”

Section: Discussionmentioning

confidence: 96%

“…Infection of human monocytes by C. pneumoniae has been reported to result in the upregulation of cytokines and chemokines [39], [40]. Stimulation of human PBMC with C. pneumoniae induces the production of chemokines IL-8, MIP-1α and MCP-1, and cytokines TNF-α, IL-1β and IL-6 [32].…”

Section: Discussionmentioning

confidence: 99%

Hydrodynamic Regulation of Monocyte Inflammatory Response to an Intracellular Pathogen

et al. 2011

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Systemic bacterial infections elicit inflammatory response that promotes acute or chronic complications such as sepsis, arthritis or atherosclerosis. Of interest, cells in circulation experience hydrodynamic shear forces, which have been shown to be a potent regulator of cellular function in the vasculature and play an important role in maintaining tissue homeostasis. In this study, we have examined the effect of shear forces due to blood flow in modulating the inflammatory response of cells to infection. Using an in vitro model, we analyzed the effects of physiological levels of shear stress on the inflammatory response of monocytes infected with chlamydia, an intracellular pathogen which causes bronchitis and is implicated in the development of atherosclerosis. We found that chlamydial infection alters the morphology of monocytes and trigger the release of pro-inflammatory cytokines TNF-α, IL-8, IL-1β and IL-6. We also found that the exposure of chlamydia-infected monocytes to short durations of arterial shear stress significantly enhances the secretion of cytokines in a time-dependent manner and the expression of surface adhesion molecule ICAM-1. As a functional consequence, infection and shear stress increased monocyte adhesion to endothelial cells under flow and in the activation and aggregation of platelets. Overall, our study demonstrates that shear stress enhances the inflammatory response of monocytes to infection, suggesting that mechanical forces may contribute to disease pathophysiology. These results provide a novel perspective on our understanding of systemic infection and inflammation.

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“…28 C. pneumoniae infection cycle in monocytes/macrophages may last from 3–7 days during which the cells secrete a plethora of inflammatory cytokines, matrix metalloproteases, procoagulants, and upregulate adhesion and LDL-up-take receptor expression levels. 31,36,48 C. pneumoniae is believed to be transmitted from the lung to other tissues including arterial wall and the brain by infected monocytes through circulation. 19,30 While most of these in vitro studies focus on monocytes in static culture, in reality, during transit from the lungs by blood flow, the monocytes experience biophysical forces such as shear stress.…”

Section: Introductionmentioning

confidence: 99%

Shear Stress Enhances Chemokine Secretion from Chlamydia pneumoniae-infected Monocytes

et al. 2013

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Chlamydia pneumoniae is a common respiratory pathogen that is considered a highly likely risk factor for atherosclerosis. C. pneumoniae is disseminated from the lung into systemic circulation via infected monocytes and lodges at the atherosclerotic sites. During transit, C. pneumoniae-infected monocytes in circulation are subjected to shear stress due to blood flow. The effect of mechanical stimuli on infected monocytes is largely understudied in the context of C. pneumoniae infection and inflammation. We hypothesized that fluid shear stress alters the inflammatory response of C. pneumoniae-infected monocytes and contributes to immune cell recruitment to the site of tissue damage. Using an in vitro model of blood flow, we determined that a physiological shear stress of 7.5 dyn/cm2 for 1 h on C. pneumoniae-infected monocytes enhances the production of several chemokines, which in turn is correlated with the recruitment of significantly large number of monocytes. Taken together, these results suggest synergistic interaction between mechanical and chemical factors in C. pneumoniae infection and associated inflammation.

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Differential effects of Chlamydia pneumoniae infection on cytokine levels in human T lymphocyte- and monocyte-derived cell cultures

Cited by 12 publications

References 39 publications

Distinct genetic and infectious profiles in Japanese neuromyelitis optica patients according to anti-aquaporin 4 antibody status

Distinct genetic and infectious profiles in Japanese neuromyelitis optica patients according to anti-aquaporin 4 antibody status

Hydrodynamic Regulation of Monocyte Inflammatory Response to an Intracellular Pathogen

Shear Stress Enhances Chemokine Secretion from Chlamydia pneumoniae-infected Monocytes

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