The Role of MicroRNA-155 in Chlamydia muridarum Infected lungs

Keck, Jonathon; Chambers, James P.; Kancharla, Aravind; Bashir, Dona Haj; Henley, Laura; Schenkel, Katherine; Castillo, Kevin; Guentzel, M. Neal; Gupta, Rishein; Arulanandam, Bernard P.

doi:10.1016/j.micinf.2020.02.005

Cited by 3 publications

(4 citation statements)

References 36 publications

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“…However, Chlamydia is not only a causative agent of sexually transmitted disease but also contributes to 16–22% of all reported cases of pneumonia in the U.S. occurring within 2 months after birth. We have established a murine intranasal chlamydial challenge model to study the protective role of IFN- γ in pulmonary Cm infection [ 14 , 17 , 18 ]. Using this animal model, we assessed the role of fetuin-A in pulmonary Cm infection.…”

Section: Resultsmentioning

confidence: 99%

“…Lung tissue lysate was used for IFU assessment following infection of McCoy cell monolayers and immunofluorescent staining as previously described [ 13 , 14 ]. Briefly, McCoy cells were grown on sterile coverslips in 24-well plates for 24 hours, followed by infection with lung lysate diluted 1 : 80 with Eagle's minimum essential medium plus 10% fetal bovine serum (EM-10 media).…”

Section: Methodsmentioning

confidence: 99%

“…All mRNA expression levels were normalized to housekeeping genes GAPDH and HSP90 and reported as expression relative to that of WT naïve mouse expression using the comparative cycle threshold method [ 16 ]. Quantification of gene expression was achieved using the CFX Maestro software (Bio-Rad), and results were reported as fold-change differences as previously described [ 14 , 15 ].…”

Section: Methodsmentioning

confidence: 99%

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Influence of Fetuin-A on Chlamydia muridarum Pulmonary Infection

Mahjabeen

Chambers

et al. 2022

International Journal of Microbiology

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Fetuin-A is an acute phase glycoprotein shown to counter in a regulatory manner proinflammatory cytokine production to maintain homeostasis during inflammation. We report here that in wild-type mice 12 days after Chlamydia muridarum (Cm) intranasal challenge, fetuin-A content in the lungs decreased 46%, while INF-γ increased 44%, consistent with a negative regulatory role of fetuin-A in inflammation. Importantly, the observed increased IFN-γ production was abrogated in fetuin-A-deficient AHSG mice suggesting that IFN-γ induction following Cm infection is fetuin-A dependent. Assessment of expression of genes associated with inflammation revealed fetuin-A-dependent upregulation of TBX21 (a Th1 cell-specific transcription factor) in the lungs of Cm-infected WT mice that correlated with IFN-γ induction. Additionally, the effect of fetuin-A deficiency in mounting an adaptive immune response to Cm infection was demonstrated using a splenocyte recall assay. Although preliminary in nature, these findings are suggestive of fetuin-A involvement following Cm pulmonary infection and underscores the need to investigate further the role of fetuin-A in the immune response and the consequences of its gene deletion.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Influence of Fetuin-A on Chlamydia muridarum Pulmonary Infection

Mahjabeen

Chambers

et al. 2022

International Journal of Microbiology

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“…Together, miR-155 can tune in type 1 immune response though regulating M1 polarization and directly inducing Th1 differentiation, therefore it may play a role in regulation of anti-chlamydial protective immunity. Indeed, the enhanced susceptibility to chlamydia infection in miR-155-/- mice have been reported recently ( Keck et al, 2020 ), but the underlying mechanism is largely unknown. The target genes of miR-155 need to be identify during NK and macrophage crosstalk in the context of chlamydial infection.…”

Section: Discussionmentioning

confidence: 99%

Natural Killer Cells Regulate Pulmonary Macrophages Polarization in Host Defense Against Chlamydial Respiratory Infection

Zhao

Zhou

et al. 2022

Front. Cell. Infect. Microbiol.

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NK cells and pulmonary macrophages both are important components of innate immunity. The interaction between NK cells and pulmonary macrophages during chlamydial infection is poorly understood. In this study, we explored the effect of NK cells on regulation of pulmonary macrophage function during chlamydial respiratory infection. We found that NK depletion led to polarization of pulmonary macrophages from M1 to M2 phenotype, and it is related to reduced miR-155 expression in lung macrophage. Using adoptive transfer approach, we found that the recipients receiving lung macrophages isolated from C. muridarum-infected NK-cell-depleted mice exhibited an increased bacterial load and severe inflammation in the lung upon chlamydial challenge infection when compared with the recipients of lung macrophages from infected isotype control antibody treated mice. Herein, the effects of NK cells on macrophage polarization were examined in vitro. We found that NK cells from chlamydial-infected mice (iNK) significantly induced M1 polarization compared to that from uninfected mice (uNK). Inhibition of miR-155 expression in macrophages reduced M1 polarization induced by iNK, while miR-155 over-expression enhanced it. Furthermore, neutralization of IFN-γ in the coculture system decreased the expression of miR-155 by macrophages, and resulted in weakened M1 polarization. The data indicates that NK cells promote M1 polarization through up-regulation of miR-155 in macrophages by producing IFN-γ during chlamydial infection, and NK-regulated macrophage polarization is functionally relevant to host defense against the infection.

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Epigenetic changes induced by pathogenic Chlamydia spp

Stein,

Thompson

2023

Pathogens and Disease

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Chlamydia trachomatis, C. pneumoniae, and C. psittaci, the three Chlamydia species known to cause human disease, have been collectively linked to several pathologies, including conjunctivitis, trachoma, respiratory disease, acute and chronic urogenital infections and their complications, and psittacosis. In vitro, animal, and human studies also established additional correlations, such as between C. pneumoniae and atherosclerosis and between C. trachomatis and ovarian cancer. As part of their survival and pathogenesis strategies as obligate intracellular bacteria, Chlamydia spp. modulate all three major types of epigenetic changes, which include DNA methylation, histone post-translational modifications, and microRNA-mediated gene silencing. Some of these epigenetic changes may be implicated in key aspects of pathogenesis, such as the ability of the Chlamydia spp. to induce epithelial-to-mesenchymal transition, interfere with DNA damage repair, suppress cholesterol efflux from infected macrophages, act as a co-factor in HPV-mediated cervical cancer, prevent apoptosis, and preserve the integrity of mitochondrial networks in infected host cells. A better understanding of the individual and collective contribution of epigenetic changes to pathogenesis will enhance our knowledge about the biology of Chlamydia spp. and facilitate the development of novel therapies and biomarkers.

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The Role of MicroRNA-155 in Chlamydia muridarum Infected lungs

Cited by 3 publications

References 36 publications

Influence of Fetuin-A on Chlamydia muridarum Pulmonary Infection

Influence of Fetuin-A on Chlamydia muridarum Pulmonary Infection

Natural Killer Cells Regulate Pulmonary Macrophages Polarization in Host Defense Against Chlamydial Respiratory Infection

Epigenetic changes induced by pathogenic Chlamydia spp

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