MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology
Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophys...
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| Veröffentlicht in: | Pathogens (Basel) 2021-05, Vol.10 (5), p.566, Article 566 |
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| description | Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b(-/-)) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b(-/-) mice were unable to clear the infection compared to WT mice; also, miR-378b(-/-) mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b(-/-) mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b(-/-) mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease. |
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MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b(-/-)) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b(-/-) mice were unable to clear the infection compared to WT mice; also, miR-378b(-/-) mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b(-/-) mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b(-/-) mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease.</description><identifier>ISSN: 2076-0817</identifier><identifier>EISSN: 2076-0817</identifier><identifier>DOI: 10.3390/pathogens10050566</identifier><identifier>PMID: 34067003</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Asymptomatic ; Biomarkers ; Chlamydia ; Chlamydia muridarum ; Chlamydial pathogenesis ; CRISPR ; Cytokines ; Fallopian tubes ; Fertility ; Gene expression ; Genital tract ; Immune response ; Infections ; Infectivity ; Infertility ; Inflammation ; Inflammatory diseases ; Life Sciences & Biomedicine ; Microbiology ; MicroRNAs ; miR-378b−/− mice ; miRNA ; Pathogenesis ; Pathology ; Pelvic inflammatory disease ; Pregnancy ; Reproductive system ; RNA polymerase ; Salpingitis ; Science & Technology ; Sexually transmitted diseases ; STD ; Uterus ; Vagina ; Womens health</subject><ispartof>Pathogens (Basel), 2021-05, Vol.10 (5), p.566, Article 566</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>5</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000654393400001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c493t-920041d26475d164d9e30e1bc1cff02dde927e280fb92ad81b82c429dbfe931d3</citedby><cites>FETCH-LOGICAL-c493t-920041d26475d164d9e30e1bc1cff02dde927e280fb92ad81b82c429dbfe931d3</cites><orcidid>0000-0003-4759-6254 ; 0000-0001-7135-1260</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8151610/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8151610/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34067003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lundy, Stephanie R.</creatorcontrib><creatorcontrib>Abney, Kobe</creatorcontrib><creatorcontrib>Ellerson, Debra</creatorcontrib><creatorcontrib>Igietseme, Joseph U.</creatorcontrib><creatorcontrib>Carroll, Darin</creatorcontrib><creatorcontrib>Eko, Francis O.</creatorcontrib><creatorcontrib>Omosun, Yusuf O.</creatorcontrib><title>MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology</title><title>Pathogens (Basel)</title><addtitle>PATHOGENS</addtitle><addtitle>Pathogens</addtitle><description>Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b(-/-)) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b(-/-) mice were unable to clear the infection compared to WT mice; also, miR-378b(-/-) mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b(-/-) mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b(-/-) mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease.</description><subject>Asymptomatic</subject><subject>Biomarkers</subject><subject>Chlamydia</subject><subject>Chlamydia muridarum</subject><subject>Chlamydial pathogenesis</subject><subject>CRISPR</subject><subject>Cytokines</subject><subject>Fallopian tubes</subject><subject>Fertility</subject><subject>Gene expression</subject><subject>Genital tract</subject><subject>Immune response</subject><subject>Infections</subject><subject>Infectivity</subject><subject>Infertility</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Life Sciences & Biomedicine</subject><subject>Microbiology</subject><subject>MicroRNAs</subject><subject>miR-378b−/− mice</subject><subject>miRNA</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Pelvic inflammatory disease</subject><subject>Pregnancy</subject><subject>Reproductive system</subject><subject>RNA polymerase</subject><subject>Salpingitis</subject><subject>Science & Technology</subject><subject>Sexually transmitted diseases</subject><subject>STD</subject><subject>Uterus</subject><subject>Vagina</subject><subject>Womens health</subject><issn>2076-0817</issn><issn>2076-0817</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1rFDEUhgdRbKn9Ad7IgDeCjOZrZpIbQRdbF1oUaa9DPs7sZplNxiSj7L83261Lqzeem3w9501O3lNVLzF6R6lA7yeV12EFPmGEWtR23ZPqlKC-axDH_dMH85PqPKUNKsHRfv28OqEMdT1C9LT6dO2-N7Tnur4Odh5VhlQv1qPa7qxTzdLb2YCtb6cJYn0J3mU11jdRmVx_298_htXuRfVsUGOC8_vxrLq9-Hyz-NJcfb1cLj5eNYYJmhtBEGLYko71rcUdswIoAqwNNsOAiLUgSA-Eo0ELoizHmhPDiLB6AEGxpWfV8qBrg9rIKbqtijsZlJN3GyGupIrZmREkJ4QMFqgyGtigeiWsIppTzRj0hNOi9eGgNc16C9aAz1GNj0Qfn3i3lqvwU3Lc4g6jIvDmXiCGHzOkLLcuGRhH5SHMSZKWlkJRi0lBX_-FbsIcffmqPUVwJ1oiCoUPlIkhpQjD8TEYyb3h8h_DS86rh1UcM_7YW4C3B-AX6DAk48AbOGKlI7qWUVHwErjQ_P_pRWmF7IJfhNln-hvS9chW</recordid><startdate>20210507</startdate><enddate>20210507</enddate><creator>Lundy, Stephanie R.</creator><creator>Abney, Kobe</creator><creator>Ellerson, Debra</creator><creator>Igietseme, Joseph U.</creator><creator>Carroll, Darin</creator><creator>Eko, Francis O.</creator><creator>Omosun, Yusuf O.</creator><general>Mdpi</general><general>MDPI AG</general><general>MDPI</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T7</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-4759-6254</orcidid><orcidid>https://orcid.org/0000-0001-7135-1260</orcidid></search><sort><creationdate>20210507</creationdate><title>MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology</title><author>Lundy, Stephanie R. ; 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MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b(-/-)) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b(-/-) mice were unable to clear the infection compared to WT mice; also, miR-378b(-/-) mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b(-/-) mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b(-/-) mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>34067003</pmid><doi>10.3390/pathogens10050566</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-4759-6254</orcidid><orcidid>https://orcid.org/0000-0001-7135-1260</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Asymptomatic Biomarkers Chlamydia Chlamydia muridarum Chlamydial pathogenesis CRISPR Cytokines Fallopian tubes Fertility Gene expression Genital tract Immune response Infections Infectivity Infertility Inflammation Inflammatory diseases Life Sciences & Biomedicine Microbiology MicroRNAs miR-378b−/− mice miRNA Pathogenesis Pathology Pelvic inflammatory disease Pregnancy Reproductive system RNA polymerase Salpingitis Science & Technology Sexually transmitted diseases STD Uterus Vagina Womens health |
| title | MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology |
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