Chlamydia trachomatis infection of the Fallopian tubes. Histological findings in two patients.

Møller, Birger R.; Weström, L; Ahrons, S.; Ripa, K T; Svensson, Lovisa; Mecklenburg, Claes von; Henrikson, H.; Mårdh, Per‐Anders

doi:10.1136/sti.55.6.422

Cited by 38 publications

(25 citation statements)

References 15 publications

(7 reference statements)

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“…Additional cytokines detected that have roles in leukocyte recruitment included IL-15, an important T-cell growth factor that also serves as a chemoattractant for T lymphocytes (70), and IL-1␣ and TNF-␣, which play indirect roles in leukocyte recruitment by upregulating ICAM-1, E-selectin, and VCAM-1 on adjacent endothelia (41). Recruitment of neutrophils, monocytes, and lymphocytes without recruitment of eosinophils is consistent with the histology seen in humans with C. trachomatis salpingitis (17,47). Cytokines released at sites of infection trigger antimicrobial activity in NK cells, T cells, and phagocytes.…”

Section: Discussionmentioning

confidence: 77%

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Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

2004

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Epithelial cells play an important role in host defense as sentinels for invading microbial pathogens.Chlamydia trachomatis is an intracellular bacterial pathogen that replicates in reproductive tract epithelium. Epithelial cells lining the reproductive tract likely play a key role in triggering inflammation and adaptive immunity during Chlamydia infections. For this report a murine oviduct epithelial cell line was derived in order to determine how epithelial cells influence innate and adaptive immune responses during Chlamydia infections. As expected, oviduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemokines, including CXCL16, and regulators of the acute-phase response, including interleukin-1␣ (IL-1␣), IL-6, and tumor necrosis factor alpha. In addition, infected epithelial cells expressed cytokines that augment gamma interferon (IFN) production, including IFN-␣/␤ and IL-12-p70. To my knowledge this is the first report of a non-myeloid/lymphoid cell type making IL-12-p70 in response to an infection. Equally interesting, infected epithelial cells significantly upregulated transforming growth factor alpha precursor expression, suggesting a mechanism by which they might play a direct role in the pathological scarring seen as a consequence of Chlamydia infections. Data from these in vitro studies predict that infected oviduct epithelium contributes significantly to host innate and adaptive defenses but may also participate in the immunopathology seen with Chlamydia infections.

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Section: Discussionmentioning

confidence: 77%

“…During C. trachomatis infections with the urogenital serovars, progression of the infection into the upper female reproductive tract causes marked inflammation of the Fallopian tubes (47). Clinical data suggests that C. trachomatis evades immune-mediated elimination to cause persistent infections in some individuals (4,11,45,54,57,64,68).…”

mentioning

confidence: 99%

Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

2004

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“…In women, progression of C. trachomatis infection into the upper reproductive tract causes significant inflammation and injury to the Fallopian tubes (3). Chlamydia-induced scarring of the Fallopian tubes is the cause of ϳ50% of tubal factor infertility and 25% of ectopic pregnancies in developed countries (4,5).…”

Section: Pattern Recognition Molecules Activated Bymentioning

confidence: 99%

“…Mammalian cells sense the presence of invading microbial pathogens through recognition of pathogen-associated molecular patterns (PAMPs) 3 present in microbial structural subunits including microbial cell wall (e.g., peptidoglycan), cell membrane (e.g., LPS), and virulence proteins (e.g., flagellin) (28). TLRs are membrane-bound receptors that bind PAMPs and trigger host defense responses, including cytokine secretion.…”

Section: Pattern Recognition Molecules Activated Bymentioning

confidence: 99%

Pattern Recognition Molecules Activated by Chlamydia muridarum Infection of Cloned Murine Oviduct Epithelial Cell Lines

Derbigny

Kerr

Johnson

2005

The Journal of Immunology

103

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Chlamydia trachomatis is the most common bacterial sexually transmitted disease in the United States and a major cause of female infertility due to infection-induced Fallopian tube scarring. Epithelial cells are likely central to host defense and pathophysiology as they are the principal cell type productively infected by C. trachomatis. We generated cloned murine oviduct epithelial cell lines without viral or chemical transformation to investigate the role of the TLRs and cytosolic nucleotide binding site/leucine-rich repeat proteins Nod1 and Nod2 in epithelial responses to Chlamydia muridarum infection. RT-PCR assays detected mRNA for TLR2 (TLRs 1 and 6), TLR3, and TLR5. No mRNA was detected for TLRs 4, 7, 8, and 9. Messenger RNAs for Nod1 and Nod2 were present in the epithelial cell lines. Oviduct epithelial cell lines infected with C. muridarum or exposed to the TLR2 agonist peptidoglycan secreted representative acute phase cytokines IL-6 and GM-CSF in a MyD88-dependent fashion. Infected epithelial cell lines secreted the immunomodulatory cytokine IFN-β, even though C. muridarum does not have a clear pathogen-associated molecular pattern (PAMP) for triggering IFN-β transcription. The oviduct epithelial lines did not secrete IFN-β in response to the TLR2 agonist peptidoglycan or to the TLR3 agonist poly(I:C). Our data identify TLR2 as the principal TLR responsible for secretion of acute phase cytokines by C. muridarum-infected oviduct epithelial cell lines. The pattern recognition molecule responsible for infection-induced IFN-β secretion by oviduct epithelial cells remains to be determined.

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“…In 2007, ∼1.1 million cases of Chlamydia were reported to the Centers for Disease Control and Infection, with more than half of the cases occurring in females aged 15-24 y (2). Infection of the upper female reproductive tract with urogenital serovars of C. trachomatis can result in inflammation of the fallopian tubes, which can potentially lead to pelvic inflammatory disease, scarring, and, ultimately, infertility (3)(4)(5). The damage to mucosal epithelium and scarring caused by an untreated and persistent C. trachomatis infection in the murine female upper reproductive tract was demonstrated to be the result of a local immune response to the infection (6).…”

mentioning

confidence: 99%

The Chlamydia muridarum-Induced IFN-β Response Is TLR3-Dependent in Murine Oviduct Epithelial Cells

Derbigny¹,

Johnson²,

Toomey³

et al. 2010

The Journal of Immunology

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Epithelial cells lining the murine genital tract act as sentinels for microbial infection, play a major role in the initiation of the early inflammatory response, and can secrete factors that modulate the adaptive immune response when infected with Chlamydia. C. muridarum-infected murine oviduct epithelial cells secrete the inflammatory cytokines IL-6 and GM-CSF in a TLR2-dependent manner. Further, C. muridarum infection induces IFN-β synthesis in the oviduct epithelial cells in a TRIF-dependent manner. Because murine oviduct epithelial cells express TLR3 but not TLRs 4, 7, 8, or 9, we hypothesized that TLR3 or an unknown TRIF-dependent pattern recognition receptor was the critical receptor for IFN-β production. To investigate the role of TLR3 in the Chlamydia-induced IFN-β response in oviduct epithelial cells, we used small interfering RNA, dominant-negative TLR3 mutants, and TLR3-deficient oviduct epithelial cells to show that the IFN-β secreted during C. muridarum infection requires a functional TLR3. Interestingly, we demonstrate that the TLR3 signaling pathway is not required for IFN-β synthesis in C. muridarum-infected macrophages, suggesting that there are alternate and redundant pathways to Chlamydia-induced IFN-β synthesis that seem to be dependent upon the cell type infected. Finally, because there is no obvious dsRNA molecule associated with Chlamydia infection, the requirement for TLR3 in Chlamydia-induced IFN-β synthesis in infected oviduct epithelial cells implicates a novel ligand that binds to and signals through TLR3.

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Chlamydia trachomatis infection of the Fallopian tubes. Histological findings in two patients.

Cited by 38 publications

References 15 publications

Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

Murine Oviduct Epithelial Cell Cytokine Responses toChlamydia muridarumInfection Include Interleukin-12-p70 Secretion

Pattern Recognition Molecules Activated by Chlamydia muridarum Infection of Cloned Murine Oviduct Epithelial Cell Lines

The Chlamydia muridarum-Induced IFN-β Response Is TLR3-Dependent in Murine Oviduct Epithelial Cells

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