[1]. Witkin SS, Minis E, Athanasiou A, Leizer J, Linhares IM. Chlamydia trachomatis: the Persistent Pathogen. Clin Vaccine Immunol. 2017;24(10):e00203-17.
[2]. Cossé MM, Hayward RD, Subtil A. One Face of Chlamydia trachomatis: The Infectious Elementary Body. Curr Top Microbiol Immunol. 2018;412:35-58.
[3]. GBD 2016 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016 [published correction appears in Lancet. 2017 Oct 28;390(10106):e38]. Lancet. 2017;390(10100):1211-1259. doi:10.1016/S0140-6736(17)32154-2
[4]. Satterwhite CL, Torrone E, Meites E, et al. Sexually transmitted infections among US women and men: prevalence and incidence estimates, 2008. Sex Transm Dis 2013; 40:187–193.
[5]. Witkin, S.S., et al., Chlamydia trachomatis: the Persistent Pathogen. Clin Vaccine Immunol, 2017. 24(10).
[6]. Ammerdorffer, A., et al., Chlamydia trachomatis and chlamydia-like bacteria: new enemies of human pregnancies. Curr Opin Infect Dis, 2017. 30(3): p. 289-296.
[7]. Spiliopoulou, A., et al., Chlamydia trachomatis: time for screening? Clin Microbiol Infect, 2005. 11(9): p. 687-9.
[8]. Ahmad B, Patel BC. Trachoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; June 4, 2020.
[9]. Mohammadzadeh F, Dolatian M, Jorjani M, et al. Urogenital chlamydia trachomatis treatment failure with azithromycin: A meta-analysis. Int J Reprod Biomed (Yazd). 2019;17(9):603-620.
[10]. Schena, M., et al., Quantitative monitoring of gene expression patterns with a complementary DNA microarray. Science, 1995. 270(5235): p. 467-70.
[11]. Lockhart, D.J., et al., Expression monitoring by hybridization to high-density oligonucleotide arrays. Nat Biotechnol, 1996. 14(13): p. 1675-80.
[12]. Kuhn, K., et al., A novel, high-performance random array platform for quantitative gene expression profiling. Genome Res, 2004. 14(11): p. 2347-56.
[13]. Wang, P., et al., The changes of gene expression profiling between segmental vitiligo, generalized vitiligo and healthy individual. J Dermatol Sci, 2016. 84(1): p. 40-49.
[14]. Singh, P., et al., Expression profiling of toxicity pathway genes by real-time PCR array in cypermethrin-exposed mouse brain. Toxicol Mech Methods, 2011. 21(3): p. 193-9.
[15]. Gebicke-Haerter, P., Expression profiling methods used in drug abuse research. Addict Biol, 2005. 10(1): p. 37-46.
[16]. Rank, R.G. and J.A. Whittum-Hudson, Protective immunity to chlamydial genital infection: evidence from animal studies. J Infect Dis, 2010. 201 Suppl 2: p. S168-77.
[17]. Rajeeve, K., et al., Chlamydia trachomatis paralyses neutrophils to evade the host innate immune response. Nat Microbiol, 2018. 3(7): p. 824-835.
[18]. Randow, F., J.D. MacMicking and L.C. James, Cellular self-defense: how cell-autonomous immunity protects against pathogens. Science, 2013. 340(6133): p. 701-6.
[19]. Finethy, R. and J. Coers, Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis. FEMS Microbiol Rev, 2016. 40(6): p. 875-893.
[20]. He, Q., et al., Chlamydial infection in vitamin D receptor knockout mice is more intense and prolonged than in wild-type mice. J Steroid Biochem Mol Biol, 2013. 135: p. 7-14.
[21]. Pietras EM. Inflammation: a key regulator of hematopoietic stem cell fate in health and disease. Blood. 2017 Oct 12;130(15):1693-1698. doi: 10.1182/blood-2017-06-780882. Epub 2017 Sep 5. PMID: 28874349; PMCID: PMC5639485.
[22]. Kim JH, Kim K, Kim I, Seong S, Lee KB, Kim N. BCAP promotes osteoclast differentiation through regulation of the p38-dependent CREB signaling pathway. Bone. 2018 Feb;107:188-195. doi: 10.1016/j.bone.2017.12.005. Epub 2017 Dec 6. PMID: 29223746.
[23]. Kaul R, Tao S, Wenman WM. Cyclic AMP inhibits protein synthesis in Chlamydia trachomatis at a transcriptional level. Biochim Biophys Acta. 1990 Jun 12;1053(1):106-12. doi: 10.1016/0167-4889(90)90032-9. PMID: 2163685.
[24]. Kurihara Y, Itoh R, Shimizu A, Walenna NF, Chou B, Ishii K, Soejima T, Fujikane A, Hiromatsu K. Chlamydia trachomatis targets mitochondrial dynamics to promote intracellular survival and proliferation. Cell Microbiol. 2019 Jan;21(1):e12962. doi: 10.1111/cmi.12962. Epub 2018 Oct 30. PMID: 30311994.
[25]. Qian Z, Zhang Z, Wang Y. T cell receptor signaling pathway and cytokine-cytokine receptor interaction affect the rehabilitation process after respiratory syncytial virus infection. PeerJ. 2019 Jun 12;7:e7089. doi: 10.7717/peerj.7089. PMID: 31223533; PMCID: PMC6571000.
[26]. Louche, A., S.P. Salcedo and S. Bigot, Protein-Protein Interactions: Pull-Down Assays. Methods Mol Biol, 2017. 1615: p. 247-255.
[27]. Lin, J.S. and E.M. Lai, Protein-Protein Interactions: Co-Immunoprecipitation. Methods Mol Biol, 2017. 1615: p. 211-219.
[28]. Natividad, A., et al., Innate immunity in ocular Chlamydia trachomatis infection: contribution of IL8 and CSF2 gene variants to risk of trachomatous scarring in Gambians. BMC Med Genet, 2009. 10: p. 138.
[29]. Rasmussen, S.J., et al., Secretion of proinflammatory cytokines by epithelial cells in response to Chlamydia infection suggests a central role for epithelial cells in chlamydial pathogenesis. J Clin Invest, 1997. 99(1): p. 77-87.
[30]. Vliagoftis, H., et al., Airway epithelial cells release eosinophil survival-promoting factors (GM-CSF) after stimulation of proteinase-activated receptor 2. J Allergy Clin Immunol, 2001. 107(4): p. 679-85.
[31]. Schlievert, P.M., et al., Staphylococcal Superantigens Stimulate Epithelial Cells through CD40 To Produce Chemokines. mBio, 2019. 10(2).
[32]. Saba, S., et al., Bacterial stimulation of epithelial G-CSF and GM-CSF expression promotes PMN survival in CF airways. Am J Respir Cell Mol Biol, 2002. 27(5): p. 561-7.
[33]. Balloy, V., et al., Normal and Cystic Fibrosis Human Bronchial Epithelial Cells Infected with Pseudomonas aeruginosa Exhibit Distinct Gene Activation Patterns. PLoS One, 2015. 10(10): p. e0140979.