{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T20:13:58Z","timestamp":1777493638524,"version":"3.51.4"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2013,2,1]],"date-time":"2013-02-01T00:00:00Z","timestamp":1359676800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Puerperal sepsis is a leading cause of maternal mortality worldwide. Streptococcus pyogenes [group A Streptococcus; (GAS)] is a major etiologic agent of severe postpartum sepsis, yet little is known regarding the pathogenesis of these infections. Tissue macrophages provide innate defense against GAS, and their actions are highly regulated. The intracellular second messenger cAMP can negatively regulate macrophage actions against GAS. Because leukotriene (LT) B4 has been shown to suppress intracellular cAMP in macrophages, we hypothesized that it could enhance innate defenses against GAS. We assessed the capacity of LTB4 to modulate antistreptococcal actions of human macrophages, including placental and decidual macrophages and used a novel intrauterine infection model of GAS in mice lacking the 5-lipoxygenase enzyme to determine the role of endogenous LTs in host defense against this pathogen. Animals lacking 5-lipoxygenase were significantly more vulnerable to intrauterine GAS infection than were wild-type mice and showed enhanced dissemination of bacteria out of the uterus and a more robust inflammatory response than did wild-type mice. In addition, LTB4 reduced intracellular cAMP levels via the BLT1 receptor and was a potent stimulant of macrophage phagocytosis and NADPH oxidase\u2013dependent intracellular killing of GAS. Importantly, interference was observed between the macrophage immunomodulatory actions of LTB4 and the cAMP-inducing lipid PGE2, suggesting that interplay between pro- and anti-inflammatory compounds may be important in vivo. This work underscores the potential for pharmacological targeting of lipid mediator signaling cascades in the treatment of invasive GAS infections.<\/jats:p>","DOI":"10.4049\/jimmunol.1202932","type":"journal-article","created":{"date-parts":[[2013,1,17]],"date-time":"2013-01-17T07:28:45Z","timestamp":1358407725000},"page":"1614-1622","source":"Crossref","is-referenced-by-count":49,"title":["Leukotriene B4 Enhances Innate Immune Defense against the Puerperal Sepsis Agent <i>Streptococcus pyogenes<\/i>"],"prefix":"10.1093","volume":"190","author":[{"given":"Elyara M","family":"Soares","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI 48109"},{"name":"Departamento de An\u00e1lises Cl\u00ednicas, Toxicol\u00f3gicas e Bromatol\u00f3gicas, Faculdade de Ci\u00eancias Farmac\u00eauticas de Ribeir\u00e3o Preto, Universidade de S\u00e3o Paulo , Ribeir\u00e3o Preto, SP, 14040-903,","place":["Brazil"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katie L","family":"Mason","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI 48109"},{"name":"Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lisa M","family":"Rogers","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlos H","family":"Serezani","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucia H","family":"Faccioli","sequence":"additional","affiliation":[{"name":"Departamento de An\u00e1lises Cl\u00ednicas, Toxicol\u00f3gicas e Bromatol\u00f3gicas, Faculdade de Ci\u00eancias Farmac\u00eauticas de Ribeir\u00e3o Preto, Universidade de S\u00e3o Paulo , Ribeir\u00e3o Preto, SP, 14040-903,","place":["Brazil"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David M","family":"Aronoff","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI 48109"},{"name":"Department of Microbiology and Immunology, University of Michigan Medical School , Ann Arbor, MI 48109"},{"name":"Reproductive Sciences Program, Department of Microbiology and Immunology, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2013,2,15]]},"reference":[{"key":"2025032406321799800_r1","doi-asserted-by":"crossref","first-page":"685","DOI":"10.1016\/S1473-3099(05)70267-X","article-title":"The global burden of group A streptococcal diseases","volume":"5","author":"Carapetis","year":"2005","journal-title":"Lancet Infect. 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