{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T07:18:44Z","timestamp":1791098324541,"version":"4.1.0"},"reference-count":39,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Immunol"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Yersinia pestis<\/jats:italic>\n                      is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with\n                      <jats:italic>Y. pestis<\/jats:italic>\n                      pro-inflammatory cytokine expression is undetectable in lung tissues.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Here, we report that, intranasal infection of mice with CO92\n                      <jats:italic>delta yopH<\/jats:italic>\n                      mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92\n                      <jats:italic>delta yopH<\/jats:italic>\n                      colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92\n                      <jats:italic>delta yopH<\/jats:italic>\n                      infection with 40% of the mice succumbing to infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1471-2172-11-29","type":"journal-article","created":{"date-parts":[[2010,6,16]],"date-time":"2010-06-16T16:33:05Z","timestamp":1276705985000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia"],"prefix":"10.1186","volume":"11","author":[{"given":"Angelene M","family":"Cantwell","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah S","family":"Bubeck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter H","family":"Dube","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,6,16]]},"reference":[{"key":"313_CR1","doi-asserted-by":"crossref","first-page":"35","DOI":"10.1128\/CMR.10.1.35","volume":"10","author":"RD Perry","year":"1997","unstructured":"Perry RD, Fetherston JD: Yersinia pestis: etiologic agent of plague. 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