22/10/2014 | AGENDA - IMIBIO-SL
Disertará investigadora alemana de la Universidad de Tübingen
Será el martes 28 a las 11:30 hs. en el aula 44 del I Bloque.

La Dra. Stella E. Autenrieth, estará visitando el Instituto Multidisciplinario de Investigaciones Biológicas (IMIBIO-CONICET/UNSL) proveniente del Departamento of Internal Medicine II, University of Tübingen, Germany.

En el marco de su visita desarrollará la charla titulada “The innate immune system favors emergency monopoiesis at the expense of DC differentiation to control bacterial infections”,que tendrá lugar el martes 28 de octubre a las 11:30 horas en el Aula 44 del Bloque I de la Universidad Nacional de San Luis. Esta charla será en inglés.

Resumen de su trabajo

“The innate immune system favors emergency monopoiesis at the expense of DC differentiation to control bacterial infections”
Dendritic cells (DCs) are critical in host defense against infection, bridging the innate and adaptive immune system. Patients with sepsis display reduced circulating and splenic DCs and impaired DC function that may contribute to prolonged immune suppression and exacerbation ofinfection. However, the mechanisms of pathogen-induced DC depletion remain poorly understood. Here, a mouse model of systemic bacterial infection was employed to analyze the impact of different bacterial pathogens on DC development in vivo. We found that the numbers of bone marrow (BM) hematopoietic progenitors committed to the DC lineages were reduced following systemic infection with different Gram-positive and Gram-negative bacteria. In parallel, a TLR4-dependent increase of committed monocyte progenitors in the BM as well as mature monocytes in the spleen was observed. In line, adoptively transferred FLT3+myeloid progenitors (MPs) developed preferentially to monocytes at the expense of DCs in infected animals. Analyses performed on mixed BM chimeras suggested that both the reduction of DC progenitors and the induction of monopoiesis following infection were dependent on extrinsic TLR4 signaling driving the secretion of IFN-g regulated chemokines. Consistently, these effects were completely abrogatedby suppression of IFN-g signaling.
Elevated monocyte numbers in the spleen triggered by infection were due to a CCR2-dependent egress from the BM. In CCR2-deficient mice, in which monocytosisreportedly is abrogated, we observed a significantly increased bacterial load in the spleen and a reduced survival rate, highlighting the importance of monocytes for bacterial clearance. Together, our data provide evidence for a general response of myeloid progenitors upon bacterial infection to enhance monocyte production, thereby increasing the availability of innate immune cells as a first line of defense against invading pathogens. Concomitantly the development of DCs is impaired, which may be responsible for transient immunosuppression in e.g. bacterial sepsis.

 

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