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Antimicrobial Resistance and Infection Control (1)
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USA300 Methicillin-resistant Staphylococcus aureus in Cuba
Peraza, Gilda Toraño
Klaassen, Corné H
Velázquez, Dayneris Menéndez
Meis, Jacques F
Antimicrobial Resistance and Infection Control
Methicillin-resistant Staphylococcus aureus is an increasing problem in the Caribbean. We investigated the molecular epidemiology of MRSA isolates on Cuba.
The predominant clone was of the spa type t149, followed by community-associated MRSA USA300.
We report the first molecular typing results of MRSA isolates from Cuba.
MRSA; Cuba; Caribbean; Infection control; Hospital-associated-infection; Low-resource setting
Caspase-12 and the Inflammatory Response to Yersinia pestis
McCall, Matthew B. B.
de Vries, Maaike C.
de Jong, Dirk
Joosten, Leo A. B.
Tissingh, Rudi A.
Reubsaet, Frans A. G.
van der Meer, Jos W. M.
van der Ven, André J. A. M.
Netea, Mihai G.
Caspase-12 functions as an antiinflammatory enzyme inhibiting caspase-1 and the NOD2/RIP2 pathways. Due to increased susceptibility to sepsis in individuals with functional caspase-12, an early-stop mutation leading to the loss of caspase-12 has replaced the ancient genotype in Eurasia and a significant proportion of individuals from African populations. In African-Americans, it has been shown that caspase-12 inhibits the pro-inflammatory cytokine production.
We assessed whether similar mechanisms are present in African individuals, and whether evolutionary pressures due to plague may have led to the present caspase-12 genotype population frequencies. No difference in cytokine induction through the caspase-1 and/or NOD2/RIP2 pathways was observed in two independent African populations, among individuals with either an intact or absent caspase-12. In addition, stimulations with Yersinia pestis and two other species of Yersinia were preformed to investigate whether caspase-12 modulates the inflammatory reaction induced by Yersinia. We found that caspase-12 did not modulate cytokine production induced by Yersinia spp.
Our experiments demonstrate for the first time the involvement of the NOD2/RIP2 pathway for recognition of Yersinia. However, caspase-12 does not modulate innate host defense against Y. pestis and alternative explanations for the geographical distribution of caspase-12 should be sought.
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