Long-term systemic bacterial infection suppresses brain and peripheral serotonergic system, leading to neurobehavioral dysfunction.

Author(s):  
Upasana Sahu
Cell Systems ◽  
2018 ◽  
Vol 6 (5) ◽  
pp. 579-592.e4 ◽  
Author(s):  
John D. Lapek ◽  
Robert H. Mills ◽  
Jacob M. Wozniak ◽  
Anaamika Campeau ◽  
Ronnie H. Fang ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e69802 ◽  
Author(s):  
Alan G. Barbour ◽  
Charlotte M. Hirsch ◽  
Arash Ghalyanchi Langeroudi ◽  
Simone Meinardi ◽  
Eric R. G. Lewis ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85623 ◽  
Author(s):  
Crystal J. Neely ◽  
Laurel B. Kartchner ◽  
April E. Mendoza ◽  
Brandon M. Linz ◽  
Jeffrey A. Frelinger ◽  
...  

2021 ◽  
Author(s):  
Arun Prakash ◽  
Mickael Bonnet ◽  
Katy M. Monteith ◽  
Pedro F. Vale

Disease tolerance describes a hosts ability to maintain health independently of the ability to clear microbe loads. However, we currently know little about the mechanisms that underlie disease tolerance or how known mechanisms of tissue damage signalling and repair may contribute to variation in tolerance. The Jak/Stat pathway plays a pivotal role in Drosophila humoral innate immunity, signalling tissue damage and triggering cellular renewal, making it a potential mechanism underlying the disease tolerance phenotype. Here, we show that disrupting the Jak/Stat pathway in Drosophila melanogaster alters disease tolerance during Pseudomonas entomophila systemic infection. Overall, flies with disrupted Jak/Stat show variation in survival that is not explained by variation in pathogen loads. For instance, mutations disrupting the function of ROS producing dual oxidase (duox) or the negative regulator of Jak/Stat, Socs36E render males less tolerant to systemic bacterial infection but not females. We also investigated whether the negative regulator of Jak/Stat, G9a which has previously been associated with tolerance of viral infections is also implicated in tolerance of bacterial infection. While female flies lacking G9a showed higher mortality and reduced bacterial clearance, disease tolerance did not differ between G9a mutants and the wildtype. This suggests that G9a does not affect tolerance during systemic bacterial infection as it appears to do with viral infection. Overall, our findings highlight that Jak/Stat signalling mediates disease tolerance during systemic bacterial infection and that this response differs between males and females. Our work therefore suggests that differences in Jak/Stat mediated disease tolerance may be a potential source of sexually dimorphic response to infection in Drosophila.


Author(s):  
Meita Hendrianingtyas ◽  
MI. Tjahjati DM

Patients in intensive care unit (ICU) have a high risk for systemic bacterial infection. Serum procalcitonin (PCT) known as a markerto predict bacterial infection, systemic inflammation responsse (SIRS) or sepsis. Another simple and easy indicator is by using leucocytecount-differential count, absolute neutrophyl count (ANC), and immatur/total (I/T) neutrophyl ratio. The aim of this study was toknow the comparation of the leucocyte count-differential count, ANC, and I/T ratio with procalcitonin serum value in patients suspectto systemic bacterial infection at ICU. A cross sectional study on 20 patients suspected with systemic bacterial infection in ICU. The datawas classified in 3 groups based on PCT serum value: group A (< 0.5 ng/mL), group B (0.5–2 ng/mL) and group C (> 2 ng/mL). Thedata was analysed by one way ANOVA test if normally distributed, and by Kruskall-Wallis test if not normally distributed. Significancywas confirmed at p < 0.05. A post hoc and Mann-Whitney test performed on a significant result. The frequency of group A was 3 (15%),group B = 5 (25%), and group C = 12 (60%). There is no significant difference on leucocyte count in 3 groups (p = 0.953), neutrophylI/T ratio (p = 0.259), ANC (p = 0.91), eosinophyl count (p = 0.287), segment neutrophyl (p = 0.094), and monosit (p = 0.152).There was a difference on lymphocyte count (p = 0.01) between group C with group A and group B and there was a difference on staffneutrophyl count (p = 0.029) and total neutrophyl count (p = 0.003) between group A with group B and C (p = 0.029). In this studywere found differences on lymphocyte, staff neutrophyl and total neutropyl count to the PCT value


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