scholarly journals Long-term Host Immune Response Trajectories Among Hospitalized Patients With Sepsis

2019 ◽  
Vol 2 (8) ◽  
pp. e198686 ◽  
Author(s):  
Sachin Yende ◽  
John A. Kellum ◽  
Victor B. Talisa ◽  
Octavia M. Peck Palmer ◽  
Chung-Chou H. Chang ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Hospitalized Patients

Unravelling some mysteries of porcine respiratory and reproductive syndrome virus (PRRSV) infections: new insights from modelling studies

2009 ◽  
Vol 2009 ◽  
pp. 30-30
Author(s):  
A Doeschl-Wilson ◽  
I Kyriazakis ◽  
L Galina-Pantoja
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Growing Pigs ◽  
Modelling Studies ◽  
Porcine Respiratory ◽  
Insight Into

Porcine reproductive and respiratory syndrome (PRRS) is an endemic pig disease in most European countries, causing respiratory distress, fever and growth reductions in growing pigs and increased litter mortality in sows. The disease is characterised by exceptionally long-term viral persistence within the host, a weak innate host immune response and delayed adaptive host immune response, and large between animal variation in the immune response (Murtaugh et al., 2004). Although numerous in-vitro and in-vivo studies produced valid insight into the fine details of the virus dynamics and its interaction with the host’s immune response, several fundamental questions concerning the role of diverse immune components and host genetics remain unanswered. In this study mathematical models were developed to investigate the role of diverse processes caused by the virus or the immune response on the infection characteristics.

A role for altered phagosome maturation in the long-term persistence ofHelicobacter pyloriinfection

2012 ◽  
Vol 303 (2) ◽  
pp. G169-G179 ◽  
Author(s):  
Glenn N. Borlace ◽  
Stacey J. Keep ◽  
Mark J. R. Prodoehl ◽  
Hilary F. Jones ◽  
Ross N. Butler ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Human Gastric Mucosa ◽  
Phagosome Maturation ◽  
Duodenal Ulcers ◽  
Immune Effector ◽  
Effector Cells ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

The vigorous host immune response that is mounted against Helicobacter pylori is unable to eliminate this pathogenic bacterium from its niche in the human gastric mucosa. This results in chronic inflammation, which can develop into gastric or duodenal ulcers in 10% of infected individuals and gastric cancer in 1% of infections. The determinants for these more severe pathologies include host (e.g., high IL-1β expression polymorphisms), bacterial [e.g., cytotoxicity-associated gene ( cag) pathogenicity island], and environmental (e.g., dietary nitrites) factors. However, it is the failure of host immune effector cells to eliminate H. pylori that underlies its persistence and the subsequent H. pylori-associated disease. Here we discuss the mechanisms used by H. pylori to survive the host immune response and, in particular, the role played by altered phagosome maturation.

Studies on the mechanism of long term survival of Taenia taeniaeformis in rats

1978 ◽  
Vol 52 (1) ◽  
pp. 1-6 ◽  
Author(s):  
B. H. Kwa ◽  
F. Y. Liew
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
The Other ◽  
Cell Adherence ◽  
Term Survival ◽  
Blocking Antibody ◽  
Long Term Survival ◽  
Other Hand ◽  
Taenia Taeniaeformis

ABSTRACTAn attempt was made to determine if blocking antibody is involved in protecting cysticerci of Taenia taeniaeformis against a host immune response. Immunoflourescence microscopy confirmed that host antibody is present on the parasite surface within the capsule. To test if the larvae can still survive after such a coat of blocking antibody is removed, the larvae were trypsinised and then implanted into recipients. The results indicate that blocking antibody could be involved in the survival of 1 year old established larvae. Untrypsinised larvae were normal 14 days after implantation into control or immunised rats. Trypsinised larvae implanted in control rats were alive but showed on intense cell adherence on their surface. On the other hand, trypsinised larvae implanted into immunised rats were dead and completely encapsulated. However, experiments with 1 month old larvae were inconclusive.

scholarly journals Rv3722c Promotes Mycobacterium tuberculosis Survival in Macrophages by Interacting With TRAF3

2021 ◽  
Vol 11 ◽  
Author(s):  
Yingying Lei ◽  
Xiaojian Cao ◽  
Weize Xu ◽  
Bing Yang ◽  
Yangyang Xu ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Host Cell ◽  
Host Immune Response ◽  
Secreted Proteins ◽  
Cell Immune Response ◽  
Term Survival ◽  
Knock Down ◽  
Tnf Α

Mycobacterium tuberculosis (M.tb) secretes numerous proteins to interfere with host immune response for its long-term survival. As one of the top abundant M.tb secreted proteins, Rv3722c was found to be essential for bacilli growth. However, it remains elusive how this protein interferes with the host immune response and regulates M.tb survival. Here, we confirmed that Rv3722c interacted with host TRAF3 to promote M.tb replication in macrophages. Knock-down of TRAF3 attenuated the effect of Rv3722c on the intracellular M.tb survival. The interaction between Rv3722c and TRAF3 hampered MAPK and NF-κB pathways, resulting in a significant increase of IFN-β expression and decrease of IL-1β, IL-6, IL-12p40, and TNF-α expression. Our study revealed that Rv3722c interacted with TRAF3 and interrupted its downstream pathways to promote M.tb survival in macrophages. These findings facilitate further understanding of the mechanism of M.tb secreted proteins in regulating the host cell immune response and promoting its intracellular survival.

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