Registration for a live webinar on 'Precision medicine treatment for anticancer drug resistance' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Resistance vs. tolerance to infection
- Tolerance to infection: tissue damage control (1)
- Tolerance to infection: tissue damage control (2)
- Tolerance to infection: tissue damage control (3)
- Tolerance to infection: tissue damage control (4)
- Host tolerance to infection in mammals
- Tolerance to Plasmodium infection
- Molecular basis of damage control and tolerance
- Tissue damage control: stress-responsive genes
- The stress-responsive heme oxygenase-1 (HO-1)
- Plasmodium infection and HO-1 gene expression
- HO-1 expression provides tissue damage control
- Tolerance to Plasmodium infection by HO-1 (1)
- Tolerance to Plasmodium infection by HO-1 (2)
- Were stress-responsive genes naturally selected?
- Sickle cell anemia: a molecular disease
- The molecular basis for sickle cell anemia
- Sickle cell trait is protective against malaria
- Plasmodium infection: cerebral malaria
- Cerebral malaria: pathology (1)
- Cerebral malaria: pathology (2)
- CD8+ T cell-driven neuroinflammation
- Hemolytic CD8+ T cell-driven neuroinflammation
- Sickle cell anemia
- Accumulation of free heme in the plasma
- The sickle HbSAD mouse
- Sickle HbSAD mice: lack of overt pathology
- Sickle HbSAD mice: plasma free heme
- Free heme suppresses cerebral malaria in mice
- Free heme confers host tolerance to malaria
- Sickle HbSAD mice survive cerebral malaria (1)
- Sickle HbSAD mice survive cerebral malaria (2)
- Sickle HbSAD mice survive cerebral malaria (3)
- Sickle HbSAD mice induce HO-1 expression (1)
- Expression HO-1 in sickle HbSAD mice
- Nrf2 regulates the expression of HO-1
- Sickle HbSAD mice develop tolerance via Nrf2 (1)
- Sickle HbSAD mice develop tolerance via Nrf2 (2)
- Sickle HbSAD mice induce HO-1 expression (2)
- Decreased HO-1 expression in Hmox1+/- mice
- Sickle HbSAD mice develop tolerance via HO-1 (1)
- Sickle HbSAD mice develop tolerance via HO-1 (2)
- Sickle HbSAD mice develop tolerance via HO-1 (3)
- Sickle HbSAD mice develop tolerance via HO-1 (4)
- HbSAD mice do not develop brain edema (1)
- HbSAD mice do not develop brain edema (2)
- The protective effect of sickle hemoglobin
- HbSAD mice repress CD8+ T cell activation (1)
- Effect of accumulation of low levels of free heme
- HbSAD mice repress CD8+ T cell activation (2)
- HbSAD mice repress CD8+ T cell activation (3)
- A mechanism of sickle cell protection
- Conclusions
- Acknowledgements (1)
- Acknowledgements (2)
Topics Covered
- Host defense strategies against pathogenic microorganisms and parasites
- Expression of stress-responsive genes provide tissue damage control, uncoupling different forms of stress associated with inflammation and immunity from tissue damage and disease
- Tissue damage control confers host tolerance to infection
- Heme oxygenase-1 is a stress-responsive gene that provides tissue damage control
- Heme oxygenase-1 confers host tolerance to Plasmodium infection
- Preservation of Heme oxygenase-1 system during human evolution
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Soares, M.P. (2012, April 29). Tissue damage control confers host tolerance to infection [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 25, 2024, from https://doi.org/10.69645/SVOX5559.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Miguel P. Soares has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Biochemistry
Transcript
Please wait while the transcript is being prepared...
0:00
Tissue damage control confers
host tolerance to infection.
0:06
Resistance versus
tolerance to infection.
It is now well established
that there are two host offense
strategies against pathogenic
microorganisms and parasites.
It can be divided into two
conceptually different components.
The first is resistance
to infection.
This is a defense strategy
that protects the infected host
by reducing its pathogenic burden.
Resistance is a function of
the immune system, which works
by detection,
neutralization, destruction,
or expulsion of pathogens.
Tolerance to infection is a second
host defense strategy that reduces
the negative impact of
infection on host fitness,
as does resistance to infection.
Unlike resistance to
infection however, tolerance
does not affect directly
pathogen burden.
Rather, tolerance limits host
susceptibility to tissue damage
or other fitness costs caused
either directly by pathogens
or indirectly by the immune
response against them.
1:08
Tolerance to infection
and tissue damage control.
Infectious diseases reflect the
extent of cell, tissue, organ,
or system damage caused
directly by pathogens
or indirectly by the
host immune response
elicited by those pathogens.
Host protective strategies
that limit the severity
of infectious diseases must
incorporate mechanisms that limit
the extent of cell, tissue, organ,
and ultimately, system damage.
We'll refer to those mechanisms
as tissue damage control.