Jarrett2015 - Modelling the interaction between immune response, bacterial dynamics and inflammatory damage
Ontology highlight
ABSTRACT:
SUBMITTER: 
Matthew Roberts
PROVIDER: BIOMD0000000920 | BioModels | 2020-03-11
REPOSITORIES: BioModels
Publications
Modelling the interaction between the host immune response, bacterial dynamics and inflammatory damage in comparison with immunomodulation and vaccination experiments.
Jarrett Angela M AM Cogan N G NG Shirtliff M E ME
Mathematical medicine and biology : a journal of the IMA 20140508 3
The immune system is a complex system of chemical and cellular interactions that responds quickly to queues that signal infection and then reverts to a basal level once the challenge is eliminated. Here, we present a general, four-component model of the immune system's response to a Staphylococcal aureus (S. aureus) infection, using ordinary differential equations. To incorporate both the infection and the immune system, we adopt the style of compartmenting the system to include bacterial dynami ...[more]
Similar Datasets
Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis. 3 samples in two biological replicates. One control and two samples infected with two different strains of S. aureus
2014-06-01 | E-GEOD-54230 | biostudies-arrayexpress
Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis. One control and two samples infected with two different strains of S. aureus
2014-06-01 | E-GEOD-54231 | biostudies-arrayexpress
Project description:Baker2013 - Cytokine Mediated Inflammation in
Rheumatoid Arthritis
This model by Baker M. 2013, describes
the interaction between pro and anti-inflammatory cytokine
signalling in rheumatoid arthritis.
Using two ordinary differential equations, the first model
[BIOMD0000000550]
analyses bifurcation and describes different pathological states by
altering inflammatory regulation parameters.
The second model
[BIOMD0000000549]
includes the effect that ageing has on pro-inflammatory signalling,
allowing for time-dependant properties and disease progression to
be observed. The author also describes potential dosing for
reversal of the disease state.
This model is described in the article:
Mathematical modelling of
cytokine-mediated inflammation in rheumatoid arthritis.
Baker M, Denman-Johnson S, Brook BS,
Gaywood I, Owen MR.
Math Med Biol 2013 Dec; 30(4):
311-337
Abstract:
Rheumatoid arthritis (RA) is a chronic inflammatory disease
preferentially affecting the joints and leading, if untreated,
to progressive joint damage and disability. Cytokines, a group
of small inducible proteins, which act as intercellular
messengers, are key regulators of the inflammation that
characterizes RA. They can be classified into pro-inflammatory
and anti-inflammatory groups. Numerous cytokines have been
implicated in the regulation of RA with complex up and down
regulatory interactions. This paper considers a two-variable
model for the interactions between pro-inflammatory and
anti-inflammatory cytokines, and demonstrates that mathematical
modelling may be used to investigate the involvement of
cytokines in the disease process. The model displays a range of
possible behaviours, such as bistability and oscillations,
which are strongly reminiscent of the behaviour of RA e.g.
genetic susceptibility and remitting-relapsing disease. We also
show that the dose regimen as well as the dose level are
important factors in RA treatments.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000550.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2014-09-25 | BIOMD0000000550 | BioModels
Project description:Baker2013 - Cytokine Mediated Inflammation in
Rheumatoid Arthritis - Age Dependant
This model by Baker M. 2013, describes
the interaction between pro and anti-inflammatory cytokine
signalling in rheumatoid arthritis.
Using two ordinary differential equations, the first model
[BIOMD0000000550]
analyses bifurcation and describes different pathological states by
altering inflammatory regulation parameters.
The second model
[BIOMD0000000549]
includes the effect that ageing has on pro-inflammatory signalling,
allowing for time-dependant properties and disease progression to
be observed. The author also describes potential dosing for
reversal of the disease state.
This model is described in the article:
Mathematical modelling of
cytokine-mediated inflammation in rheumatoid arthritis.
Baker M, Denman-Johnson S, Brook BS,
Gaywood I, Owen MR.
Math Med Biol 2013 Dec; 30(4):
311-337
Abstract:
Rheumatoid arthritis (RA) is a chronic inflammatory disease
preferentially affecting the joints and leading, if untreated,
to progressive joint damage and disability. Cytokines, a group
of small inducible proteins, which act as intercellular
messengers, are key regulators of the inflammation that
characterizes RA. They can be classified into pro-inflammatory
and anti-inflammatory groups. Numerous cytokines have been
implicated in the regulation of RA with complex up and down
regulatory interactions. This paper considers a two-variable
model for the interactions between pro-inflammatory and
anti-inflammatory cytokines, and demonstrates that mathematical
modelling may be used to investigate the involvement of
cytokines in the disease process. The model displays a range of
possible behaviours, such as bistability and oscillations,
which are strongly reminiscent of the behaviour of RA e.g.
genetic susceptibility and remitting-relapsing disease. We also
show that the dose regimen as well as the dose level are
important factors in RA treatments.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000549.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2014-09-25 | BIOMD0000000549 | BioModels
Project description:Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype
| PRJNA421349 | ENA
Project description:Sanchez2017 - Inflammatory responses during acute hyperinsulinemia
This model is described in the article:
The CD4+ T cell regulatory
network mediates inflammatory responses during acute
hyperinsulinemia: a simulation study
Mariana E. Martinez-Sanchez, Marcia
Hiriart, Elena R. Alvarez-Buylla
BMC Systems Biology
Abstract:
Obesity is frequently linked to insulin resistance, high
insulin levels, chronic inflammation, and alterations in the
behaviour of CD4+ T cells. Despite the biomedical importance of
this condition, the system-level mechanisms that alter CD4+ T
cell differentiation and plasticity are not well understood. We
model how hyperinsulinemia alters the dynamics of the CD4+ T
regulatory network, and this, in turn, modulates cell
differentiation and plasticity. Different polarizing
microenvironments are simulated under basal and high levels of
insulin to assess impacts on cell-fate attainment and
robustness in response to transient perturbations. In the
presence of high levels of insulin Th1 and Th17 become more
stable to transient perturbations, and their basin sizes are
augmented, Tr1 cells become less stable or disappear, while
TGF? producing cells remain unaltered. Hence, the model
provides a dynamic system-level framework and explanation to
further understand the documented and apparently paradoxical
role of TGF? in both inflammation and regulation of immune
responses, as well as the emergence of the adipose Treg
phenotype. Furthermore, our simulations provide new predictions
on the impact of the microenvironment in the coexistence of the
different cell types, suggesting that in pro-Th1, pro-Th2 and
pro-Th17 environments effector and regulatory cells can
coexist, but that high levels of insulin severely diminish
regulatory cells, especially in a pro-Th17 environment. This
work provides a first step towards a system-level formal and
dynamic framework to integrate further experimental data in the
study of complex inflammatory diseases.
This model is hosted on
BioModels Database
and identified by:
MODEL1606020000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-06-27 | MODEL1606020000 | BioModels
Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis.
2014-06-01 | GSE54230 | GEO
Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis.
2014-06-01 | GSE54231 | GEO
Project description:Dunster2014 - WBC Interactions (Model1)
This is a sub-model of a three-step
inflammatory response modelling study. The model includes distinct
populations of white blood cells namely, macrophages and active and
apoptotic neutrophil populations. Neutrophil apoptosis rate is
predicted to be crucial for the qualitative nature of the
system.
This model is described in the article:
The resolution of
inflammation: a mathematical model of neutrophil and macrophage
interactions.
Dunster JL, Byrne HM, King JR.
Bull. Math. Biol. 2014 Aug; 76(8):
1953-1980
Abstract:
There is growing interest in inflammation due to its
involvement in many diverse medical conditions, including
Alzheimer's disease, cancer, arthritis and asthma. The
traditional view that resolution of inflammation is a passive
process is now being superceded by an alternative hypothesis
whereby its resolution is an active, anti-inflammatory process
that can be manipulated therapeutically. This shift in mindset
has stimulated a resurgence of interest in the biological
mechanisms by which inflammation resolves. The
anti-inflammatory processes central to the resolution of
inflammation revolve around macrophages and are closely related
to pro-inflammatory processes mediated by neutrophils and their
ability to damage healthy tissue. We develop a spatially
averaged model of inflammation centring on its resolution,
accounting for populations of neutrophils and macrophages and
incorporating both pro- and anti-inflammatory processes. Our
ordinary differential equation model exhibits two outcomes that
we relate to healthy and unhealthy states. We use bifurcation
analysis to investigate how variation in the system parameters
affects its outcome. We find that therapeutic manipulation of
the rate of macrophage phagocytosis can aid in resolving
inflammation but success is critically dependent on the rate of
neutrophil apoptosis. Indeed our model predicts that an
effective treatment protocol would take a dual approach,
targeting macrophage phagocytosis alongside neutrophil
apoptosis.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000616.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2016-08-16 | BIOMD0000000616 | BioModels
Project description:Here, the effects of high glucose levels on influenza severity were investigated using an in vitro model of the pulmonary epithelial-endothelial barrier. We show that compared to low glucose levels, high glucose conditions prior to influenza A virus infection increased virus-induced barrier damage. Increased barrier damage was not associated with increased cell death nor increased virus replication, but rather an increased pro-inflammatory response in endothelial cells and the subsequent damage of the epithelial junctional complex.
2020-02-14 | GSE145232 | GEO