General Information:

Id: 3,653
Diseases: Q fever
pathogen-host system
Coxiella burnetii/mammalia
review
Reference: Amara AB et al.(2012) Immune Response and Coxiella burnetii Invasion Adv. Exp. Med. Biol. 984: 287-298 [PMID: 22711638]

Interaction Information:

Comment The phagocytosis of phase I C. burnetii is mediated by alphav-beta3 integrin and leads to a low phagocytosis rate and intracellular surviva.
Formal Description
Interaction-ID: 34712

organism

Coxiella burnetii, phase I

interacts (colocalizes) with

complex/PPI

Alphav-beta3 integrin complex

Comment The phagocytosis of phase I C. burnetii is mediated by alphav-beta3 integrin and leads to a low phagocytosis rate and intracellular surviva.
Formal Description
Interaction-ID: 34717

organism

Coxiella burnetii, phase I

increases_activity of

process

pathogen survival

Comment The phagocytosis of phase II C. burnetii is mediated by alphav-beta3 integrin and CR3 (alphaM-beta2 integrin, CD11b/CD18) resulting in high phagocytosis rate and bacterial eliminatio.
Formal Description
Interaction-ID: 34720

organism

Coxiella burnetii, phase II

interacts (colocalizes) with

complex/PPI

Alphav-beta3 integrin complex

Comment The phagocytosis of phase II C. burnetii is mediated by alphav-beta3 integrin and CR3 (alphaM-beta2 integrin, CD11b/CD18) resulting in high phagocytosis rate and bacterial eliminatio.
Formal Description
Interaction-ID: 34726

organism

Coxiella burnetii, phase II

decreases_activity of

process

pathogen survival

Comment The phagocytosis of phase II C. burnetii is mediated by alphav-beta3 integrin and CR3 (alphaM-beta2 integrin, CD11b/CD18) resulting in high phagocytosis rate and bacterial eliminatio.
Formal Description
Interaction-ID: 34730

organism

Coxiella burnetii, phase II

interacts (colocalizes) with

complex/PPI

AlphaM-beta2 integrin complex

Comment The activation state of monocytes and macrophages after encountering C. burnetii are apparently different.
Formal Description
Interaction-ID: 34756

process

Coxiella burnetii infection

increases_activity of

Comment The activation state of monocytes and macrophages after encountering C. burnetii are apparently different.
Formal Description
Interaction-ID: 34757

process

Coxiella burnetii infection

increases_activity of

Comment Monocytes show a pro-inflammatory M1-type response, macrophages are polarized toward an M2-type. In circulating monocytes, C. burnetii stimulates the M1-type response that control bacterial replication.
Formal Description
Interaction-ID: 34759

increases_activity of

process

M1 polarization

in response to C. burnetii infection
Comment Monocytes show a pro-inflammatory M1-type response, macrophages are polarized toward an M2-type. In macrophages, C. burnetii stimulates an atypical M2-type response that is unable to control C. burnetii replication, as observed during acute Q fever.
Formal Description
Interaction-ID: 34764

increases_activity of

process

atypical M2 polarization

in response to C. burnetii infection
Comment Macrophages infected with C. burnetii release the following M2-type related proteins: IL-10, TGF-beta-1, CCL18, mannose receptor, active form of arginase-1.
Formal Description
Interaction-ID: 34766

process

atypical M2 polarization

increases_quantity of

gene/protein

IL10

in macrophages; in response to C. burnetii infection
Comment Macrophages infected with C. burnetii release the following M2-type related proteins: IL-10, TGF-beta-1, CCL18, mannose receptor and the active form of arginase-1.
Formal Description
Interaction-ID: 34767

process

atypical M2 polarization

increases_quantity of

gene/protein

TGFB1

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for TGFB1
Comment Macrophages infected with C. burnetii release the following M2-type related proteins: IL-10, TGF-beta-1, CCL18, mannose receptor and the active form of arginase-1.
Formal Description
Interaction-ID: 34768

process

atypical M2 polarization

increases_quantity of

gene/protein

CCL18

in macrophages; in response to C. burnetii infection
Comment Macrophages infected with C. burnetii release the following M2-type related proteins: IL-10, TGF-beta-1, CCL18, mannose receptor and the active form of arginase-1.
Formal Description
Interaction-ID: 34769

process

atypical M2 polarization

increases_quantity of

gene/protein

MRC1

in macrophages; in response to C. burnetii infection
Comment Macrophages infected with C. burnetii release high levels of IL-6 and CXCL8, two molecules associated with M1 polarization.
Formal Description
Interaction-ID: 34770

process

atypical M2 polarization

increases_quantity of

gene/protein

IL6

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for IL6
Comment Macrophages infected with C. burnetii release high levels of IL-6 and CXCL8, two molecules associated with M1 polarization.
Formal Description
Interaction-ID: 34771

process

atypical M2 polarization

increases_quantity of

gene/protein

CXCL8

in response to C. burnetii infection
Comment Macrophages infected with C. burnetii release the following M2-type related proteins: IL-10, TGF-beta-1, CCL18, mannose receptor and the active form of arginase-1.
Formal Description
Interaction-ID: 34772

process

atypical M2 polarization

increases_quantity of

gene/protein

ARG1

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for ARG1
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34773

process

M1 polarization

increases_quantity of

gene/protein

TNF

in monocytes; in response to C. burnetii infection
Drugbank entries Show/Hide entries for TNF
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34774

process

M1 polarization

increases_quantity of

gene/protein

IL6

in monocytes; in response to C. burnetii infection
Drugbank entries Show/Hide entries for IL6
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34775

process

M1 polarization

increases_quantity of

gene/protein

IL12

in monocytes; in response to C. burnetii infection
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34776

process

M1 polarization

increases_quantity of

gene/protein

CD80

in monocytes; in response to C. burnetii infection
Drugbank entries Show/Hide entries for CD80
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34777

process

M1 polarization

increases_quantity of

gene/protein

CCR7

in monocytes; in response to C. burnetii infection
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34778

process

M1 polarization

increases_quantity of

gene/protein

IFNG

in monocytes; in response to C. burnetii infection
Drugbank entries Show/Hide entries for IFNG
Comment In circulating monocytes, C. burnetii stimulates an M1-type activation that controls bacterial replication. The M1-type activation is associated with the release of: TNF, IL-6, IL-12, CD80, CCR7, IFN-gamma and NO production.
Formal Description
Interaction-ID: 34779

process

M1 polarization

increases_quantity of

drug/chemical compound

Reactive nitrogen species

in response to C. burnetii infection
Comment Intracellular trafficking is under the control of IL-10, which is responsible for bacterial persistence and the development of chronic Q fever.
Formal Description
Interaction-ID: 34787

gene/protein

IL10

increases_activity of

process

pathogen survival

Comment There is no expression of the M1 typical molecules TNF, IL-12, CD80 and CCR7 in macrophages in response to C. burnetii infection.
Formal Description
Interaction-ID: 34788

process

atypical M2 polarization

NOT increases_quantity of

gene/protein

TNF

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for TNF
Comment There is no expression of the M1 typical molecules TNF, IL-12, CD80 and CCR7 in macrophages in response to C. burnetii infection.
Formal Description
Interaction-ID: 34789

process

atypical M2 polarization

NOT increases_quantity of

gene/protein

IL12

in macrophages; in response to C. burnetii infection
Comment There is no expression of the M1 typical molecules TNF, IL-12, CD80 and CCR7 in macrophages in response to C. burnetii infection.
Formal Description
Interaction-ID: 34790

process

atypical M2 polarization

NOT increases_quantity of

gene/protein

CD80

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for CD80
Comment There is no expression of the M1 typical molecules TNF, IL-12, CD80 and CCR7 in macrophages in response to C. burnetii infection.
Formal Description
Interaction-ID: 34791

process

atypical M2 polarization

NOT increases_quantity of

gene/protein

CCR7

in macrophages; in response to C. burnetii infection
Comment There is no increase of the M1 typical nitric oxide production in macrophages in response to C. burnetii infection.
Formal Description
Interaction-ID: 34792

process

atypical M2 polarization

NOT increases_quantity of

drug/chemical compound

Reactive nitrogen species

in macrophages; in response to C. burnetii infection
Comment In addition to bone marrow cells, adipose tissue is a candidate to house C. burnetii. Adipose tissue macrophages are the probable targets of C. burnetii but adipocytes may also harbor C. burnetii.
Formal Description
Interaction-ID: 34794

process

Coxiella burnetii infection

is localized in

tissue/cell line

adipose tissue

Comment C. burnetii has been shown to be present in placenta.
Formal Description
Interaction-ID: 34801

process

Coxiella burnetii infection

is localized in

tissue/cell line

placenta

Comment It has been shown that IL-10 is the main factor in the chronic development of Q fever.
Formal Description
Interaction-ID: 34805

disease

Q fever, chronic

increases_quantity of

gene/protein

IL10

Comment It has been shown that IL-10 induces C. burnetii replication in monocytes.
Formal Description
Interaction-ID: 34808

gene/protein

IL10

increases_activity of

process

Coxiella burnetii replication

in monocytes
Comment IL-10 decreases the TNF production, because TNF was shown to restore the microbicidal activity against C. burnetii in IL-10-treated monocytes.
Formal Description
Interaction-ID: 34813

gene/protein

IL10

decreases_quantity of

gene/protein

TNF

in monocytes
Drugbank entries Show/Hide entries for TNF
Comment IL-10 upregulates the release of monocyte type II receptors of TNF (TNF-RII). There is an increase of TNF-RII during chronic Q fever.
Formal Description
Interaction-ID: 34817

gene/protein

IL10

increases_quantity of

gene/protein

TNFRSF1B

in monocytes
Drugbank entries Show/Hide entries for TNFRSF1B
Comment The transendothelial migration of mononuclear cells is defective in patients with Q fever endocarditis, the neutralization of IL-10 corrects the defect.
Formal Description
Interaction-ID: 34826

gene/protein

IL10

decreases_activity of

in monocytes
Comment Vanin-1 is a membrane-anchored pantetheinase involved in control of tissue inflammation. The results show that vanin-1 plays a role in granuloma formation in response to C. burnetii by skewing macrophage activation toward an M2 program.
Formal Description
Interaction-ID: 34840

gene/protein

VNN1

affects_activity of

in bone marrow-derived macrophages
Comment Vanin-1 is a membrane-anchored pantetheinase involved in control of tissue inflammation. The results show that vanin-1 plays a role in granuloma formation in response to C. burnetii by skewing macrophage activation toward an M2 program.
Formal Description
Interaction-ID: 34841

gene/protein

VNN1

affects_activity of

process

M2 polarization

in bone marrow-derived macrophages
Comment C. burnetii infection of macrophages inhibits cell apoptosis via the upregulation of c/IAP2 (BIRC3) and A1/bfl1 (BCL2A1), which prevents the activation of caspase 3 and the BH3-only proteins.
Formal Description
Interaction-ID: 34842

process

Coxiella burnetii infection

decreases_activity of

process

host cell apoptosis

in macrophages
Comment C. burnetii infection of macrophages inhibits cell apoptosis via the upregulation of c/IAP2 (BIRC3) and A1/bfl1 (BCL2A1), which prevents the activation of caspase 3 and the BH3-only proteins.
Formal Description
Interaction-ID: 34843

process

Coxiella burnetii infection

increases_quantity of

gene/protein

BCL2A1

in macrophages
Comment C. burnetii infection of macrophages inhibits cell apoptosis via the upregulation of c/IAP2 (BIRC3) and A1/bfl1 (BCL2A1), which prevents the activation of caspase 3 and the BH3-only proteins.
Formal Description
Interaction-ID: 34844

process

Coxiella burnetii infection

increases_quantity of

gene/protein

BIRC3

in macrophages
Comment C. burnetii infection of macrophages inhibits cell apoptosis via the upregulation of c/IAP2 (BIRC3) and A1/bfl1 (BCL2A1), which prevents the activation of caspase 3 and the BH3-only proteins.
Formal Description
Interaction-ID: 34845

gene/protein

BCL2A1

decreases_activity of

process

host cell apoptosis

in macrophages
Comment C. burnetii infection of macrophages inhibits cell apoptosis via the upregulation of c/IAP2 (BIRC3) and A1/bfl1 (BCL2A1), which prevents the activation of caspase 3 and the BH3-only proteins.
Formal Description
Interaction-ID: 34846

gene/protein

BIRC3

decreases_activity of

process

host cell apoptosis

in macrophages
Comment The survival strategy of C. burnetii is to prevent apoptosis.
Formal Description
Interaction-ID: 34852

process

pathogen survival

decreases_activity of

process

host cell apoptosis

Comment The neutralization of IL-10 and TGF-beta-1 prevents the replication of C. burnetii due to the engulfment of apoptotic lymphocytes, suggesting that IL-10 and TGF-beta-1 are critically involved in bacterial replication.
Formal Description
Interaction-ID: 34858

gene/protein

TGFB1

increases_activity of

process

Coxiella burnetii replication

in macrophages; in response to C. burnetii infection
Drugbank entries Show/Hide entries for TGFB1
Comment A patient study to analyse the levels of regulatory T cell subsets in acute or chronic Q fever showed no significant differences between acute Q fever patients and healthy subjects. But there was a significant increase in Tregs expressing Foxp3 in patients with Q fever endocarditis.
Formal Description
Interaction-ID: 34884

disease

Q fever, chronic

increases_quantity of

gene/protein

FOXP3

in regulatory T cell subsets
Comment In macrophages, C. burnetii induces an atypical M2 profile that is unable to control C. burnetii replication, as observed during acute Q fever.
Formal Description
Interaction-ID: 34962

process

atypical M2 polarization

NOT decreases_activity of

process

Coxiella burnetii replication

in macrophages
Comment In circulating monocytes, C. burnetii stimulates an M1 profile that control bacterial replication.
Formal Description
Interaction-ID: 34963

process

M1 polarization

decreases_activity of

process

Coxiella burnetii replication

in monocytes
Comment Phagosome-lysosome fusion is impaired in patients with chronic Q fever relative to patients with acute Q fever. The neutralization of endogenous IL-10 reestablishes the fusion.
Formal Description
Interaction-ID: 34964

gene/protein

IL10

decreases_activity of

Comment The number of granulomas is low in the spleen and liver of infected transgenic mice, as also shown in patients with chronic Q fever.
Formal Description
Interaction-ID: 34965

disease

Q fever, chronic

NOT increases_activity of

Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in monocytes: CD14, IL-10 and IL-1ra.
Formal Description
Interaction-ID: 34966

process

M2 polarization

increases_quantity of

gene/protein

CD14

in monocytes
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in monocytes: CD14, IL-10 and IL-1ra.
Formal Description
Interaction-ID: 34967

process

M2 polarization

increases_quantity of

gene/protein

IL10

in monocytes
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in monocytes: CD14, IL-10 and IL-1ra.
Formal Description
Interaction-ID: 34968

process

M2 polarization

increases_quantity of

gene/protein

IL1RN

in monocytes
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in macrophages: IL-10, TGF-beta-1, IL-1ra, and MR.
Formal Description
Interaction-ID: 34969

process

M2 polarization

increases_quantity of

gene/protein

IL10

in macrophages
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in macrophages: IL-10, TGF-beta-1, IL-1ra, and MR.
Formal Description
Interaction-ID: 34970

process

M2 polarization

increases_quantity of

gene/protein

TGFB1

in macrophages
Drugbank entries Show/Hide entries for TGFB1
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in macrophages: IL-10, TGF-beta-1, IL-1ra, and MR.
Formal Description
Interaction-ID: 34971

process

M2 polarization

increases_quantity of

gene/protein

IL1RN

in macrophages
Comment In chronic Q fever C. burnetii replication is related to an M2 program, characterized by the up-regulation of the following molecules in macrophages: IL-10, TGF-beta-1, IL-1ra, and MR.
Formal Description
Interaction-ID: 34972

process

M2 polarization

increases_quantity of

gene/protein

MRC1

in macrophages
Comment The engulfment of apoptotic cells by monocytes and macrophages increases C. burnetii replication by redirecting their activation states toward M2 profiles that are non-protective against most pathogens.
Formal Description
Interaction-ID: 34973

increases_activity of

process

M2 polarization

Comment The engulfment of apoptotic cells by monocytes and macrophages increases C. burnetii replication by redirecting their activation states toward M2 profiles that are non-protective against most pathogens.
Formal Description
Interaction-ID: 34974

increases_activity of

process

Coxiella burnetii replication

Comment The authors propose a model in which apoptotic cells play a key role in the establishment of Q fever endocarditis.
Formal Description
Interaction-ID: 34975

disease

Q fever, chronic

increases_activity of

Comment In an inflammatory context (such as that found in the presence of IFN-gamma ), the effect of apoptotic cell engulfment is inhibited.
Formal Description
Interaction-ID: 34976

disease

Q fever, acute

decreases_activity of

Comment A patient study to analyse the levels of regulatory T cell subsets in acute or chronic Q fever showed no significant differences between acute Q fever patients and healthy subjects. But there was a significant increase in Tregs expressing Foxp3 in patients with Q fever endocarditis.
Formal Description
Interaction-ID: 36492

disease

Q fever, acute

NOT increases_quantity of

gene/protein

FOXP3

in regulatory T cell subsets