RGD Reference Report - Impaired expression of inflammatory cytokines and chemokines at early stages of infection with Leishmania amazonensis. - Rat Genome Database

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Impaired expression of inflammatory cytokines and chemokines at early stages of infection with Leishmania amazonensis.

Authors: Ji, J  Sun, J  Soong, L 
Citation: Ji J, etal., Infect Immun. 2003 Aug;71(8):4278-88.
RGD ID: 5688168
Pubmed: PMID:12874303   (View Abstract at PubMed)
PMCID: PMC166010   (View Article at PubMed Central)

Infection of mice with Leishmania major results in disease progression or resolution, largely depending on the genetic backgrounds of the mouse strains. Infection with Leishmania amazonensis, on the other hand, causes progressive cutaneous lesions in most inbred strains of mice. We hypothesized that deficient activation of early immune responses contributes to the pathogenesis in L. amazonensis-infected mice. To distinguish early molecular events that determine the outcome of Leishmania infections, we examined cytokine gene expression in C57BL/6 mice infected with either L. amazonensis or L. major (a healing model). After 2 to 4 weeks, L. amazonensis-infected mice had significantly delayed and depressed expression of inflammatory cytokines (interleukin-12 [IL-12], gamma interferon, IL-1 alpha, IL-1 beta), CC chemokines (CC chemokine ligand 3 [CCL3]/macrophage inflammatory protein 1 alpha [MIP-1 alpha], CCL4/MIP-1 beta, CCL5/RANTES, MIP-2), and chemokine receptors (CCR1, CCR2, CCR5) in foot tissues and draining lymph nodes compared to the expression in L. major-infected controls. These findings correlated with defective T-cell responsiveness to parasite stimulation in vivo and in vitro. Adoptive transfer of L. amazonensis-specific Th1 cells prior to infection overcame the immune defects of the animals, leading to complete control of the disease. Studies with gene knockout mice suggested that IL-10, but not IL-4, contributed partially to compromised immunity in L. amazonensis-infected hosts. The data suggest that there is impairment in multiple immune functions at early stages of infection with L. amazonensis parasites and provide a compelling rationale to explore immune augmentation as an intervention in American cutaneous leishmaniasis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CCR1Humancutaneous leishmaniasis  ISOCcr1 (Mus musculus) RGD 
CCR2Humancutaneous leishmaniasis  ISOCcr2 (Mus musculus)mRNA:increased expression:foot and lymph nodeRGD 
Ccr1Ratcutaneous leishmaniasis  ISOCcr1 (Mus musculus) RGD 
Ccr1Mousecutaneous leishmaniasis  IEP  RGD 
Ccr2Ratcutaneous leishmaniasis  ISOCcr2 (Mus musculus)mRNA:increased expression:foot and lymph nodeRGD 
Ccr2Mousecutaneous leishmaniasis  IEP mRNA:increased expression:foot and lymph nodeRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ccr1  (C-C motif chemokine receptor 1)
Ccr2  (C-C motif chemokine receptor 2)

Genes (Mus musculus)
Ccr1  (C-C motif chemokine receptor 1)
Ccr2  (C-C motif chemokine receptor 2)

Genes (Homo sapiens)
CCR1  (C-C motif chemokine receptor 1)
CCR2  (C-C motif chemokine receptor 2)


Additional Information