Chemokines expression during Leptospira interrogans serovar Copenhageni infection in resistant BALB/c and susceptible C3H/HeJ mice

Silva, Josefa Bezerra da; Ramos, Tatiane Mendes Varela; Franco, Marcelo De; Paiva, Delhi; Ho, Paulo Lee; Martins, Elizabeth A. L.; Pereira, Martha María

doi:10.1016/j.micpath.2009.05.002

Cited by 31 publications

(26 citation statements)

References 31 publications

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“…IL-17 is known to be responsible for induction of downstream chemokines, such as KC/CXCL1, which are chemotactic for neutrophils (58). The induction of KC/ CXCL1 following infection has been documented for a wide variety of pathogens, including bacterial infections such as Pseudomonas aeruginosa (45,51,56), Chlamydia muridarum (63), Citrobacter rodentium (50,55), Listeria monocytogenes (53), Streptococcus pneumoniae (48,54), Leptospira interrogans (8), and Borrelia burgdorferi (3). In the present studies, KC/ CXCL1 induction was evaluated following systemic A. baumannii infection in C3HeB/FeJ mice.…”

Section: Characterization Of Systemic a Baumannii Infection Five CLmentioning

confidence: 99%

Innate Immune Responses to Systemic Acinetobacter baumannii Infection in Mice: Neutrophils, but Not Interleukin-17, Mediate Host Resistance

et al. 2011

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Acinetobacter baumannii is a nosocomial pathogen with a high prevalence of multiple-drug-resistant strains, causing pneumonia and sepsis. The current studies further develop a systemic mouse model of this infection and characterize selected innate immune responses to the organism. Five clinical isolates, with various degrees of antibiotic resistance, were assessed for virulence in two mouse strains, and between male and female mice, using intraperitoneal infection. A nearly 1,000-fold difference in virulence was found between bacterial strains, but no significant differences between sexes or mouse strains were observed. It was found that microbes disseminated rapidly from the peritoneal cavity to the lung and spleen, where they replicated. A persistent septic state was observed. The infection progressed rapidly, with mortality between 36 and 48 h. Depletion of neutrophils with antibody to Ly-6G decreased mean time to death and increased mortality. Interleukin-17 (IL-17) promotes the response of neutrophils by inducing production of the chemokine keratinocyte-derived chemoattractant (KC/CXCL1), the mouse homolog of human IL-8. Acinetobacter infection resulted in biphasic increases in both IL-17 and KC/CXCL1. Depletion of neither IL-17 nor KC/CXCL1, using specific antibodies, resulted in a difference in bacterial burdens in organs of infected mice at 10 h postinfection. Comparison of bacterial burdens between IL-17a؊/؊ and wild-type mice confirmed that the absence of this cytokine did not sensitize mice to Acinetobacter infection. These studies definitely demonstrate the importance of neutrophils in resistance to systemic Acinetobacter infection. However, neither IL-17 nor KC/CXCL1 alone is required for effective host defense to systemic infection with this organism.

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Section: Characterization Of Systemic a Baumannii Infection Five CLmentioning

confidence: 99%

Innate Immune Responses to Systemic Acinetobacter baumannii Infection in Mice: Neutrophils, but Not Interleukin-17, Mediate Host Resistance

et al. 2011

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“…Early findings that some strains are refractory to infection by pathogenic Leptospira spirochetes after about 4 weeks of age led to a relative reluctance to conduct investigations with this model. Although this is true for the development of acute disease in BALB/c mice (18)(19)(20), it is also apparent that other strains, such as DBA, C3H, and C57BL/6, can be infected at between 3 and 6 weeks of age and that mice of these strains show signs and symptoms of both acute and chronic infection (8)(9)(10)(11)(20)(21)(22)(23).…”

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confidence: 99%

Mouse Model for Sublethal Leptospira interrogans Infection

et al. 2015

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bAlthough Leptospira can infect a wide range of mammalian species, most studies have been conducted in golden Syrian hamsters, a species particularly sensitive to acute disease. Chronic disease has been well characterized in the rat, one of the natural reservoir hosts. Studies in another asymptomatic reservoir host, the mouse, have occasionally been done and have limited infection to mice younger than 6 weeks of age. We analyzed the outcome of sublethal infection of C3H/HeJ mice older than age 10 weeks with Leptospira interrogans serovar Copenhageni. Infection led to bloodstream dissemination of Leptospira, which was followed by urinary shedding, body weight loss, hypothermia, and colonization of the kidney by live spirochetes 2 weeks after infection. In addition, Leptospira dissemination triggered inflammation in the kidney but not in the liver or lung, as determined by increased levels of mRNA transcripts for the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosis factor alpha, interleukin-1␤, inducible nitric oxide synthase, interleukin-6, and gamma interferon in kidney tissue. The acquired humoral response to Leptospira infection led to the production of IgG mainly of the IgG1 subtype. Flow cytometric analysis of splenocytes from infected mice revealed that cellular expansion was primarily due to an increase in the levels of CD4؉ and double-negative T cells (not CD8؉ cells) and that CD4 ؉ T cells acquired a CD44 high CD62L low effector phenotype not accompanied by increases in memory T cells. A mouse model for sublethal Leptospira infection allows understanding of the bacterial and host factors that lead to immune evasion, which can result in acute or chronic disease or resistance to infection (protection).

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“…), suggesting that the gene expression levels of these effectors might be predictors of a poor outcome in leptospirosis. Moreover, different expression profiles of the chemokines monocyte chemoattractant protein-1 (MCP-1)/ CCL2, MIP-1␣/CCL3, and IL-8/CXCL8 were noticed in tissue and serum samples between resistant BALB/c and susceptible C3H/HeJ mice inoculated with a high dose of pathogenic L. interrogans serovar Copenhageni (10). These results indicated that resistance to leptospirosis is partially correlated with the increase in MIP-1␣/CCL3 levels observed in BALB/c mice, while an increasing and sustained expression of MCP-1/CCL2 and IL-8/CXCL8 in the lungs of C3H/HeJ mice correlated with the severity and progression of the disease.…”

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confidence: 99%

Gene Expression Profiles of Immune Mediators and Histopathological Findings in Animal Models of Leptospirosis: Comparison between Susceptible Hamsters and Resistant Mice

et al. 2011

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Leptospirosis is a widespread zoonosis characterized by multiple organ failure and variable host susceptibility toward pathogenic Leptospira strains. In this study, we put the role of inflammatory mediators in parallel with bacterial burdens and organ lesions by comparing a susceptible animal model, the hamster, and a resistant one, the Oncins France 1 (OF1) mouse, both infected with virulent Leptospira interrogans serovar Icterohaemorrhagiae strain Verdun. Histological observations evidenced edema, congestion, hemorrhage, and inflammatory infiltration in the organs of hamsters, in contrast to limited changes in mice. Using reverse transcription-quantitative PCR techniques, we showed that the relative Leptospira burden progressively increased in hamster tissues, while a rapid clearance was observed in mouse tissues. The early regulation of the proinflammatory mediators interleukin-1␤ (IL-1␤), IL-6, tumor necrosis factor alpha, and cyclo-oxygenase-2 and the chemokines gamma interferon-inducible protein 10 kDa/CXCL10 and macrophage inflammatory protein-1␣/CCL3 in mouse tissues contrasted with their delayed and massive overexpression in hamster tissues. Conversely, the induction of the anti-inflammatory cytokine IL-10 was faster in the resistant than in the susceptible animal model. The role of these cytokines in the pathophysiology of leptospirosis and the implications of their differential regulation in the development of this disease are discussed.

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Chemokines expression during Leptospira interrogans serovar Copenhageni infection in resistant BALB/c and susceptible C3H/HeJ mice

Cited by 31 publications

References 31 publications

Innate Immune Responses to Systemic Acinetobacter baumannii Infection in Mice: Neutrophils, but Not Interleukin-17, Mediate Host Resistance

Innate Immune Responses to Systemic Acinetobacter baumannii Infection in Mice: Neutrophils, but Not Interleukin-17, Mediate Host Resistance

Mouse Model for Sublethal Leptospira interrogans Infection

Gene Expression Profiles of Immune Mediators and Histopathological Findings in Animal Models of Leptospirosis: Comparison between Susceptible Hamsters and Resistant Mice

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