Description of an in vivo model for the assessment of eosinophil chemoattractants in the mouse

Teixeira, Mauro Martins; Williams, Timothy J.; Hellewell, Paul G.

doi:10.1590/s0074-02761997000800029

Cited by 5 publications

(4 citation statements)

References 17 publications

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“…It is noteworthy that the inhibition observed (28%) may be underestimated as the egg itself accounts for some of the granuloma area that, if excluded, would revert in a larger percent inhibition. The slight fall in EPO activity found in the present study is in agreement with previous data in that eosinophils should be less recruited in the absence of CCL3 (49). A reduction in the number of eosinophils may have contributed to the smaller size of granulomas present in the liver of CCL3-deficient mice.…”

Section: Discussionsupporting

confidence: 92%

Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

Souza¹,

Roffê²,

Pinho³

et al. 2005

Infect Immun

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In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1␣ (MIP-1␣/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.Schistosomiasis is one of the most prevalent helminth diseases in the world and is caused by blood flukes of the Schistosoma genus (36). In infected individuals, the granulomatous inflammation in response to egg deposition in the liver in the case of Schistosoma mansoni is the major pathological finding and accounts for most of the clinical symptoms. Worm oviposition at 5 to 6 weeks poses a strong Th2 bias in the immune response against infection (6) while also inhibiting the Th1 component (12,42). Nonetheless, the granulomatous response that is maximal during the first few weeks after initial oviposition is also subjected to immunomodulation. Apart from interleukin-10 (IL-10) (29), other factors may also be involved in this process. For example, recent literature suggests that, in animal models, the granulomatous response that occurs at chronic time points is dependent on the soluble form of the IL-13 receptor ␣2 (27). In patients, failure in modulating the response might lead to the development severe schistosomiasis later in life (15). Indeed, a direct consequence of the persistence of an exacerbated immune response appears to be the development of large granulomatous reactions associated with intense collagen deposition (20) and the development of hepatosplenic schistosomiasis. Therefore, there is much scientific interest in the understanding of the mechanisms and inflammatory mediators underlying egg-induced granulomatous response, with the ultimate goal of proposing strategies to modulate fibrosis. It is known, however, that prevention of granuloma formation may be dangerous, since lethality ...

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Section: Discussionsupporting

confidence: 92%

Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

Souza¹,

Roffê²,

Pinho³

et al. 2005

Infect Immun

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“…The infiltration is most likely caused directly by C5a, a known eosinophil chemoattract ( Yancey 1988, Gerard & Gerard 1994). Interestingly, in this model, the lack of C5a‐mediated chemotaxis on eosinophils could not be compensated by redundant mechanisms, as for example those driven by eotaxin or MIP‐1α ( Texeira et al . 1997 ).…”

Section: Discussionmentioning

confidence: 98%

Contribution of C5‐mediated mechanisms to host defence against Echinococcus granulosus hydatid infection

Ferreira

Breijo

Sim

et al. 2000

Parasite Immunology

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The aim of this work was to investigate the contribution of complement C5-mediated mechanisms, with an emphasis on inflammation, to host defences against Echinococcus granulosus hydatid disease. Thus, we compared the systemic and local inflammatory responses induced by the parasite, and the outcome of infection, between congenic C5-sufficient (B10.D2 n/SnJ) and C5-deficient (B10.D2 o/SnJ) mice challenged with protoscoleces. Indirect evidence of in-vivo complement activation during the establishment phase was obtained; infection induced serum amyloid P and eosinophil responses which were dependent on C5. Early recruitment of polymorphonuclear cells was not dependent on the presence of C5. The higher capacity of C5-sufficient mice to recruit eosinophils was also observed during the cystic phase of infection, and mice recruiting more eosinophils developed lower parasite masses. Analysis of the outcome of infection after 8 months showed that C5-sufficient mice were more resistant to infection than C5-deficient mice in terms of individuals with no cysts; this trend was not statistically significant. In addition, C5-deficient mice developed higher numbers of large (> 5 mm in diameter) cysts and higher cyst weights than C5-sufficient mice indicating that C5-mediated mechanisms are detrimental for parasite growth. Taken together, our results suggest that complement, through C5-mediated effectors, contributes to host defences by both restricting the establishment of infection and controlling the growth of established cysts. This contribution may, at least partially, be associated with the ability of C5a to promote eosinophil infiltration.

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“…Indeed, they are potent eosinophil and lymphocyte chemoattractants (3,29,35,39,41,42), which comprise the principle infiltrating cells in the mouse model of FI-RSV-induced enhanced pathology (23,43,44). Alternatively, the relatively homeostatic kinetics of MCP-1, MIP-1␣, MIP-1␤, MIP-2, Ltn, and RANTES gene expression at early time points postchallenge in this group suggest that these chemokines are not implicated in initiation of the associated pathology.…”

Section: Discussionmentioning

confidence: 99%

Differential Histopathology and Chemokine Gene Expression in Lung Tissues following Respiratory Syncytial Virus (RSV) Challenge of Formalin-Inactivated RSV- or BBG2Na-Immunized Mice

Power

Huss

Michaud

et al. 2001

J Virol

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A BALB/c mouse model of enhanced pulmonary pathology following vaccination with formalin-inactivated alum-adsorbed respiratory syncytial virus (FI-RSV) and live RSV challenge was used to determine the type and kinetics of histopathologic lesions induced and chemokine gene expression profiles in lung tissues. These data were compared and contrasted with data generated following primary and/or secondary RSV infection or RSV challenge following vaccination with a promising subunit vaccine, BBG2Na. Severe peribronchiolitis and perivascularitis coupled with alveolitis and interstitial inflammation were the hallmarks of lesions in the lungs of FI-RSV-primed mice, with peak histopathology evident on days 5 and 9. In contrast, primary RSV infection resulted in no discernible lesions, while challenge of RSV-primed mice resulted in rare but mild peribronchiolitis and perivascularitis, with no evidence of alveolitis or interstitial inflammation. Importantly, mice vaccinated with a broad dose range ( Respiratory syncytial virus (RSV), a Pneumovirus of the family Paramyxoviridae, is a major respiratory pathogen. Infection often results in acute bronchiolitis or pneumonia in infants and young children and can result in persistently abnormal pulmonary function throughout childhood. In addition, adults become reinfected despite enhanced serum antibody responses. Consequently, development of an RSV vaccine is considered a World Health Organization priority. The occurrence of a severe pulmonary disease, characterized by the presence of abnormally numerous inflammatory cells (18), after subsequent natural infection in children given a formalin-inactivated RSV (FI-RSV) vaccine has greatly interfered in the development of a successful and safe RSV vaccine (21).We explored a subunit approach to the development of a RSV vaccine and have described the construction and expression of a RSV (Long strain) G envelope glycoprotein fragment as part of a chimeric protein in Escherichia coli (20,25). The polypeptide of amino acids 130 to 230 of the G protein (G2Na) is fused to BB, the albumin-binding domain of streptococcal protein G, producing BBG2Na. The immune responses induced by BBG2Na demonstrate a potent lung protective efficacy against RSV challenge in both mouse and cotton rat models of RSV infection (25). Importantly, this potent protective efficacy was maintained irrespective of whether BBG2Na was administered intraperitoneally (i.p.), intramuscularly (i.m.) or subcutaneously (s.c.) (15). The G2Na fragment contains at least five murine B-cell protectopes, one of which incorporates a stretch of amino acid residues that are completely conserved among all known RSV subgroup A and B human isolates (9) and all of which overlap with peptide reactivities in human RSV convalescent sera (24). Furthermore, we recently reported that immunizations with BBG2Na do not induce evidence of pulmonary inflammation upon RSV challenge, as demonstrated by the absence of aberrant and massive lung infiltration of macrophages, eosinophils, and T cells (23). ...

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Description of an in vivo model for the assessment of eosinophil chemoattractants in the mouse

Cited by 5 publications

References 17 publications

Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

Contribution of C5‐mediated mechanisms to host defence against Echinococcus granulosus hydatid infection

Differential Histopathology and Chemokine Gene Expression in Lung Tissues following Respiratory Syncytial Virus (RSV) Challenge of Formalin-Inactivated RSV- or BBG2Na-Immunized Mice

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