Different inflammatory stimuli in the footpad of mice influence the kinetics of resident peritoneal cells

Palos, M. C.; Azevedo, M. C. A.; Thies, Felipe Garutti; Osugui, Lika; Álvares, Anuska Marcelino; Laurindo, María Fernanda Lucatelli; Russo, Ricardo T.; Popi, Ana Flávia; Mariano, Mário

doi:10.1007/s00011-012-0514-y

Cited by 7 publications

(6 citation statements)

References 13 publications

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“…However, CD8 + T cells decreased in the peritoneal cavity, suggesting their migration to the site of pathogen proliferation. This finding is in corroboration to previous studies that have already shown cells in the peritoneal cavity to migrate to other sites (Almeida et al, 2001; Palos et al, 2012).…”

Section: Discussionsupporting

confidence: 93%

Cyclophosphamide Treatment Mimics Sub-Lethal Infections With Encephalitozoon intestinalis in Immunocompromised Individuals

et al. 2019

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Microsporidia, including Encephalitozoon intestinalis, are emerging pathogens which cause opportunistic infections in immunocompromised patients, such as those with AIDS, cancer, the elderly and people on immunosuppressive drugs. Intestinal mucosa (IM) is crucial for developing an efficient adaptive immune response against pathogenic micro-organisms, thereby preventing their colonization and subsequent infection. As immunosuppressive drugs affect the intestinal immune response is little known. In the present study, we investigated the immune response to E. intestinalis infection in the IM and gut-associated lymphoid tissue (GALT) in cyclophosphamide (Cy) immunosuppressed mice, to mimic an immunocompromised condition. Histopathology revealed lymphoplasmacytic enteritis at 7 and 14 days-post-infection (dpi) in all infected groups, however, inflammation diminished at 21 and 28 dpi. Cy treatment also led to a higher number of E. intestinalis spores and lesions, which reduced at 28 dpi. In addition, flow cytometry analysis demonstrated CD4+ and CD8+ T cells to be predominant immune cells, with up-regulation in both Th1 and Th2 cytokines at 7 and 14 dpi, as demonstrated by histopathology. In conclusion, Cy treatment reduced GALT (Peyer’s plaques and mesenteric lymph nodes) and peritoneum populations but increased the T-cell population in the intestinal mucosa and the production of pro-and anti-inflammatory cytokines, which were able to eliminate this opportunistic fungus and reduced the E. intestinalis infection.

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Section: Discussionsupporting

confidence: 93%

Cyclophosphamide Treatment Mimics Sub-Lethal Infections With Encephalitozoon intestinalis in Immunocompromised Individuals

et al. 2019

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“…These researchers described a macrophage cell trafficking pathway, that is, the migration of these cells from the peritoneal cavity to a tumour lesion; they demonstrated that in rats subcutaneously inoculated with AK‐5 tumour cells, an influx of immune cells occurs in the peritoneal cavity, with hyperactivation of macrophages and elevated levels of cytokines, NO and O 2 − . Other studies have demonstrated the migration of peritoneal cells to other tissues . In this context, we can infer that our results concerning total and differential numbers of peritoneal lavage cells appear to reflect the changes observed in the footpad with a significant increase in the total number of cells recovered by peritoneal lavage during the infectious process, particularly at 8 months postinoculation compared to control animals.…”

Section: Discussionsupporting

confidence: 72%

Murine experimental leprosy: Evaluation of immune response by analysis of peritoneal lavage cells and footpad histopathology

Vilani-Moreno

Barbosa

Sartori

et al. 2019

Int J Experimental Path

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Summary This study evaluated the immune response of nude and BALB/c mice inoculated in the footpads (FP) with Mycobacterium leprae after 3, 5 and 8 months. At each timepoint peritoneal cells, peripheral blood, FP and popliteal lymph nodes (PLN) were collected. Peritoneal cell cultures were performed to measure the H2O2, O2−, NO, IL‐2, IL‐4, IL‐10, IL‐12, IFN‐γ and TNF levels. Serum levels of anti‐PGL‐I antibodies were also quantified. The results showed that the infection was progressive in nude mice with bacterial multiplication, development of macroscopic lesions in the FP and presence of bacilli in the PLN at 8 months. In BALB/c mice, the infection reached a plateau of bacillary multiplication at 5 months and regressed at 8 months. Histopathological analysis of FP revealed a mononuclear inflammatory infiltrate with a large number of neutrophils at 5 months, with a higher number in nude mice. At 8 months, the number of neutrophils decreased and the infiltrate was predominantly mononuclear in both mouse strains. There was no H2O2, O2−, IL‐2, IL‐4, IL‐10 and IFN‐γ production in the course of infection in nude mice; however, in BALB/c, O2− and IL‐12 production was higher at 5 months and NO, IFN‐γ and TNF production was higher at 8 months when there was a decrease in the number of bacilli. The level of anti‐PGL‐I antibodies was higher in BALB/c mice. Thus, nude and BALB/c mice can be used as experimental models for the study of various aspects of leprosy.

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“…At 60 days post-infection, necrosis had started to progress in L. major infection (Figure B,C). A positive control of inflammation was also analyzed by injecting LPS into the footpad dermis of another set of animals …”

Section: Resultsmentioning

confidence: 99%

Comparative Proteomic Analysis of Murine Cutaneous Lesions Induced by Leishmania amazonensis or Leishmania major

et al. 2019

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Cutaneous leishmaniasisis is the most common clinical form of leishmaniasis and one of the most relevant neglected diseases. It is known that the progress of the disease is species specific and the host's immune response plays an important role in its outcome. However, the pathways that lead to parasite clearance or survival remain unknown. In this work, skin tissue from mice experimentally infected with L. amazonensis, one of the causative agents of cutaneous leishmaniasis in the Amazon region, L. major, another causative agent of cutaneous leishmaniasis in Africa, the Middle East, China, and India, or lipopolysaccharides from Escherichia coli as an inflammation model were investigated using label-free proteomics to unveil Leishmaniaspecific protein alterations. Proteomics is a powerful tool to investigate host−pathogen relationships to address biological questions. In this work, proteins from mice skin biopsies were identified and quantified using nano-LC coupled with tandem mass spectrometry analyses. Integrated Proteomics Pipeline was used for peptide/protein identification and quantification. Western blot was used for validation of protein quantification by mass spectrometry, and protein pathways were predicted using Ingenuity Pathway Analysis. In this proteomics study, several proteins were pointed out as hypothetical targets to guide future studies on Leishmania-specific modulation of proteins in the host. We identified hundreds of exclusively modulated proteins after Leishmania spp. infection and 17 proteins that were differentially modulated in the host after L. amazonensis or L. major infection.

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Different inflammatory stimuli in the footpad of mice influence the kinetics of resident peritoneal cells

Abstract: These data show that cells from the peritoneal cavity are influenced by pathologies in remote regions of the animal. How this novel phenomenon influences overall immune responses, courses of infection and tumor growth are open to further investigation.

Cited by 7 publications

References 13 publications

Cyclophosphamide Treatment Mimics Sub-Lethal Infections With Encephalitozoon intestinalis in Immunocompromised Individuals

Cyclophosphamide Treatment Mimics Sub-Lethal Infections With Encephalitozoon intestinalis in Immunocompromised Individuals

Murine experimental leprosy: Evaluation of immune response by analysis of peritoneal lavage cells and footpad histopathology

Comparative Proteomic Analysis of Murine Cutaneous Lesions Induced by Leishmania amazonensis or Leishmania major

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